Updated on 2025/07/25

写真a

 
KAKITA Akiyoshi
 
Organization
Brain Research Institute Professor
Graduate School of Medical and Dental Sciences Biological Functions and Medical Control Professor
Title
Professor
External link

Degree

  • 医学博士 ( 1993.9   新潟大学 )

Research Areas

  • Life Science / Anatomy and histopathology of nervous system

Research History

  • Niigata University   Brain Research Institute Center for Bioresources Department of Pathological Neuroscience   Professor

    2011.10

  • Niigata University   Graduate School of Medical and Dental Sciences Biomedical Sciences   Professor

    2011.10

  • Niigata University   Graduate School of Medical and Dental Sciences Biological Functions and Medical Control   Professor

    2011.10

  • Niigata University   Brain Research Institute Center for Bioresources Department of Pathological Neuroscience   Associate Professor

    2002.4 - 2011.9

  • Niigata University   Brain Research Institute   Associate Professor

    2000.10 - 2002.3

  • Niigata University   Brain Research Institute   Research Assistant

    1995.11 - 2000.10

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Papers

  • Chemical Landscape for Tissue Clearing based on Hydrophilic Reagents Reviewed

    Kazuki Tainaka, Tatsuya C. Murakam, Etsuo A. Susaki, Chika Shimizu, Rie Saito, Kei Takahashi, Akiko Hayashi-Takagi, Hiroshi Sekiya, Yasunobu Arima, Satoshi Nojima, Masako Ikemura, Tetsuo Ushiku, Yoshihiro Shimizu, Masaaki Murakami, Kenji F. Tanaka, Masamitsu Iino, Haruo Kasai, Toshikuni Sasaoka, Kazuto Kobayashi, Kohei Miyazono, Eiichi Morii, Tadashi Isa, Masashi Fukayama, Akiyoshi Kakita, Hiroki R. Ueda

    Cell Reports   24 ( 8 )   2196 - 2210   2108.8

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Cell Press  

    We describe a strategy for developing hydrophilic chemical cocktails for tissue delipidation, decoloring, refractive index (RI) matching, and decalcification, based on comprehensive chemical profiling. More than 1,600 chemicals were screened by a high-throughput evaluation system for each chemical process. The chemical profiling revealed important chemical factors: salt-free amine with high octanol/water partition-coefficient (logP) for delipidation, N-alkylimidazole for decoloring, aromatic amide for RI matching, and protonation of phosphate ion for decalcification. The strategic integration of optimal chemical cocktails provided a series of CUBIC (clear, unobstructed brain/body imaging cocktails and computational analysis) protocols, which efficiently clear mouse organs, mouse body including bone, and even large primate and human tissues. The updated CUBIC protocols are scalable and reproducible, and they enable three-dimensional imaging of the mammalian body and large primate and human tissues. This strategy represents a future paradigm for the rational design of hydrophilic clearing cocktails that can be used for large tissues.

    DOI: 10.1016/j.celrep.2018.07.056.

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  • Long-Term Clinical Landscapes of Spinal Hypertrophic Pachymeningitis With Anti-Neutrophil Cytoplasmic Antibody–Associated Vasculitis

    Akihiro Nakajima, Mariko Hokari, Fumihiro Yanagimura, Etsuji Saji, Hiroshi Shimizu, Yasuko Toyoshima, Kaori Yanagawa, Musashi Arakawa, Akiko Yokoseki, Takahiro Wakasugi, Kouichirou Okamoto, Kei Watanabe, Keitaro Minato, Yutaka Otsu, Yukiko Nozawa, Daisuke Kobayashi, Kazuhiro Sanpei, Hirotoshi Kikuchi, Shunsei Hirohata, Kazuaki Awamori, Aya Nawata, Mitsunori Yamada, Hitoshi Takahashi, Masatoyo Nishizawa, Hironaka Igarashi, Noboru Sato, Akiyoshi Kakita, Osamu Onodera, Izumi Kawachi

    Neurology   104 ( 8 )   2025.4

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    Publishing type:Research paper (scientific journal)   Publisher:Ovid Technologies (Wolters Kluwer Health)  

    DOI: 10.1212/wnl.0000000000213420

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  • Visualizing epileptogenic regions using the chemical exchange saturation transfer method in a patient with drug-resistant focal epilepsy: a case report

    Yosuke Ito, Masafumi Fukuda, Ken Ohno, Tomoyoshi Ota, Masaki Watanabe, Tsuyoshi Matsuda, Masahiro Hatakeyama, Hiroshi Masuda, Hiroki Kitaua, Akiyoshi Kakita, Hitoshi Shimada, Makoto Oishi, Hironaka Igarashi

    Journal of Medical Case Reports   19 ( 1 )   2025.4

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    Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    DOI: 10.1186/s13256-025-05191-5

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    Other Link: https://link.springer.com/article/10.1186/s13256-025-05191-5/fulltext.html

  • “Chocolate Chip Sign” on Susceptibility-Weighted Imaging

    Shoichiro Ando, Rie Saito, Sho Kitahara, Masahiro Uemura, Yuya Hatano, Masaki Watanabe, Taisuke Kato, Yosuke Ito, Atchayaram Nalini, Tomohiko Ishihara, Shigeo Murayama, Hironaka Igarashi, Akiyoshi Kakita, Osamu Onodera

    Neurology Genetics   11 ( 2 )   2025.4

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    Publishing type:Research paper (scientific journal)   Publisher:Ovid Technologies (Wolters Kluwer Health)  

    DOI: 10.1212/nxg.0000000000200237

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  • Novel Aspects of Hereditary Spastic Paraplegia: A Clinicopathologic and Biochemical Study of a Patient With a Heterozygous GCH1 Variant. International journal

    Shoko Hongo, Tetsuhiko Ikeda, Mari Tada, Rina Aida, Tetsuo Ozawa, Norikazu Hara, Akinori Miyashita, Takashi Nakajima, Osamu Onodera, Takeshi Ikeuchi, Hiroshi Ichinose, Akiyoshi Kakita

    Neuropathology and applied neurobiology   51 ( 1 )   e70006   2025.2

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/nan.70006

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  • Diagnosis of Leptomeningeal Disease in Diffuse Midline Gliomas by Detection of H3F3A K27M Mutation in Circulating Tumor DNA of Cerebrospinal Fluid. International journal

    Satoshi Shibuma, Jotaro On, Manabu Natsumeda, Akihide Koyama, Haruhiko Takahashi, Jun Watanabe, Masaki Mitobe, Satoshi Nakata, Yuki Tanaka, Yoshihiro Tsukamoto, Masayasu Okada, Junichi Yoshimura, Mari Tada, Hiroshi Shimizu, Soichi Oya, Junko Murai, Kouichirou Okamoto, Hiroyuki Kawashima, Akiyoshi Kakita, Makoto Oishi

    Pediatric blood & cancer   e31535   2025.1

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    INTRODUCTION: Leptomeningeal disease (LMD) in diffuse midline gliomas (DMGs) can lead to devastating symptoms such as severe pain, urinary incontinence, and tetraparesis, with limited treatment options. We determined whether detecting H3F3A K27M-mutant droplets in cerebrospinal fluid (CSF) circulating tumor deoxyribonucleic acid (ctDNA) could be a biomarker for detecting LMD in DMGs. METHODS: Twenty-five CSF samples were obtained from 22 DMG patients. Histological confirmation of H3F3A K27M mutation was obtained in 10 (45.5%) cases. ctDNA was extracted from CSF, and H3F3A K27M-mutant and wildtype droplets were detected using digital droplet polymerase chain reaction (ddPCR). LMD was diagnosed by CSF cytology and pre- and post-contrast head and spine magnetic resonance (MR) imaging. RESULTS: The number of H3F3A K27M-mutant droplets (median 27 [range: 1-379] vs. median 0 [range: 0-1]; p < 0.0001) and variant allele frequency (VAF) (median 48.9% [range: 7.5%-87.5%] vs. median 0.0% [range: 0.0%-50.0%]; p < 0.0001) were significantly higher in the LMD/early-LMD group compared to no-LMD group. In two cases (Cases 4 and 11) without clinical evidence of LMD, multiple H3F3A K27M-mutant droplets were detected in CSF ctDNA. In those cases, extensive spinal dissemination was detected 6 months after the initial liquid biopsy. One case (Case 15) with high Schlafen11 (SLFN11) expression responded well to treatment for LMD and survived for 532 days after the diagnosis of LMD. CONCLUSION: This study provides evidence that detecting H3F3A K27M-mutant droplets in CSF ctDNA is diagnostic for LMD and is more sensitive than traditional methods such as CSF cytology and MR imaging.

    DOI: 10.1002/pbc.31535

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  • Girdin deficiency causes developmental and epileptic encephalopathy with hippocampal sclerosis and interneuronopathy

    Machiko Iida, Motoki Tanaka, Tsuyoshi Takagi, Tohru Matsuki, Kimihiro Kimura, Kazuki Shibata, Yohei Kobayashi, Yuka Mizutani, Haruki Kuwamura, Keitaro Yamada, Hiroki Kitaura, Akiyoshi Kakita, Mayu Sakakibara, Naoya Asai, Masahide Takahashi, Masato Asai

    Epilepsia   2024.12

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Wiley  

    Abstract

    Objective

    Loss‐of‐function mutations in the GIRDIN/CCDC88A gene cause developmental epileptic encephalopathy (DEE) in humans. However, its pathogenesis is largely unknown. Global knockout mice of the corresponding orthologous gene (gKOs) have a preweaning lethal phenotype with growth failure, preventing longitudinal analysis. We aimed to overcome this lethality and elucidate DEE pathogenesis.

    Methods

    We developed a novel lifelong feeding regimen (NLFR), which consists of providing mash food from postnatal day 14 (P14) until weaning (P28), followed by agar‐bound food exclusively after weaning. Videography, electroencephalography (EEG), and histological analyses were performed. Conditional Girdin/Ccdc88a knockout mice (cKOs) of variable lineages (Nestin, Emx1, or Nkx2‐1) were generated to identify the region responsible for epilepsy.

    Results

    Under the NLFR, gKOs survived beyond 1 year and displayed fully penetrant, robust epileptic phenotypes, including early‐onset (P22.3 in average) generalized tonic–clonic seizures (GTCSs) (averaging eight per day), which were completely synchronized with fast rhythms on EEG, frequent interictal electroencephalographic spikes (averaging 430 per hour), and progressive deformation of visceral organs. In addition, gKOs had absence seizures, which were not always time‐locked to frequent spike waves on EEG. The frequent GTCSs and interictal spikes in gKOs were suppressed by known antiepileptic drugs. Histologically, bilateral hippocampi in gKOs exhibited congenital cornu‐ammonis splitting, granule cell dispersion, and astrogliosis. Furthermore, analysis of conditional knockouts using multiple Cre‐deleters identified a defect in the delivery of interneuron precursors from the medial ganglionic eminence into the hippocampal primordium during embryogenesis as a major cause of epileptogenesis.

    Significance

    These findings give rise to a new approach of lifelong caregiving to overcome the problem of preweaning lethality in animal models. We propose a useful model for studying DEE with hippocampal sclerosis and interneuronopathy. gKOs with NLFR combine the contradictory properties of robust epileptic phenotypes and long‐term survivability, which can be used to investigate spontaneous epileptic wave propagation and therapeutic intervention in hippocampal sclerosis.

    DOI: 10.1111/epi.18204

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  • Blood–brain barrier dysfunction in multiple system atrophy: A human postmortem study

    Ramil Gabdulkhaev, Hiroshi Shimizu, Masato Kanazawa, Yasuko Kuroha, Arika Hasegawa, Jiro Idezuka, Kazuki Tainaka, Osamu Onodera, Akiyoshi Kakita

    Neuropathology   2024.12

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    Multiple system atrophy (MSA) is a rare neurodegenerative disease characterized by an accumulation of phosphorylated α‐synuclein (p‐αsyn) in oligodendrocytes in the form of glial cytoplasmic inclusions (GCIs). In MSA, not only mature oligodendrocytes but also oligodendrocyte precursor cells (OPCs) are affected. The latter play an important role in remyelination by differentiating into mature oligodendrocytes, as well as maintaining the blood–brain barrier (BBB) by promoting the expression of tight junction proteins. We have hypothesized that in MSA, the BBB is impaired as a result of aberrant interactions between affected OPCs and the cerebral vasculature. To verify this hypothesis, we conducted a neuropathological examination of postmortem brains from MSA patients and control subjects, focusing on the primary motor area, one of the main regions affected in MSA. Using double immunofluorescence, we quantified the expression of tight junction protein claudin‐5 in capillary endothelial cells and found that it was significantly lower in MSA than in controls in both the gray matter and white matter. Furthermore, a significantly higher amount of fibrinogen was extravasated into the brain parenchyma in MSA patients than in controls. In addition, leakage of IgG was detected almost specifically in MSA brain parenchyma, as visualized in three dimensions by combining techniques of chemical tissue clearing and light sheet microscopy. Finally, we confirmed accumulation of p‐αsyn‐positive GCIs along the cerebral vasculature within OPCs. These results suggest that BBB dysfunction and associated fibrinogen extravasation are constant findings in MSA, presumably triggered by the deposition of p‐αsyn in perivascular OPCs.

    DOI: 10.1111/neup.13021

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  • Distinct tau pathologies in the nucleus basalis of Meynert between early-onset and late-onset Alzheimer's disease patients revealed by positron emission tomography. Reviewed International journal

    Hisaomi Suzuki, Kenji Tagai, Maiko Ono, Hiroshi Shimizu, Hironobu Endo, Hideki Matsumoto, Manabu Kubota, Yuko Kataoka, Sho Moriguchi, Shin Kurose, Masanori Ichihashi, Hitoshi Shinotoh, Kiwamu Matsuoka, Naomi Kokubo, Harutsugu Tatebe, Sayo Matsuura, Yasuharu Yamamoto, Yuki Momota, Kazunori Kawamura, Ming-Rong Zhang, Yuhei Takado, Hitoshi Shimada, Takahiko Tokuda, Mitsumoto Onaya, Masaru Mimura, Akiyoshi Kakita, Naruhiko Sahara, Hiroyuki Uchida, Makoto Higuchi, Keisuke Takahata

    Journal of Alzheimer's disease : JAD   13872877241297382 - 13872877241297382   2024.11

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    BACKGROUND: Tau accumulation in the nucleus basalis of Meynert (nbM) has been documented in Alzheimer's disease (AD), but its relationship to neuropathological changes in other brain regions and cognitive deficits remains unclear, particularly between early-onset AD (EOAD) and late-onset AD (LOAD). OBJECTIVE: To evaluate tau accumulation patterns in the nbM and other brain regions in EOAD and LOAD using 18F-florzolotau PET and examine correlations with cognitive function. METHODS: Thirty-eight amyloid-positive AD patients (15 EOAD, 23 LOAD) and 46 healthy controls underwent 18F-florzolotau PET. Tau levels were quantified in the nbM and Braak-staging regions. Postmortem brain samples were examined to assess 18F-florzolotau binding to tau deposits. RESULTS: EOAD showed a higher overall tau burden, including in the nbM, compared with LOAD. However, nbM tau levels correlated more strongly with cognitive decline in LOAD than EOAD. The relationship between nbM tau and neocortical tau differed between EOAD and LOAD. Histopathology revealed abundant 18F-florzolotau labeling of neurofibrillary tangles (NFTs) and ghost tangles in AD nbM samples. CONCLUSIONS: This study provides the first in vivo PET evidence of differential nbM tau pathology between EOAD and LOAD, with higher accumulation but weaker correlation to cognition in EOAD. The distinct relationships between nbM and cortical tau in EOAD and LOAD suggest divergent pathological trajectories. 18F-florzolotau PET successfully visualized NFTs and extracellular ghost tangles in the nbM across AD stages. These findings highlight the importance of considering age of onset when evaluating tau pathology and its clinical correlates in AD.

    DOI: 10.1177/13872877241297382

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  • SMN2 gene copy number affects the incidence and prognosis of motor neuron diseases in Japan

    Tomohiko Ishihara, Akihide Koyama, Naoki Atsuta, Mari Tada, Saori Toyoda, Kenta Kashiwagi, Sachiko Hirokawa, Yuya Hatano, Akio Yokoseki, Ryoichi Nakamura, Genki Tohnai, Yuishin Izumi, Ryuji Kaji, Mitsuya Morita, Asako Tamura, Osamu Kano, Masashi Aoki, Satoshi Kuwabara, Akiyoshi Kakita, Gen Sobue, Osamu Onodera

    BMC Medical Genomics   17 ( 1 )   2024.11

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    Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    DOI: 10.1186/s12920-024-02026-y

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    Other Link: https://link.springer.com/article/10.1186/s12920-024-02026-y/fulltext.html

  • Surgical outcome and contributing presurgical evaluations in children with magnetic resonance imaging-negative epilepsy and periodic seizure cycles Reviewed

    Yoshihiko Saito, Kenji Sugai, Masaki Iwasaki, Noriko Sato, Akiyoshi Kakita, Yuko Saito, Taisuke Ohtsuki, Masayuki Sasaki

    Epilepsy Research   2024.11

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    DOI: 10.1016/j.eplepsyres.2024.107492

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  • Indications for a brain biopsy in neurological diseases of unknown etiology: The role of magnetic resonance imaging findings and liquid biopsy in yielding definitive pathological diagnoses. International journal

    Toshiya Kizaki, Masato Kanazawa, Takanobu Ishiguro, Manabu Natsumeda, Mari Tada, Hiroshi Shimizu, Kouichirou Okamoto, Makoto Oishi, Akiyoshi Kakita, Yukihiko Fujii, Osamu Onodera

    Journal of the neurological sciences   463   123150 - 123150   2024.8

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    Brain biopsies are often considered for patients who cannot be diagnosed with various laboratory test results. However, physicians tend to be hesitant regarding their application in possibly non-neoplastic brain diseases, due to the invasiveness and risks. The aim was to determine the indications for brain biopsies in cases of neurological diseases of unknown etiology. We retrospectively evaluated diagnostic accuracy, laboratory findings (including a liquid biopsy for malignant lymphoma), magnetic resonance imaging (MRI) characteristics and the post-treatment outcomes of patients undergoing brain biopsies for neurological diseases of unknown etiology. The data of patients who had undergone a brain biopsy during their admission to Niigata University Hospital, between 2011 and 2024, were reviewed. Moreover, the laboratory data and MRI findings between patients with definitive and nonspecific biopsy diagnoses were compared. Twenty-six patients underwent a brain biopsy, and a definitive diagnosis was obtained in 14 patients (53.8%). Even in cases where a nonspecific diagnosis was made, biopsy findings helped rule out malignancy and guide clinical diagnosis and treatment decisions. The liquid biopsy for malignant lymphoma was performed in eight patients, with one yielding a positive result, consistent with primary central nervous system lymphoma. The sensitivity and specificity of liquid biopsy were 0.5 and 1, respectively. Diffusely contrasted cortical lesions and the presence of mass effects on MRI, were significantly associated with a definitive diagnosis, compared to a nonspecific diagnosis. In conclusion, brain MRI and liquid biopsies can assist in determining the appropriate indications for brain biopsies in neurological diseases of unknown etiology.

    DOI: 10.1016/j.jns.2024.123150

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  • 難治性てんかんとしての海馬硬化症における神経成長関連タンパク質のリン酸化解析

    岡田 正康, 北浦 弘樹, 柿田 明美, 大石 誠, 五十嵐 道弘

    JSBMS Letters   49 ( Suppl. )   112 - 112   2024.8

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    Language:Japanese   Publisher:(一社)日本医用マススペクトル学会  

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  • Primary spinal cord gliomas: Pathologic features associated with prognosis. International journal

    Yuki Tanaka, Manabu Natsumeda, Masayuki Ohashi, Rie Saito, Nayuta Higa, Toshiaki Akahane, Hideki Hashidate, Junko Ito, Satoshi Fujii, Atsushi Sasaki, Akihide Tanimoto, Ryosuke Hanaya, Kei Watanabe, Makoto Oishi, Hiroyuki Kawashima, Akiyoshi Kakita

    Journal of neuropathology and experimental neurology   2024.7

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    Primary spinal cord gliomas are rare and are associated with high mortality. Unlike brain tumors, the clinicopathological features of spinal cord gliomas are not well defined. We analyzed clinical, histopathology, and immunohistochemical features and overall survival (OS) of 25 patients with primary spinal cord gliomas treated between 1994 and 2023 at 4 institutions. IDH1 R132H, H3K27M, and p53 were assessed by immunohistochemistry (IHC). Four (16%), 5 (20%), 2 (8%), and 13 (52%) patients were diagnosed as having grades 1, 2, 3, and 4 gliomas according to the World Health Organization (WHO) 2021 classification, respectively. One case (4%), with a circumscribed diffuse midline glioma, H3K27-altered, had a rare molecular profile and could not be graded. IHC demonstrated H3K27M positivity, indicative of H3F3A K27M or HIST1H3B K27M mutation, in 9 (36%) patients. H3K27me3-loss was evident in 13 (52%) patients. In one patient with a grade 1 tumor that showed negative staining for H3K27M and H3K27me3 loss, numbers of EZHIP-positive cells were increased, suggesting diffuse midline glioma, H3K27-altered (WHO grade 4). H3K27me3 loss, frequency of p53 positive cells (≥10%), MIB-1 index (≥10%), and high histopathological grades significantly correlated with poor OS. These results indicate the pathological and immunohistochemical characteristics of primary spinal cord gliomas that impact prognosis.

    DOI: 10.1093/jnen/nlae084

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  • Inherited C-terminal TREX1 variants disrupt homology-directed repair to cause senescence and DNA damage phenotypes in Drosophila, mice, and humans

    Samuel D. Chauvin, Shoichiro Ando, Joe A. Holley, Atsushi Sugie, Fang R. Zhao, Subhajit Poddar, Rei Kato, Cathrine A. Miner, Yohei Nitta, Siddharth R. Krishnamurthy, Rie Saito, Yue Ning, Yuya Hatano, Sho Kitahara, Shin Koide, W. Alexander Stinson, Jiayuan Fu, Nehalee Surve, Lindsay Kumble, Wei Qian, Oleksiy Polishchuk, Prabhakar S. Andhey, Cindy Chiang, Guanqun Liu, Ludovic Colombeau, Raphaël Rodriguez, Nicolas Manel, Akiyoshi Kakita, Maxim N. Artyomov, David C. Schultz, P. Toby Coates, Elisha D. O. Roberson, Yasmine Belkaid, Roger A. Greenberg, Sara Cherry, Michaela U. Gack, Tristan Hardy, Osamu Onodera, Taisuke Kato, Jonathan J. Miner

    Nature Communications   15 ( 1 )   2024.6

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    Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    Abstract

    Age-related microangiopathy, also known as small vessel disease (SVD), causes damage to the brain, retina, liver, and kidney. Based on the DNA damage theory of aging, we reasoned that genomic instability may underlie an SVD caused by dominant C-terminal variants in TREX1, the most abundant 3′−5′ DNA exonuclease in mammals. C-terminal TREX1 variants cause an adult-onset SVD known as retinal vasculopathy with cerebral leukoencephalopathy (RVCL or RVCL-S). In RVCL, an aberrant, C-terminally truncated TREX1 mislocalizes to the nucleus due to deletion of its ER-anchoring domain. Since RVCL pathology mimics that of radiation injury, we reasoned that nuclear TREX1 would cause DNA damage. Here, we show that RVCL-associated TREX1 variants trigger DNA damage in humans, mice, and Drosophila, and that cells expressing RVCL mutant TREX1 are more vulnerable to DNA damage induced by chemotherapy and cytokines that up-regulate TREX1, leading to depletion of TREX1-high cells in RVCL mice. RVCL-associated TREX1 mutants inhibit homology-directed repair (HDR), causing DNA deletions and vulnerablility to PARP inhibitors. In women with RVCL, we observe early-onset breast cancer, similar to patients with BRCA1/2 variants. Our results provide a mechanistic basis linking aberrant TREX1 activity to the DNA damage theory of aging, premature senescence, and microvascular disease.

    DOI: 10.1038/s41467-024-49066-7

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    Other Link: https://www.nature.com/articles/s41467-024-49066-7

  • Pharmacological evaluation of E2730, a novel selective uncompetitive GAT1 inhibitor, on epileptiform activities in resected brain tissues from human focal cortical dysplasia ex vivo. International journal

    Hiroki Kitaura, Kazuyuki Fukushima, Masafumi Fukuda, Yosuke Ito, Akiyoshi Kakita

    Epilepsy research   202   107364 - 107364   2024.5

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    Focal cortical dysplasia (FCD) is an important etiology of focal epilepsy in children and adults. However, only a few preclinical models sufficiently reproduce the characteristic histopathologic features of FCD. To improve the success rate of clinical trials for antiseizure medications (ASMs) in patients with FCD, more human-relevant preclinical models are needed, and epileptic foci resected from patients are a powerful tool for this purpose. Here, we conducted ex vivo studies using epileptic foci resected from patients with FCD type II to evaluate the pharmacologic effects of the ASM candidate E2730, a selective uncompetitive inhibitor of γ-aminobutyric acid transporter 1. We used the same ex vivo assay system to assess carbamazepine (CBZ), an ASM often prescribed for focal epilepsy, as a reference. At the higher dose tested (200 µM), both E2730 and CBZ suppressed spontaneous epileptiform activities almost completely. At the lower dose (100 µM), CBZ reduced the area of brain tissue showing epileptiform activity, whereas E2730 significantly decreased the number of epileptiforms. These findings suggest that E2730-both as a single agent and in combination with CBZ-merits evaluation in clinical trials involving patients with FCD.

    DOI: 10.1016/j.eplepsyres.2024.107364

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  • 頭蓋骨転移した胸部SMARCA4欠損未分化腫瘍の1例

    渋間 啓, 西田 京香, 小倉 良介, 岡田 正康, 棗田 学, 加藤 卓, 梅津 哉, 大石 誠, 柿田 明美

    Brain Tumor Pathology   41 ( Suppl. )   159 - 159   2024.5

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    Language:Japanese   Publisher:日本脳腫瘍病理学会  

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  • 間脳下垂体腫瘍病理診断の現状と治療:PitNETを含め 機能性PitNETの治療中に転移を来たし,下垂体転写因子の有無で鑑別した2症例の経験

    岡田 正康, 棗田 学, 塚本 佳広, 梅津 哉, 柿田 明美, 大石 誠

    Brain Tumor Pathology   41 ( Suppl. )   079 - 079   2024.5

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  • Stage-dependent immunity orchestrates AQP4 antibody-guided NMOSD pathology: a role for netting neutrophils with resident memory T cells in situ

    Akihiro Nakajima, Fumihiro Yanagimura, Etsuji Saji, Hiroshi Shimizu, Yasuko Toyoshima, Kaori Yanagawa, Musashi Arakawa, Mariko Hokari, Akiko Yokoseki, Takahiro Wakasugi, Kouichirou Okamoto, Hirohide Takebayashi, Chihiro Fujii, Kyoko Itoh, Yo-ichi Takei, Shinji Ohara, Mitsunori Yamada, Hitoshi Takahashi, Masatoyo Nishizawa, Hironaka Igarashi, Akiyoshi Kakita, Osamu Onodera, Izumi Kawachi

    Acta Neuropathologica   147 ( 1 )   2024.4

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    Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    DOI: 10.1007/s00401-024-02725-x

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    Other Link: https://link.springer.com/article/10.1007/s00401-024-02725-x/fulltext.html

  • Recent advances in liquid biopsy of central nervous system lymphomas: case presentations and review of the literature

    Manabu Natsumeda, Satoshi Shibuma, Haruhiko Takahashi, Jotaro On, Yoshihiro Mouri, Kaoru Tomikawa, Hidemoto Fujiwara, Jun Watanabe, Yoshihiro Tsukamoto, Masayasu Okada, Rui Takeda, Hiroshi Shimizu, Jun Takizawa, Akiyoshi Kakita, Makoto Oishi

    Brain Tumor Pathology   41 ( 2 )   85 - 91   2024.4

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    Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    DOI: 10.1007/s10014-024-00483-y

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  • Acute respiratory failure caused by brainstem demyelinating lesions in an older patient with an atypical relapsing autoimmune disorder

    Shoko Hongo, Hiroshi Shimizu, Etsuji Saji, Akihiro Nakajima, Kouichirou Okamoto, Izumi Kawachi, Osamu Onodera, Akiyoshi Kakita

    Neuropathology   2024.4

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    An 84‐year‐old man presented with somnolence, dysphagia, and right hemiplegia, all occurring within a month, approximately one year after initial admission due to subacute, transient cognitive decline suggestive of acute disseminated encephalomyelitis involving the cerebral white matter. Serial magnetic resonance imaging (MRI) studies over that period revealed three high‐intensity signal lesions on fluid‐attenuated inversion recovery images, appearing in chronological order in the left upper and left lower medulla oblongata and left pontine base. Despite some clinical improvement following methylprednisolone pulse therapy, the patient died of respiratory failure. Autopsy revealed four fresh, well‐defined lesions in the brainstem, three of which corresponded to the lesions detected radiologically. The remaining lesion was located in the dorsal medulla oblongata and involved the right solitary nucleus. This might have appeared at a later disease stage, eventually causing respiratory failure. Histologically, all four lesions showed loss of myelin, preservation of axons, and infiltration of lymphocytes, predominantly CD8‐positive T cells, consistent with the histological features of autoimmune demyelinating diseases, particularly the confluent demyelination observed in the early and acute phases of multiple sclerosis (MS). In the cerebral white matter, autoimmune demyelination appeared superimposed on ischemic changes, consistent with the cerebrospinal fluid (CSF) and MRI findings on initial admission. No anti‐AQP4 or MOG antibodies or those potentially causing autoimmune encephalitis/demyelination were detected in either the serum or CSF. Despite several similarities to MS, such as the relapsing–remitting disease course and lesion histology, the entire clinicopathological picture in the present patient, especially the advanced age at onset and development of brainstem lesions in close proximity within a short time frame, did not fit those of MS or other autoimmune diseases that are currently established. The present results suggest that exceptionally older individuals can be affected by an as yet unknown inflammatory demyelinating disease of the CNS.

    DOI: 10.1111/neup.12976

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  • Availability of individual proteins for quantitative analysis in postmortem brains preserved in two different brain banks

    Atsuko Nagaoka, Mizuki Hino, Ryuta Izumi, Risa Shishido, Miki Ishibashi, Masataka Hatano, Makoto Sainouchi, Akiyoshi Kakita, Hiroaki Tomita, Yasuto Kunii

    Neuropsychopharmacology Reports   2024.4

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    Abstract

    Aim

    Postmortem brain research is necessary for elucidating the pathology of schizophrenia; an increasing number of studies require a combination of suitable tissue samples preserved at multiple brain banks. In this study, we examined whether a comparative study of protein expression levels can be conducted using postmortem brain samples preserved in different facilities.

    Methods

    We compared the demographic factors of postmortem brain samples preserved in two institutions and measured and compared the expression levels of glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) and glial fibrillary acidic protein (GFAP) in the prefrontal cortex and superior temporal gyrus. GAPDH is generally used as a loading control for western blotting, and GFAP is considered as an astrocyte marker in the brain.

    Results

    We found significant differences between the two institutions in postmortem interval, age at death, and preservation time. To reduce the effects of these differences on our measurements, the parameters were set as covariates in our analyses of covariance. Subsequently, no differences in GAPDH and GFAP expression were found between institutions.

    Conclusions

    When studies are conducted using brain samples preserved in different brain banks, differences in demographic factors should be carefully considered and taken into account by statistical methods to minimize their impact as much as possible. Since there was no significant difference in the protein expression levels of GAPDH and GFAP in either region between the two institutions that preserved the postmortem brains, we concluded that it is possible to perform protein quantitative analysis assuming that there is no effect of difference between two institutions.

    DOI: 10.1002/npr2.12430

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  • 神経皮膚黒色症剖検例における多領域ゲノム解析

    高橋 陽彦, 棗田 学, 塚本 佳広, 岡田 正康, 原 範和, 小山 哲秀, 宮下 哲典, 結城 明彦, 清水 宏, 柿田 明美, 池内 健, 大石 誠

    小児の脳神経   49 ( 2 )   228 - 228   2024.4

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  • 神経皮膚黒色症剖検例における多領域ゲノム解析

    高橋 陽彦, 棗田 学, 塚本 佳広, 岡田 正康, 原 範和, 小山 哲秀, 宮下 哲典, 結城 明彦, 清水 宏, 柿田 明美, 池内 健, 大石 誠

    小児の脳神経   49 ( 2 )   228 - 228   2024.4

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  • Successful Multimodal Treatment of Intracranial Growing Teratoma Syndrome with Malignant Features. International journal

    Daiken Satake, Manabu Natsumeda, Kaishi Satomi, Mari Tada, Taro Sato, Noritaka Okubo, Keita Kawabe, Haruhiko Takahashi, Yoshihiro Tsukamoto, Masayasu Okada, Masakazu Sano, Haruko Iwabuchi, Nao Shibata, Masaru Imamura, Chihaya Imai, Hirokazu Takami, Koichi Ichimura, Ryo Nishikawa, Hajime Umezu, Akiyoshi Kakita, Makoto Oishi

    Current oncology (Toronto, Ont.)   31 ( 4 )   1831 - 1838   2024.3

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    Molecular analysis of the growing teratoma syndrome has not been extensively studied. Here, we report a 14-year-old boy with a growing mass during treatment for a mixed germ cell tumor of the pineal region. Tumor markers were negative; thus, growing teratoma syndrome was suspected. A radical resection via the occipital transtentorial approach was performed, and histopathological examination revealed a teratoma with malignant features. Methylation classifier analysis confirmed the diagnosis of teratoma, and DMRT1 loss and 12p gain were identified by copy number variation analysis, potentially elucidating the cause of growth and malignant transformation of the teratoma. The patient remains in remission after intense chemoradiation treatment as a high-risk germ cell tumor.

    DOI: 10.3390/curroncol31040138

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  • The cycad genotoxin methylazoxymethanol, linked to Guam ALS/PDC, induces transcriptional mutagenesis. International journal

    Bert M Verheijen, Claire Chung, Ben Thompson, Hyunjin Kim, Asa Nakahara, Jasper J Anink, James D Mills, Jeong H Lee, Eleonora Aronica, Kiyomitsu Oyanagi, Akiyoshi Kakita, Jean-Francois Gout, Marc Vermulst

    Acta neuropathologica communications   12 ( 1 )   30 - 30   2024.2

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  • Marked alteration of phosphoinositide signaling‐associated molecules in postmortem prefrontal cortex with bipolar disorder

    Mizuki Hino, Yasuto Kunii, Risa Shishido, Atsuko Nagaoka, Junya Matsumoto, Hiroyasu Akatsu, Yoshio Hashizume, Hideki Hayashi, Akiyoshi Kakita, Hiroaki Tomita, Hirooki Yabe

    Neuropsychopharmacology Reports   2024.1

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    Abstract

    Aim

    The etiology of bipolar disorder (BD) remains unknown; however, lipid abnormalities in BD have received increasing attention in recent years. In this study, we examined the expression levels of enzyme proteins associated with the metabolic pathway of phosphoinositides (PIs) and their downstream effectors, protein kinase B (Akt1) and glycogen synthase kinase 3β (GSK3β), which have been assumed to be the targets of mood stabilizers such as lithium, in the postmortem brains of patients with BD.

    Methods

    The protein expression levels of phosphatidylinositol 4‐phosphate 5‐kinase type‐1 gamma (PIP5K1C), phosphatidylinositol 4‐kinase alpha (PIK4CA), phosphatase and tensin homolog deleted from chromosome 10 (PTEN), Akt1, and GSK3β were measured using enzyme‐linked immunosorbent assays and multiplex fluorescent bead‐based immunoassays in the prefrontal cortex (PFC). Specifically, PTEN, Akt1, GSK3β, and PIP5K1C were measured in seven BD patients and 48 controls. Additionally, PIK4CA was analyzed in 10 cases and 34 controls.

    Results

    PTEN expression levels were markedly decreased in the PFCs of patients with BD, whereas those of Akt and GSK3β were prominently elevated. Moreover, patients medicated with lithium exhibited higher Akt1 expression levels and lower PTEN expression levels in comparison with the untreated group.

    Conclusion

    Our results suggest that the expression levels of Akt1/GSK3β and its upstream regulator PTEN are considerably altered.

    DOI: 10.1002/npr2.12409

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  • Missense mutation of NRAS is associated with malignant progression in neurocutaneous melanosis. International journal

    Haruhiko Takahashi, Manabu Natsumeda, Norikazu Hara, Akihide Koyama, Hiroshi Shimizu, Akinori Miyashita, Daiken Satake, Yoshihiro Mouri, Jun Tsukano, Keita Kawabe, Yoshihiro Tsukamoto, Masayasu Okada, Ryosuke Ogura, Akihiko Yuki, Hajime Umezu, Akiyoshi Kakita, Takeshi Ikeuchi, Makoto Oishi

    Acta neuropathologica communications   12 ( 1 )   14 - 14   2024.1

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    Neurocutaneous melanosis (NCM) is a rare congenital neurocutaneous syndrome characterized by congenital melanocytic nevus of skin and abnormal proliferation of leptomeningeal melanocytes. Early acquisition of post-zygotic somatic mutations has been postulated to underlie the pathogenesis of NCM. The pathogenesis of NCM remains to be fully elucidated, and treatment options have not been established. Here, we report for the first time, multiregional genomic analyses in a 3-year-old autopsied girl with leptomeningeal melanomatosis associated with NCM, in which a ventriculo-peritoneal (VP) shunt was inserted for the treatment of hydrocephalus. The patient expired six months after the onset due to respiratory failure caused by abdominal dissemination via VP shunt. We performed multiregional exome sequencing to identify genomic differences among brain and abdominal tumors, nevus, and normal tissues. A total of 87 somatic mutations were found in 71 genes, with a significantly large number of gene mutations found in the tumor site. The genetic alterations detected in the nevus were only few and not shared with other sites. Three mutations, namely GNAQ R183Q, S1PR3 G89S and NRAS G12V, considered pathogenic, were found, although S1PR3 mutations have not been previously reported in melanocytic tumors. GNAQ and S1PR3 mutations were shared in both tumor and normal sites. Moreover, the mutant allele frequencies of the two mutations were markedly higher in tumor sites than in normal sites, with copy-neutral loss-of-heterozygosity (CN-LOH) occurring in tumor. NRAS mutation was found only in the abdominal tumor and was thought to be responsible for malignant progression in the present case. Multiregional comprehensive genetic analysis may lead to discovering novel driver mutations associated with tumorigenesis and targeted therapy.

    DOI: 10.1186/s40478-024-01723-0

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  • Reliable detection of genetic alterations in cyst fluid DNA for the diagnosis of brain tumors. International journal

    Jotaro On, Manabu Natsumeda, Haruhiko Takahashi, Akihide Koyama, Satoshi Shibuma, Nao Shibata, Jun Watanabe, Shoji Saito, Yu Kanemaru, Yoshihiro Tsukamoto, Masayasu Okada, Ryosuke Ogura, Takeyoshi Eda, Mari Tada, Hiroshi Shimizu, Jun-Ichi Adachi, Kazuhiko Mishima, Ryo Nishikawa, Akiyoshi Kakita, Makoto Oishi

    Journal of neuro-oncology   2024.1

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    PURPOSE: Liquid biopsy of cyst fluid in brain tumors has not been extensively studied to date. The present study was performed to see whether diagnostic genetic alterations found in brain tumor tissue DNA could also be detected in cell-free DNA (cfDNA) of cyst fluid in cystic brain tumors. METHODS: Cyst fluid was obtained from 22 patients undergoing surgery for a cystic brain tumor with confirmed genetic alterations in tumor DNA. Pathological diagnoses based on WHO 2021 classification and diagnostic alterations in the tumor DNA, such as IDH1 R132H and TERT promoter mutation for oligodendrogliomas, were detected by Sanger sequencing. The same alterations were analyzed by both droplet digital PCR (ddPCR) and Sanger sequencing in cyst fluid cfDNA. Additionally, multiplex ligation-dependent probe amplification (MLPA) assays were performed to assess 1p/19q status, presence of CDKN2A loss, PTEN loss and EGFR amplification, to assess whether differentiating between astrocytomas and oligodendrogliomas and grading is possible from cyst fluid cfDNA. RESULTS: Twenty-five genetic alterations were found in 22 tumor samples. All (100%) alterations were detected in cyst fluid cfDNA by ddPCR. Twenty of the 25 (80%) alterations were also detected by Sanger sequencing of cyst fluid cfDNA. Variant allele frequency (VAF) in cyst fluid cfDNA was comparable to that of tumor DNA (R = 0.62, Pearson's correlation). MLPA was feasible in 11 out of 17 (65%) diffuse gliomas, with close correlation of results between tumor DNA and cyst fluid cfDNA. CONCLUSION: Cell-free DNA obtained from cyst fluid in cystic brain tumors is a reliable alternative to tumor DNA when diagnosing brain tumors.

    DOI: 10.1007/s11060-023-04555-5

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  • Multi-omics analyses of choroid plexus carcinoma cell lines reveal potential targetable pathways and alterations. International journal

    Dina Hesham, Jotaro On, Nouran Alshahaby, Nada Amer, Sameh Magdeldin, Masayasu Okada, Yoshihiro Tsukamoto, Tetsuya Hiraishi, Chihaya Imai, Shujiro Okuda, Toshifumi Wakai, Akiyoshi Kakita, Makoto Oishi, Shahenda El-Naggar, Manabu Natsumeda

    Journal of neuro-oncology   166 ( 1 )   27 - 38   2024.1

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    PURPOSE: Choroid plexus carcinomas (CPCs) are extremely rare brain tumors and carry a dismal prognosis. Treatment options are limited and there is an urgent need to develop models to further research. In the present study, we established two CPC cell lines and performed multi-omics analyses. These cell lines serve as valuable models to propose new treatments in these rare but deadly brain tumors. METHODS: Multi-omic profiling including, (i) methylation array (EPIC 850 K), (ii) whole genome sequencing (WGS), (iii) CANCERPLEX cancer genome panel testing, (iv) RNA sequencing (RNA-seq), and (v) proteomics analyses were performed in CCHE-45 and NGT131 cell lines. RESULTS: Both cell lines were classified as methylation class B. Both harbored pathogenic TP53 point mutations; CCHE-45 additionally displayed TP53 loss. Furthermore, alterations of the NOTCH and WNT pathways were also detected in both cell lines. Two protein-coding gene fusions, BZW2-URGCP, and CTTNBP2-ERBB4, mutations of two oncodrivers, GBP-4 and KRTAP-12-2, and several copy number alterations were observed in CCHE-45, but not NGT131. Transcriptome and proteome analysis identified shared and unique signatures, suggesting that variability in choroid plexus carcinoma tumors may exist. The discovered difference's importance and implications highlight the possible diversity of choroid plexus carcinoma and call for additional research to fully understand disease pathogenesis. CONCLUSION: Multi-omics analyses revealed that the two choroid plexus carcinoma cell lines shared TP53 mutations and other common pathway alterations and activation of NOTCH and WNT pathways. Noticeable differences were also observed. These cell lines can serve as valuable models to propose new treatments in these rare but deadly brain tumors.

    DOI: 10.1007/s11060-023-04484-3

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  • Case report: Progressive multifocal leukoencephalopathy co-occurring with neurosarcoidosis: early brain biopsy and appropriate therapy for PML resulted in a favorable prognosis. International journal

    Qiannan Wang, Shintaro Tsuboguchi, Kouichirou Okamoto, Mari Tada, Akiyoshi Kakita, Kazuo Nakamichi, Makoto Oishi, Masato Kanazawa, Osamu Onodera

    Frontiers in immunology   15   1447992 - 1447992   2024

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    Progressive multifocal leukoencephalopathy (PML) is a rare central nervous system disease caused by JC virus (JCV) infection. Human immunodeficiency virus (HIV) infection is the greatest risk factor for PML. Other immunological diseases, including systemic sarcoidosis, have also been reported as risk factors for PML. Herein, we report a case of PML co-occurring with neurosarcoidosis. Early diagnosis using brain biopsy and appropriate therapeutic interventions achieved favorable outcomes. PML in patients with active intracranial neurosarcoidosis is extremely rare. We believe that it is important to perform brain biopsy at an early stage to allow diagnosis, even for central nervous system involvement with a progressive parenchymal lesion in patients with sarcoidosis, if PML is possible.

    DOI: 10.3389/fimmu.2024.1447992

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  • Clinicopathologic features of two unrelated autopsied patients with Charcot-Marie-Tooth disease carrying MFN2 gene mutation. International journal

    Hideki Hayashi, Rie Saito, Hidetomo Tanaka, Norikazu Hara, Shin Koide, Yosuke Yonemochi, Tetsuo Ozawa, Mariko Hokari, Yasuko Toyoshima, Akinori Miyashita, Osamu Onodera, Kouichirou Okamoto, Takeshi Ikeuchi, Takashi Nakajima, Akiyoshi Kakita

    Acta neuropathologica communications   11 ( 1 )   207 - 207   2023.12

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  • Tau filaments from amyotrophic lateral sclerosis/parkinsonism-dementia complex adopt the CTE fold. International journal

    Chao Qi, Bert M Verheijen, Yasumasa Kokubo, Yang Shi, Stephan Tetter, Alexey G Murzin, Asa Nakahara, Satoru Morimoto, Marc Vermulst, Ryogen Sasaki, Eleonora Aronica, Yoshifumi Hirokawa, Kiyomitsu Oyanagi, Akiyoshi Kakita, Benjamin Ryskeldi-Falcon, Mari Yoshida, Masato Hasegawa, Sjors H W Scheres, Michel Goedert

    Proceedings of the National Academy of Sciences of the United States of America   120 ( 51 )   e2306767120   2023.12

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    The amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) of the island of Guam and the Kii peninsula of Japan is a fatal neurodegenerative disease of unknown cause that is characterized by the presence of abundant filamentous tau inclusions in brains and spinal cords. Here, we used electron cryo-microscopy to determine the structures of tau filaments from the cerebral cortex of three cases of ALS/PDC from Guam and eight cases from Kii, as well as from the spinal cord of two of the Guam cases. Tau filaments had the chronic traumatic encephalopathy (CTE) fold, with variable amounts of Type I and Type II filaments. Paired helical tau filaments were also found in three Kii cases and tau filaments with the corticobasal degeneration fold in one Kii case. We identified a new Type III CTE tau filament, where protofilaments pack against each other in an antiparallel fashion. ALS/PDC is the third known tauopathy with CTE-type filaments and abundant tau inclusions in cortical layers II/III, the others being CTE and subacute sclerosing panencephalitis. Because these tauopathies are believed to have environmental causes, our findings support the hypothesis that ALS/PDC is caused by exogenous factors.

    DOI: 10.1073/pnas.2306767120

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  • Marked laterality of olivopontocerebellar pathology in an autopsied patient with MSA: Implications for degeneration and α-synuclein propagation. International journal

    Misato Ozawa, Rie Saito, Takuya Konno, Reiji Koide, Shigeru Fujimoto, Osamu Onodera, Akiyoshi Kakita

    Journal of neurology, neurosurgery, and psychiatry   2023.11

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  • 緊張型脳実質内気脳症の1例

    大倉 良太, 吉田 至誠, 高橋 陽彦, 小倉 良介, 柿田 明美, 大石 誠, 藤井 幸彦

    脳神経外科速報   33 ( 6 )   e1 - e7   2023.11

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  • Clinical, imaging, and molecular features of radiation-induced glioblastomas developing more than 20 years after radiation therapy for intracranial germinomatous germ cell tumor: illustrative cases. International journal

    Yoshihiro Tsukamoto, Manabu Natsumeda, Haruhiko Takahashi, Asuka Ueno, Kiichi Sakai, Kazuki Shida, Hiroki Seto, Taiki Saito, Satoshi Shibuma, Yoko Nakayama, Yuki Tanaka, Toshimichi Nakano, Atsushi Ohta, Katsuya Maruyama, Masayasu Okada, Takeyoshi Eda, Yasuhiro Seki, Yuichirou Yoneoka, Hiroshi Shimizu, Kouichirou Okamoto, Akiyoshi Kakita, Makoto Oishi

    Journal of neurosurgery. Case lessons   6 ( 16 )   2023.10

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    BACKGROUND: Germinomatous germ cell tumor is highly sensitive to chemoradiotherapy; patients are expected to survive for decades. Many radiation-induced malignant gliomas (RIMGs) occur >10 years after radiotherapy. Standard therapy for RIMGs has not been established because of the lesion's rarity, the patient's shorter survival period, and the risk of radiation necrosis by repeat radiation. OBSERVATIONS: Two patients, a 32-year-old man and a 50-year-old man, developed glioblastomas more than 20 years after radiation monotherapy for germinoma with or without mature teratoma. The first patient showed a tumor in the left frontotemporal region with disseminated lesions and died 2 months after partial resection of the tumor without responding to the chemotherapy with temozolomide and bevacizumab. Methylation classifier analysis classified the pathology as closest to diffuse pediatric-type high-grade glioma, Rtk1 subtype. The second patient showed a tumor mass in the brainstem and left cerebellar peduncle, which worsened progressively during chemotherapy with temozolomide and bevacizumab. The tumor transiently responded to stereotactic radiotherapy with the CyberKnife. However, the patient died of RIMG recurrence-related aspiration pneumonia 11 months after the biopsy. Methylation classifier analysis classified the pathology as closest to infratentorial pilocytic astrocytoma. LESSONS: Chemoradiotherapy may improve the survival of patients with RIMGs. Furthermore, molecular features may influence the clinical, locoregional, and pathological features of RIMG.

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  • Ethnicity-dependent effect of rs1799971 polymorphism on OPRM1 expression in the postmortem brain and responsiveness to antipsychotics

    Kazusa Miyahara, Mizuki Hino, Risa Shishido, Ryuta Izumi, Atsuko Nagaoka, Hideki Hayashi, Akiyoshi Kakita, Hirooki Yabe, Hiroaki Tomita, Yasuto Kunii

    Journal of Psychiatric Research   166   10 - 16   2023.10

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    DOI: 10.1016/j.jpsychires.2023.08.007

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  • [An autopsied patient with palatal tremor and fatal bilateral vocal cord abduction paralysis associated with bilateral cerebellar dentate nucleus infarction].

    Tomoe Sato, Rie Saito, Makoto Sainouchi, Naomi Mezaki, Takeshi Miura, Takuya Mashima, Akiyoshi Kakita

    Rinsho shinkeigaku = Clinical neurology   2023.8

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    A 74-year-old male patient developed multiple infarcts of the brainstem and cerebellum, followed 14 months later by palatal tremor and bilateral vocal cord abduction paralysis, resulting in death due to type 2 respiratory failure. Pathologic analysis revealed old infarcts extending from the bilateral cerebellar cortices to the dentate nucleus, being more extensive on the right side, accompanied by Wallerian degeneration involving the left red nucleus, right central tegmentum tract, and inferior cerebellar peduncle, followed by pseudohypertrophy of the bilateral inferior olivary nuclei. These lesions, involving the Guillain-Mollaret triangle, may have been responsible for the palatal tremor. On the other hand, there were no evident causative lesions for the vocal cord abduction, including any in the nucleus ambiguus or posterior cricoarytenoid muscles. In this case it is possible that the dysfunction responsible for the palatal tremor may have affected the pathway from the central tegmentum tract, which is part of the Guillain-Mollaret triangle, to the vagus nerve arising from the nucleus ambiguus, which plays a role in vocal cord abduction, thus affecting the vocal cords and resulting in abduction paralysis.

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  • APOEのレアミスセンスバリアント

    宮下 哲典, 大日方 藍, 他田 真理, 阿部 学, 柿田 明美, 池内 健

    BIO Clinica   38 ( 7 )   602 - 603   2023.7

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  • Progressive conus medullaris lesions are suggestive of intravascular large B-cell lymphoma. International journal

    Sho Kitahara, Masato Kanazawa, Manabu Natsumeda, Aki Sato, Masanori Ishikawa, Kenju Hara, Hiroyuki Tabe, Kunihiko Makino, Kouichirou Okamoto, Nobuya Fujita, Akiyoshi Kakita, Yukihiko Fuji, Osamu Onodera

    European journal of neurology   2023.6

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    BACKGROUND AND PURPOSE: Spinal cord lesions are observed in 40% of all central nervous system lesions in intravascular large B-cell lymphoma (IVLBCL). However, because IVLBCL is a very rare disease, its clinical features are not well defined, which may delay appropriate diagnosis and treatment, whilst the acute to subacute course of brain lesions in patients with IVLBCL is well established. Therefore, this study aimed to clarify the clinical features of spinal cord lesions in patients with IVLBCL. METHODS: The medical records of patients with IVLBCL admitted to our hospital between 2010 and 2020 were searched. The inclusion criteria were preceding neurological symptoms without non-neurological symptoms and pathologically confirmed IVLBCL in various organs. Clinical features of spinal cord involvement in patients with IVLBCL were assessed and distinguished from those of brain involvement. RESULTS: Sixteen consecutive patients with IVLBCL were divided into two groups: six patients with spinal involvement (spinal cord type) and 10 patients with brain involvement (brain type). In the spinal cord type, four patients had chronic progression and two had subacute progression. Acute progression (0% vs. 80.0%) and sudden onset (0% vs. 50.0%) occurred significantly less frequently in the spinal cord than in the brain. All spinal cord lesions involved the conus medullaris. CONCLUSIONS: Spinal cord involvement in IVLBCL has a predominantly chronic progressive course that is exclusive to brain involvement. Conus medullaris lesions are suggestive of IVLBCL and are useful for early and accurate diagnosis and treatment.

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  • Phosphorylation of α-synuclein at T64 results in distinct oligomers and exerts toxicity in models of Parkinson's disease. International journal

    Hideaki Matsui, Shinji Ito, Hideki Matsui, Junko Ito, Ramil Gabdulkhaev, Mika Hirose, Tomoyuki Yamanaka, Akihide Koyama, Taisuke Kato, Maiko Tanaka, Norihito Uemura, Noriko Matsui, Sachiko Hirokawa, Maki Yoshihama, Aki Shimozawa, Shin-Ichiro Kubo, Kenji Iwasaki, Masato Hasegawa, Ryosuke Takahashi, Keisuke Hirai, Akiyoshi Kakita, Osamu Onodera

    Proceedings of the National Academy of Sciences of the United States of America   120 ( 23 )   e2214652120   2023.6

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    α-Synuclein accumulates in Lewy bodies, and this accumulation is a pathological hallmark of Parkinson's disease (PD). Previous studies have indicated a causal role of α-synuclein in the pathogenesis of PD. However, the molecular and cellular mechanisms of α-synuclein toxicity remain elusive. Here, we describe a novel phosphorylation site of α-synuclein at T64 and the detailed characteristics of this post-translational modification. T64 phosphorylation was enhanced in both PD models and human PD brains. T64D phosphomimetic mutation led to distinct oligomer formation, and the structure of the oligomer was similar to that of α-synuclein oligomer with A53T mutation. Such phosphomimetic mutation induced mitochondrial dysfunction, lysosomal disorder, and cell death in cells and neurodegeneration in vivo, indicating a pathogenic role of α-synuclein phosphorylation at T64 in PD.

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  • V180I genetic Creutzfeldt-Jakob disease: Severe degeneration of the inferior olivary nucleus in an autopsied patient with identification of the M2T prion strain. International journal

    Midori Watanabe, Kosei Nakamura, Rie Saito, Atsuko Takeuchi, Tetsuya Takahashi, Tetsuyuki Kitamoto, Osamu Onodera, Akiyoshi Kakita

    Neuropathology : official journal of the Japanese Society of Neuropathology   2023.5

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    Genetic Creutzfeldt-Jakob disease (gCJD) with a V180I mutation (V180I gCJD) is the most common type of gCJD in Japan, characterized by an older age at onset, slower progression, and moderate to severe cortical degeneration with spongiform changes and sparing of the brainstem and cerebellum. Degeneration of the inferior olivary nucleus (IO) is rarely observed in patients with CJD but is known to occur in fatal familial insomnia (FFI) and MM2-thalamic-type sporadic CJD (sCJD-MM2T) involving type 2 prion protein (M2T prion). Here we report on an 81-year-old Japanese woman who initially developed depressive symptoms followed by progressive cognitive impairment, myoclonus, and hallucinations and died after a clinical course of 23 months. Insomnia was not evident. Genetic analysis of the prion protein (PrP) identified a V180I mutation with methionine/valine heterozygosity at codon 129. Pathologic analysis demonstrated extensive spongiform degeneration, neuronal loss in the cortices, and weak synaptic-type PrP deposition. Except for IO degeneration, the clinicopathologic features and Western blotting PrP band pattern were compatible with those of previously reported V180I gCJD cases. Quantitative analysis revealed that the neuronal density of the IO, especially in the dorsal area, was considerably reduced to the same extent as that of a patient with sCJD-MM2T but preserved in other patients with V180I gCJD and sCJD-MM1 (this patient, 2.3 ± 0.53/mm2 ; a patient with sCJD-MM2T, 4.2 ± 2; a patient with V180I gCJD, 60.5 ± 9.3; and a patient with sCJD-MM1, 84.5 ± 17.9). Use of the protein misfolding cyclic amplification (PMCA) method confirmed the presence of the M2T prion strain, suggesting that the latter might be associated with IO degeneration in V180I gCJD. Autopsy studies are necessary to better understand the nature of CJD, since even if patients present with the common clinical picture, pathologic analysis might provide new insights, as was the case here.

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  • Identification of schizophrenia symptom-related gene modules by postmortem brain transcriptome analysis. International journal

    Kazusa Miyahara, Mizuki Hino, Risa Shishido, Atsuko Nagaoka, Ryuta Izumi, Hideki Hayashi, Akiyoshi Kakita, Hirooki Yabe, Hiroaki Tomita, Yasuto Kunii

    Translational psychiatry   13 ( 1 )   144 - 144   2023.5

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    Schizophrenia is a multifactorial disorder, the genetic architecture of which remains unclear. Although many studies have examined the etiology of schizophrenia, the gene sets that contribute to its symptoms have not been fully investigated. In this study, we aimed to identify each gene set associated with corresponding symptoms of schizophrenia using the postmortem brains of 26 patients with schizophrenia and 51 controls. We classified genes expressed in the prefrontal cortex (analyzed by RNA-seq) into several modules by weighted gene co-expression network analysis (WGCNA) and examined the correlation between module expression and clinical characteristics. In addition, we calculated the polygenic risk score (PRS) for schizophrenia from Japanese genome-wide association studies, and investigated the association between the identified gene modules and PRS to evaluate whether genetic background affected gene expression. Finally, we conducted pathway analysis and upstream analysis using Ingenuity Pathway Analysis to clarify the functions and upstream regulators of symptom-related gene modules. As a result, three gene modules generated by WGCNA were significantly correlated with clinical characteristics, and one of these showed a significant association with PRS. Genes belonging to the transcriptional module associated with PRS significantly overlapped with signaling pathways of multiple sclerosis, neuroinflammation, and opioid use, suggesting that these pathways may also be profoundly implicated in schizophrenia. Upstream analysis indicated that genes in the detected module were profoundly regulated by lipopolysaccharides and CREB. This study identified schizophrenia symptom-related gene sets and their upstream regulators, revealing aspects of the pathophysiology of schizophrenia and identifying potential therapeutic targets.

    DOI: 10.1038/s41398-023-02449-8

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  • FGFR3-TACC3 fusionを伴うIDH野生型神経膠腫はCTで石灰化を高率に有する

    高橋 陽彦, 棗田 学, 塚本 佳広, 清水 宏, 岡本 浩一郎, 峰晴 陽平, 荒川 芳輝, 大石 誠, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   40 ( Suppl. )   099 - 099   2023.5

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  • FGFR3-TACC3 fusionを伴うIDH野生型神経膠腫はCTで石灰化を高率に有する

    高橋 陽彦, 棗田 学, 塚本 佳広, 清水 宏, 岡本 浩一郎, 峰晴 陽平, 荒川 芳輝, 大石 誠, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   40 ( Suppl. )   099 - 099   2023.5

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  • 脳腫瘍診断におけるliquid biopsyの可能性 中枢神経再発を来すsystemic diffuse large B cell lymphomaは高率にMYD88変異を有する

    棗田 学, 温 城太郎, 高橋 陽彦, 渡邉 潤, 塚本 佳広, 大石 誠, 柿田 明美, 瀧澤 淳, 正木 康史, 林 康彦

    Brain Tumor Pathology   40 ( Suppl. )   069 - 069   2023.5

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  • プロラクチン産生下垂体腺腫が頸部に転移したPit-1陽性下垂体がんの一例

    岡田 正康, 植木 雄志, 棗田 学, 大石 誠, 近藤 修平, 梅津 哉, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   40 ( Suppl. )   144 - 144   2023.5

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  • 胚種治療後20年以上経過後に発症した放射線誘発性膠芽腫の2症例の検討

    塚本 佳広, 高橋 陽彦, 棗田 学, 坂井 貴一, 中山 遥子, 田中 裕貴, 岡本 浩一郎, 大石 誠, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   40 ( Suppl. )   113 - 113   2023.5

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  • Tau Filaments from Amyotrophic Lateral Sclerosis/Parkinsonism-Dementia Complex (ALS/PDC) adopt the CTE Fold. International journal

    Chao Qi, Bert M Verheijen, Yasumasa Kokubo, Yang Shi, Stephan Tetter, Alexey G Murzin, Asa Nakahara, Satoru Morimoto, Marc Vermulst, Ryogen Sasaki, Eleonora Aronica, Yoshifumi Hirokawa, Kiyomitsu Oyanagi, Akiyoshi Kakita, Benjamin Ryskeldi-Falcon, Mari Yoshida, Masato Hasegawa, Sjors H W Scheres, Michel Goedert

    bioRxiv : the preprint server for biology   2023.4

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    UNLABELLED: The amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) of the island of Guam and the Kii peninsula of Japan is a fatal neurodegenerative disease of unknown cause that is characterised by the presence of abundant filamentous tau inclusions in brains and spinal cords. Here we used electron cryo-microscopy (cryo-EM) to determine the structures of tau filaments from the cerebral cortex of three cases of ALS/PDC from Guam and eight cases from Kii, as well as from the spinal cord of two of the Guam cases. Tau filaments had the chronic traumatic encephalopathy (CTE) fold, with variable amounts of Type I and Type II filaments. Paired helical tau filaments were also found in two Kii cases. We also identified a novel Type III CTE tau filament, where protofilaments pack against each other in an anti-parallel fashion. ALS/PDC is the third known tauopathy with CTE-type filaments and abundant tau inclusions in cortical layers II/III, the others being CTE and subacute sclerosing panencephalitis. Because these tauopathies are believed to have environmental causes, our findings support the hypothesis that ALS/PDC is caused by exogenous factors. SIGNIFICANCE: A neurodegenerative disease of unknown cause on the island of Guam and the Kii peninsula of Japan has been widely studied, because patients can suffer from the combined symptoms of motor neuron disease, parkinsonism and dementia. Abnormal filamentous inclusions made of tau protein characterise this amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) and their formation closely correlates with neurodegeneration. Here we have used electron cryo-microscopy (cryo-EM) to show that tau filaments from ALS/PDC are identical to those from chronic traumatic encephalopathy (CTE), a disease caused by repetitive head impacts or blast waves. CTE tau filaments are also found in subacute sclerosing panencephalitis, which is a rare consequence of measles infection. ALS/PDC may therefore also be caused by environmental factors.

    DOI: 10.1101/2023.04.26.538417

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  • Administration of glucocorticoids prior to liquid biopsy dramatically reduces the detection rate of <i>MYD88 L265P</i> mutation in cerebrospinal fluid of primary CNS lymphoma patients

    Haruhiko Takahashi, Manabu Natsumeda, Jotaro On, Jun Watanabe, Mari Tada, Hiroshi Shimizu, Yoshihiro Tsukamoto, Masayasu Okada, Makoto Oishi, Jun Takizawa, Yasuhiko Hayashi, Yasufumi Masaki, Akiyoshi Kakita, Yukihiko Fujii

    Leukemia &amp; Lymphoma   64 ( 6 )   1219 - 1222   2023.4

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    DOI: 10.1080/10428194.2023.2199895

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  • 【認知症のゲノム医療】APOEの遺伝型とレアミスセンスバリアント 臨床応用への可能性

    宮下 哲典, 原 範和, 春日 健作, 菊地 正隆, 尾崎 浩一, 新飯田 俊平, 他田 真理, 柿田 明美, 池内 健

    Dementia Japan   37 ( 2 )   239 - 249   2023.4

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  • 遺伝性痙性対麻痺を呈しGTP cyclohydrolase 1ヘテロ接合性変異を認めた1剖検例

    本郷 祥子, 他田 真理, 池田 哲彦, 小澤 哲夫, 劉 李きん, 宮下 哲典, 池内 健, 小野寺 理, 中島 孝, 柿田 明美

    信州医学雑誌   71 ( 2 )   128 - 129   2023.4

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  • 遺伝性痙性対麻痺を呈しGTP cyclohydrolase 1ヘテロ接合性変異を認めた1剖検例

    本郷 祥子, 他田 真理, 池田 哲彦, 小澤 哲夫, 劉 李きん, 宮下 哲典, 池内 健, 小野寺 理, 中島 孝, 柿田 明美

    信州医学雑誌   71 ( 2 )   128 - 129   2023.4

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  • Human early-onset dementia caused by DAP12 deficiency reveals a unique signature of dysregulated microglia. International journal

    Yingyue Zhou, Mari Tada, Zhangying Cai, Prabhakar S Andhey, Amanda Swain, Kelly R Miller, Susan Gilfillan, Maxim N Artyomov, Masaki Takao, Akiyoshi Kakita, Marco Colonna

    Nature immunology   24 ( 3 )   545 - 557   2023.3

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    The TREM2-DAP12 receptor complex sustains microglia functions. Heterozygous hypofunctional TREM2 variants impair microglia, accelerating late-onset Alzheimer's disease. Homozygous inactivating variants of TREM2 or TYROBP-encoding DAP12 cause Nasu-Hakola disease (NHD), an early-onset dementia characterized by cerebral atrophy, myelin loss and gliosis. Mechanisms underpinning NHD are unknown. Here, single-nucleus RNA-sequencing analysis of brain specimens from DAP12-deficient NHD individuals revealed a unique microglia signature indicating heightened RUNX1, STAT3 and transforming growth factor-β signaling pathways that mediate repair responses to injuries. This profile correlated with a wound healing signature in astrocytes and impaired myelination in oligodendrocytes, while pericyte profiles indicated vascular abnormalities. Conversely, single-nuclei signatures in mice lacking DAP12 signaling reflected very mild microglial defects that did not recapitulate NHD. We envision that DAP12 signaling in microglia attenuates wound healing pathways that, if left unchecked, interfere with microglial physiological functions, causing pathology in human. The identification of a dysregulated NHD microglia signature sparks potential therapeutic strategies aimed at resetting microglia signaling pathways.

    DOI: 10.1038/s41590-022-01403-y

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  • 多数のタウ陽性グリア細胞質内封入体を認めた30年経過の多系統萎縮症の一剖検

    中原 亜紗, 野崎 洋明, 佐藤 晶, 五十嵐 修一, 他田 真理, 柿田 明美, 橋立 英樹

    日本病理学会会誌   112 ( 1 )   318 - 318   2023.3

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  • Elevated ratio of C-type lectin-like receptor 2 level and platelet count (C2PAC) aids in the diagnosis of post-operative venous thromboembolism in IDH-wildtype gliomas. International journal

    Kazuhiro Ando, Manabu Natsumeda, Masahide Kawamura, Kamon Shirakawa, Masayasu Okada, Yoshihiro Tsukamoto, Takeyoshi Eda, Jun Watanabe, Shoji Saito, Haruhiko Takahashi, Akiyoshi Kakita, Makoto Oishi, Yukihiko Fujii

    Thrombosis research   223   36 - 43   2023.3

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    INTRODUCTION: Podoplanin (PDPN) is known to induce platelet aggregation via interacting with the C-type lectin-like receptor-2 on platelets and is involved in postoperative venous thromboembolism (VTE) formation. In this study, we investigate the correlation between soluble C-type lectin-like receptor (sCLEC-2) levels and PDPN expression in patients with high grade gliomas and the relationship between sCLEC-2 levels and the occurrence of VTE. MATERIALS AND METHODS: Forty-four patients harboring high grade gliomas, treated surgically at the Department of Neurosurgery, Niigata University from April 2018 to August 2020, were included. Patients with high grade gliomas were divided into isocitrate dehydrogenase (IDH)- wildtype and mutant groups, and the presence or absence of VTE and the intensity of PDPN by immunohistochemistry were confirmed. Platelet counts, as well as plasma sCLEC-2 and PDPN were measured in these patients. Furthermore, the levels of sCLEC-2 concentration were divided by the platelet count (C2PAC index) for comparison. RESULTS: IDH-wildtype glioma patients highly expressed PDPN (P < 0.001) compared to IDH-mutant glioma patients. In total, 9 (20.5 %) patients were diagnosed with VTE during the follow-up period, of which 8 patients harbored IDH-wildtype gliomas, and one patient an IDH-mutant glioma. Mean sCLEC-2 levels and C2PAC index in patients with IDH-wildtype gliomas were significantly higher than that of low or no PDPN expression group, which included patients with IDH-mutant gliomas (P = 0.0004, P = 0.0002). In patients with IDH-wildtype gliomas, the C2PAC index in patients with VTE was significantly higher than in patients without VTE (P = 0.0492). The optimal cutoff point of C2PAC for predicting VTE in IDH-wildtype glioma patients was 3.7 with a sensitivity of 87.5 % and specificity of 51.9 %. CONCLUSION: Platelet activation is strongly involved in the development of VTE in patients with IDH-wildtype high grade gliomas, and C2PAC index is a potential marker to detect VTE formation after surgery.

    DOI: 10.1016/j.thromres.2023.01.018

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  • Evidence for increased DNA damage repair in the postmortem brain of the high stress-response group of schizophrenia. International journal

    Risa Shishido, Yasuto Kunii, Mizuki Hino, Ryuta Izumi, Atsuko Nagaoka, Hideki Hayashi, Akiyoshi Kakita, Hiroaki Tomita, Hirooki Yabe

    Frontiers in psychiatry   14   1183696 - 1183696   2023

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    BACKGROUND: Schizophrenia (SZ) is a disorder diagnosed by specific symptoms and duration and is highly heterogeneous, clinically and pathologically. Although there are an increasing number of studies on the association between genetic and environmental factors in the development of SZ, the actual distribution of the population with different levels of influence of these factors has not yet been fully elucidated. In this study, we focused on stress as an environmental factor and stratified SZ based on the expression levels of stress-responsive molecules in the postmortem prefrontal cortex. METHODS: We selected the following stress-responsive molecules: interleukin (IL) -1β, IL-6, IL-10, tumor necrosis factor-α, interferon-γ, glucocorticoid receptor, brain-derived neurotrophic factor, synaptophysin, S100 calcium-binding protein B, superoxide dismutase, postsynaptic density protein 95, synuclein, apolipoprotein A1 (ApoA1), ApoA2, and solute carrier family 6 member 4. We performed RNA sequencing in the prefrontal gray matter of 25 SZ cases and 21 healthy controls and conducted a hierarchical cluster analysis of SZ based on the gene expression levels of stress-responsive molecules, which yielded two clusters. After assessing the validity of the clusters, they were designated as the high stress-response SZ group and the low stress-response SZ group, respectively. Ingenuity Pathway Analysis of differentially expressed genes (DEGs) between clusters was performed, and Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was conducted on four cases each in the high and low stress-response SZ groups to validate DNA damage. RESULTS: We found higher prevalence of family history of SZ in the low stress-response SZ group (0/3 vs. 5/4, p = 0.04). Pathway analysis of DEGs between clusters showed the highest enrichment for DNA double-strand break repair. TUNEL staining showed a trend toward a lower percentage of TUNEL-positive cells in the high stress-response SZ group. CONCLUSION: Our results suggest that there are subgroups of SZ with different degrees of stress impact. Furthermore, the pathophysiology of these subgroups may be associated with DNA damage repair. These results provide new insights into the interactions and heterogeneity between genetic and environmental factors.

    DOI: 10.3389/fpsyt.2023.1183696

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  • 口蓋振戦と致死性の両側声帯外転麻痺をきたした両側小脳歯状核梗塞の1剖検例

    Tomoe Sato, Rie Saito, Makoto Sainouchi, Naomi Mezaki, Takeshi Miura, Takuya Mashima, Akiyoshi Kakita

    Rinsho Shinkeigaku   2023

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    DOI: 10.5692/clinicalneurol.cn-001859

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  • Cerebrospinal Fluid Biomarkers and Amyloid-β Elimination from the Brain in Cerebral Amyloid Angiopathy-Related Inflammation. International journal

    Kenji Sakai, Moeko Noguchi-Shinohara, Hidetomo Tanaka, Tokuhei Ikeda, Tsuyoshi Hamaguchi, Akiyoshi Kakita, Masahito Yamada, Kenjiro Ono

    Journal of Alzheimer's disease : JAD   91 ( 3 )   1173 - 1183   2023

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    BACKGROUND: Cerebrospinal fluid (CSF) biomarkers in patients with cerebral amyloid angiopathy-related inflammation (CAA-ri) have demonstrated inconsistent results. OBJECTIVE: We investigated the relationship between CSF amyloid-β protein (Aβ) and vascular pathological findings to elucidate the mechanisms of Aβ elimination from the brain in CAA-ri. METHODS: We examined Aβ40 and Aβ42 levels in CSF samples in 15 patients with CAA-ri and 15 patients with Alzheimer's disease and cerebral amyloid angiopathy (AD-CAA) using ELISA as a cross-sectional study. Furthermore, we pathologically examined Aβ40 and Aβ42 depositions on the leptomeningeal blood vessels (arteries, arterioles, and veins) using brain biopsy samples from six patients with acute CAA-ri and brain tissues of two autopsied patients with CAA-ri. RESULTS: The median Aβ40 and Aβ42 levels in the CSF showed no significant difference between pre-treatment CAA-ri (Aβ40, 6837 pg/ml; Aβ42, 324 pg/ml) and AD-CAA (Aβ40, 7669 pg/ml, p = 0.345; Aβ42, 355 pg/ml, p = 0.760). Aβ40 and Aβ42 levels in patients with post-treatment CAA-ri (Aβ40, 1770 pg/ml, p = 0.056; Aβ42, 167 pg/ml, p = 0.006) were lower than those in patients with pre-treatment CAA-ri. Regarding Aβ40 and Aβ42 positive arteries, acute CAA-ri cases showed a higher frequency of partially Aβ-deposited blood vessels than postmortem CAA-ri cases (Aβ40, 20.8% versus 3.9%, p = 0.0714; Aβ42, 27.4% versus 2.0%, p = 0.0714, respectively). CONCLUSION: Lower levels of CSF Aβ40 and Aβ42 could be biomarkers for the cessation of inflammation in CAA-ri reflecting the recovery of the intramural periarterial drainage pathway and vascular function.

    DOI: 10.3233/JAD-220838

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  • <i>SYNE1</i>-ataxia: clinicopathologic features of an autopsied patient with novel compound heterozygous mutations

    Rie Saito, Norikazu Hara, Mari Tada, Masatoshi Wakabayashi, Akinori Miyashita, Masatoyo Nishizawa, Osamu Onodera, Takeshi Ikeuchi, Akiyoshi Kakita

    Journal of Neuropathology &amp; Experimental Neurology   2022.12

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    DOI: 10.1093/jnen/nlac120

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  • Spinocerebellar ataxia type 17-digenic TBP/STUB1 disease: neuropathologic features of an autopsied patient

    Rie Saito, Yui Tada, Daisuke Oikawa, Yusuke Sato, Makiko Seto, Akira Satoh, Kodai Kume, Nozomi Ueki, Masahiro Nakashima, Shintaro Hayashi, Yasuko Toyoshima, Fuminori Tokunaga, Hideshi Kawakami, Akiyoshi Kakita

    Acta Neuropathologica Communications   10 ( 1 )   2022.12

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    Abstract

    Spinocerebellar ataxia (SCA) type 17-digenic TBP/STUB1 disease (SCA17-DI) has been recently segregated from SCA17, caused by digenic inheritance of two gene mutations – intermediate polyglutamine-encoding CAG/CAA repeat expansions (polyQ) in TBP (TBP<sub>41 − 49</sub>) and STUB1 heterozygosity – the former being associated with SCA17, and the latter with SCA48 and SCAR16 (autosomal recessive). In SCA17, most patients carry intermediate TBP<sub>41 − 49</sub> alleles but show incomplete penetrance, and the missing heritability can be explained by a new entity whereby TBP<sub>41 − 49</sub> requires the STUB1 variant to be symptomatic. The STUB1 gene encodes the chaperone-associated E3 ubiquitin ligase (CHIP) involved in ubiquitin-mediated proteasomal control of protein homeostasis. However, reports of the neuropathology are limited and role of STUB1 mutations in SCA17-DI remain unknown. Here we report the clinicopathologic features of identical twin siblings, one of whom was autopsied and was found to carry an intermediate allele (41 and 38 CAG/CAA repeats) in TBP and a heterozygous missense mutation in STUB1 (p.P243L). These patients developed autosomal recessive Huntington’s disease-like symptoms. Brain MRI showed diffuse atrophy of the cerebellum and T2WI revealed hyperintense lesions in the basal ganglia and periventricular deep white matter. The brain histopathology of the patient shared features characteristic of SCA17, such as degeneration of the cerebellar cortex and caudate nucleus, and presence of 1C2-positive neurons. Here we show that mutant CHIP fails to generate the polyubiquitin chain due to disrupted folding of the entire U box domain, thereby affecting the E3 activity of CHIP. When encountering patients with cerebellar ataxia, especially those with Huntington’s disease-like symptoms, genetic testing for STUB1 as well as TBP should be conducted for diagnosis of SCA17-DI, even in cases of sporadic or autosomal recessive inheritance.

    DOI: 10.1186/s40478-022-01486-6

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  • 疾患解析技術の最先端 認知症のトランスクリプトーム解析 ヒト剖検脳のシングル核解析から見えてくるもの

    宮下 哲典, 他田 真理, 原 範和, 長谷川 舞衣, 柿田 明美, 池内 健

    老年精神医学雑誌   33 ( 増刊II )   195 - 195   2022.11

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  • Epigenetic upregulation of Schlafen11 renders WNT- and SHH- activated medulloblastomas sensitive to cisplatin. International journal

    Satoshi Nakata, Junko Murai, Masayasu Okada, Haruhiko Takahashi, Tyler H Findlay, Kristen Malebranche, Akhila Parthasarathy, Satoshi Miyashita, Ramil Gabdulkhaev, Ilan Benkimoun, Sabine Druillennec, Sara Chabi, Eleanor Hawkins, Hiroaki Miyahara, Kensuke Tateishi, Shinji Yamashita, Shiori Yamada, Taiki Saito, Jotaro On, Jun Watanabe, Yoshihiro Tsukamoto, Junichi Yoshimura, Makoto Oishi, Toshimichi Nakano, Masaru Imamura, Chihaya Imai, Tetsuya Yamamoto, Hideo Takeshima, Atsuo T Sasaki, Fausto J Rodriguez, Sumihito Nobusawa, Pascale Varlet, Celio Pouponnot, Satoru Osuka, Yves Pommier, Akiyoshi Kakita, Yukihiko Fujii, Eric H Raabe, Charles G Eberhart, Manabu Natsumeda

    Neuro-oncology   25 ( 5 )   899 - 912   2022.10

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    BACKGROUND: Intensive chemotherapeutic regimens with craniospinal irradiation have greatly improved survival in medulloblastoma patients. However, survival markedly differs among molecular subgroups and their biomarkers are unknown. Through unbiased screening, we found Schlafen family member 11 (SLFN11), which is known to improve response to DNA damaging agents in various cancers, to be one of the top prognostic markers in medulloblastomas. Hence, we explored the expression and functions of SLFN11 in medulloblastoma. METHODS: SLFN11 expression for each subgroup was assessed by immunohistochemistry in 98 medulloblastoma patient samples and by analyzing transcriptomic databases. We genetically or epigenetically modulated SLFN11 expression in medulloblastoma cell lines and determined cytotoxic response to the DNA damaging agents cisplatin and topoisomerase I inhibitor SN-38 in vitro and in vivo. RESULTS: High SLFN11 expressing cases exhibited significantly longer survival than low expressing cases. SLFN11 was highly expressed in the WNT-activated subgroup and in a proportion of the SHH-activated subgroup. While WNT activation was not a direct cause of the high expression of SLFN11, a specific hypomethylation locus on the SLFN11 promoter was significantly correlated with high SLFN11 expression. Overexpression or deletion of SLFN11 made medulloblastoma cells sensitive and resistant to cisplatin and SN-38, respectively. Pharmacological upregulation of SLFN11 by the brain-penetrant histone deacetylase-inhibitor RG2833 markedly increased sensitivity to cisplatin and SN-38 in SLFN11-negative medulloblastoma cells. Intracranial xenograft studies also showed marked sensitivity to cisplatin by SLFN11-overexpression in medulloblastoma cells. CONCLUSIONS: High SLFN11 expression is one factor which renders favorable outcomes in WNT-activated and a subset of SHH-activated medulloblastoma possibly through enhancing response to cisplatin.

    DOI: 10.1093/neuonc/noac243

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  • SWI by 7T MR Imaging for the Microscopic Imaging Diagnosis of Astrocytic and Oligodendroglial Tumors Reviewed

    M. Natsumeda, H. Matsuzawa, M. Watanabe, K. Motohashi, R. Gabdulkhaev, Y. Tsukamoto, Y. Kanemaru, J. Watanabe, R. Ogura, M. Okada, S. Kurabe, K. Okamoto, A. Kakita, H. Igarashi, Y. Fujii

    American Journal of Neuroradiology   2022.10

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    DOI: 10.3174/ajnr.A7666

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  • Involvement of autophagic protein DEF8 in Lewy bodies. International journal

    Makoto Timon Tanaka, Yasuo Miki, Conceição Bettencourt, Taku Ozaki, Kunikazu Tanji, Fumiaki Mori, Akiyoshi Kakita, Koichi Wakabayashi

    Biochemical and biophysical research communications   623   170 - 175   2022.10

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    Dysregulation of autophagy, one of the major processes through which abnormal proteins are degraded, is a cardinal feature of synucleinopathies, including Lewy body diseases [Parkinson's disease (PD) and dementia with Lewy bodies (DLB)] and multiple system atrophy (MSA), which are characterized by the presence of abnormal α-synuclein in neurons and glial cells. Although several research groups have reported that Rubicon family proteins can regulate autophagosome-lysosome fusion or positioning, little is known about their involvement in synucleinopathies. In the present study, by studying patients with PD (N = 8), DLB (N = 13), and MSA (N = 5) and controls (N = 16), we explored the involvement of Rubicon family proteins [Rubicon, Pacer and differentially expressed in FDCP8 (DEF8)] in synucleinopathies. Immunohistochemical analysis showed that not only brainstem-type Lewy bodies but also cortical Lewy bodies were immunoreactive for DEF8 in Lewy body diseases, whereas Rubicon and Pacer were detectable in only a few brainstem-type Lewy bodies in PD. Glial cytoplasmic inclusions in patients with MSA were not immunoreactive for Rubicon, Pacer or DEF8. Immunoblotting showed significantly increased protein levels of DEF8 in the substantia nigra and putamen of patients with PD and the temporal cortex of patients with DLB. In addition, the smear band of DEF8 appeared in the insoluble fraction where that of phosphorylated α-synuclein was detected. These findings indicate the involvement of DEF8 in the formation of Lewy bodies. Quantitative and qualitative alterations in DEF8 may reflect the dysregulation of autophagy in Lewy body diseases.

    DOI: 10.1016/j.bbrc.2022.07.069

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  • Biallelic <i>COX10</i> Mutations and <i>PMP22</i> Deletion in a Family With Leigh Syndrome and Hereditary Neuropathy With Liability to Pressure Palsy

    Yasuko Kuroha, Takanobu Ishiguro, Mari Tada, Norikazu Hara, Kei Murayama, Izumi Kawachi, Kensaku Kasuga, Akinori Miyashita, Arika Hasegawa, Tetsuya Takahashi, Nae Matsubara, Osamu Onodera, Akiyoshi Kakita, Ryoko Koike, Takeshi Ikeuchi

    Neurology Genetics   8 ( 5 )   e200030 - e200030   2022.10

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    Objectives

    Leigh syndrome is a progressive encephalopathy characterized by symmetrical lesions in brain. This study aimed to investigate the clinicopathologic and genetic characteristics of a family with Leigh syndrome and hereditary neuropathy with liability to pressure palsy (HNPP).

    Methods

    Data from a Japanese family's clinical features, MRIs, muscle biopsy, and an autopsy were analyzed. A whole-exome sequence was performed, as well as real-time PCR analysis to determine copy number variations and Western blot analyses.

    Results

    The proband and her 2 siblings developed spastic paraplegia and mental retardation during childhood. The proband and her sister had peripheral neuropathy, whereas their father developed compression neuropathy. Leigh encephalopathy was diagnosed neuropathologically. Brain MRI revealed changes in cerebral white matter as well as multiple lesions in the brainstem and cerebellum. Muscle biopsy revealed type 2 fiber uniformity and decreased staining of cytochrome c oxidase. The COX10 missense mutation was identified through whole-exome sequence. A 1.4-Mb genomic deletion extending from intron 5 of COX10 to PMP22 was detected.

    Discussion

    These findings suggest that in this family, Leigh syndrome is associated with a mitochondrial respiratory chain complex IV deficiency caused by biallelic COX10 mutations coexisting with HNPP caused by heterozygous PMP22 deletion.

    DOI: 10.1212/nxg.0000000000200030

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  • High‐Contrast Imaging of α‐Synuclein Pathologies in Living Patients with Multiple System Atrophy International journal

    Kiwamu Matsuoka, Maiko Ono, Yuhei Takado, Kosei Hirata, Hironobu Endo, Toshiyuki Ohfusa, Taichi Kojima, Takeshi Yamamoto, Tomohiro Onishi, Asumi Orihara, Kenji Tagai, Keisuke Takahata, Chie Seki, Hitoshi Shinotoh, Kazunori Kawamura, Hiroshi Shimizu, Hitoshi Shimada, Akiyoshi Kakita, Ming‐Rong Zhang, Tetsuya Suhara, Makoto Higuchi

    Movement Disorders   37 ( 10 )   2159 - 2161   2022.10

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    DOI: 10.1002/mds.29186

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  • 疾患解析技術の最先端 認知症のトランスクリプトーム解析 ヒト剖検脳のシングル核解析から見えてくるもの

    宮下 哲典, 他田 真理, 原 範和, 長谷川 舞衣, 柿田 明美, 池内 健

    Dementia Japan   36 ( 4 )   721 - 721   2022.10

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  • 神経症状で初発する血管内大細胞型B細胞リンパ腫の臨床的特徴と診断方法に関する検討

    北原 匠, 金澤 雅人, 徳武 孝充, 棗田 学, 佐藤 晶, 石川 正典, 原 賢寿, 田部 浩行, 牧野 邦比古, 藤田 信也, 岡本 浩一郎, 柿田 明美, 藤井 幸彦, 小野寺 理

    臨床神経学   62 ( Suppl. )   S272 - S272   2022.10

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  • The large neuron involvement in the neostriatum in Lewy body diseases. International journal

    Kiyomitsu Oyanagi, Hideki Hayashi, Mitsunori Yamada, Akiyoshi Kakita

    Neuropathology : official journal of the Japanese Society of Neuropathology   42 ( 5 )   459 - 463   2022.10

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  • Successful Treatment of Acute Uric Acid Nephropathy with Rasburicase in a Primary Central Nervous System Lymphoma Patient Showing a Dramatic Response to Methotrexate—Case Report

    Yoshihiro Mouri, Manabu Natsumeda, Noritaka Okubo, Taro Sato, Taiki Saito, Kohei Shibuya, Shiori Yamada, Jotaro On, Yoshihiro Tsukamoto, Masayasu Okada, Makoto Oishi, Takeyoshi Eda, Junko Murai, Hiroshi Shimizu, Akiyoshi Kakita, Yukihiko Fujii

    Journal of Clinical Medicine   11 ( 19 )   5548 - 5548   2022.9

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    Background: Primary central nervous system lymphomas (PCNSLs) are sensitive to chemotherapy. The standard treatment is high-dose methotrexate (MTX)-based chemotherapy. There are no reports of successful treatment of acute uric acid nephropathy with rasburicase after MTX administration in PCNSLs. Case presentation: A 54-year-old man with a history of gout presented with a change in character and cognitive dysfunction. MRI showed a large enhancing mass spanning the bilateral frontal lobes and the right temporal lobe. After endoscopic biopsy, an MTX, procarbazine, and vincristine (MPV) regimen was initiated for the treatment of the PCNSL. After the initiation of chemotherapy, the patient experienced a gout attack, and blood examination revealed acute renal failure (ARF) and hyperuricemia. The considered causes of ARF included MTX toxicity and acute uric acid nephropathy. As the dramatic effect of MTX was observed, treatment was continued despite ARF, most probably due to acute hyperuricemia due to tumor lysis, which was treated in parallel. After an improvement in renal function, MTX was resumed, and rasburicase was initiated to control hyperuricemia. A complete response was obtained after induction chemotherapy. Hyperuricemia was controlled with rasburicase, and renal function was preserved. Conclusions: Acute uric acid nephropathy should be considered when ARF occurs after the initiation of MTX in PCNSLs, especially in newly diagnosed PCNSL patients with large tumors or hyperuricemia.

    DOI: 10.3390/jcm11195548

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  • Elucidating the multiple genetic alterations involved in the malignant transformation of a KRAS mutant neurenteric cyst. A case report. International journal

    Shoji Saito, Manabu Natsumeda, Makoto Sainouchi, Toru Takino, Kohei Shibuya, Jotaro On, Yu Kanemaru, Ryosuke Ogura, Masayasu Okada, Makoto Oishi, Yoshifumi Shimada, Toshifumi Wakai, Shujiro Okuda, Yoichi Ajioka, Akiyoshi Kakita, Yukihiko Fujii

    Neuropathology : official journal of the Japanese Society of Neuropathology   42 ( 6 )   519 - 525   2022.9

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    Neurenteric cyst (NC) shows benign histopathology and rarely demonstrate malignant transformation. We herein describe a case of NC that exhibited malignant transformation. A 65-year-old female presented with gait disturbance due to compression by a cystic mass on the dorsal surface of the medulla oblongata. Partial resection was performed twice, leading to improvement of her symptoms. Two years after the second surgery, gadolinium-perfused T1-weighted magnetic resonance imaging revealed an invasive lesion with contrast enhancement at the trigone of the left lateral ventricle for which partial resection followed by radiotherapy was performed. However, mass regrowth was observed, with the patient eventually succumbing to her disease 11 months after her third surgery. Histopathological analyses of the first and second surgical specimens identified pseudostratified cuboidal epithelial cells, with no nuclear or cellular atypia resembling gastrointestinal mucosa, lining the inner surface of the cystic wall. Based on these findings the lesion was diagnosed as NC. The third surgical specimen exhibited apparent malignant features of the epithelial cells with elongated and hyperchromatic nuclei, several mitotic figures, small necrotic foci, and a patternless or sheet-like arrangement. Based on these findings, the lesion was diagnosed as NC with malignant transformation. Next-generation sequencing revealed KRAS p.G12D mutation in all specimens. Additionally, the third surgical specimen harbored the following 12 de novo gene alterations: ARID1A loss, BAP1 p.F170L, CDKN1B loss, CDKN2A loss, CDKN2B loss, FLCN loss, PTCH1 loss, PTEN loss, PTPRD loss, SUFU loss, TP53 loss, and TSC1 loss. The aforementioned results suggest that KRAS mutation is associated with the development of the NC, and that the additional gene alterations contribute to malignant transformation of the NC.

    DOI: 10.1111/neup.12822

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  • Phosphorylation of Tau at Threonine 231 in Patients With Multiple System Atrophy and in a Mouse Model

    Makoto T Tanaka, Kunikazu Tanji, Yasuo Miki, Taku Ozaki, Fumiaki Mori, Hideki Hayashi, Akiyoshi Kakita, Koichi Wakabayashi

    Journal of Neuropathology &amp; Experimental Neurology   2022.9

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    Abstract

    Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder pathologically characterized by the presence of glial cytoplasmic inclusions (GCIs). Some MSA patients exhibit motor deficits with accompanying cognitive impairment. Of note, some patients suffering from MSA with longer disease duration have AT8-positive signals, which correspond to phosphorylated tau (P-tau) at 202/205 (P-tau202/205). However, P-tau sites other than the AT8 antibody epitope antibody are less well studied. Here, we focused on the effect of α-synuclein (Syn) expression on the phosphorylation of tau in MSA model mice. Among the 6 kinds of antibodies against P-tau, we confirmed that antibodies against P-tau at 231 (P-tau231) were phospho-specific and found that P-tau231 level was increased in parallel with disease progression in MSA model mice. Additional studies of human brains revealed that P-tau231 was mainly expressed in the temporal cortex in MSA brains and that its expression level was significantly higher in MSA patients than in controls. Immunohistochemical analysis showed that anti-P-tau231-, but not AT8, antibodies mainly immunolabeled hippocampal CA2/3 pyramidal neurons, and some GCIs in MSA. These data suggest that P-tau231 occurs in MSA differently from P-tau202/205.

    DOI: 10.1093/jnen/nlac082

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  • Alteration of Vesicle-Associated Membrane Protein-Binding Protein B in α-Synuclein Aggregates in Lewy Body Disease. International journal

    Fumiaki Mori, Yukino Nakamura, Yasuo Miki, Kunikazu Tanji, Tomoya Kon, Masahiko Tomiyama, Akiyoshi Kakita, Koichi Wakabayashi

    Journal of neuropathology and experimental neurology   81 ( 10 )   807 - 815   2022.8

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    α-Synuclein (α-Syn) binds to vesicle-associated membrane protein-binding protein B (VAPB) in the endoplasmic reticulum membrane. Recent studies have shown that α-Syn-immunoreactive Lewy pathology is characterized by membrane crowding, including vesicular structures. To elucidate the role of VAPB and vesicular structures in Parkinson's disease (PD) and in dementia with Lewy bodies (DLB), the relationships among VAPB, vesicular structures, and Lewy pathology were investigated by immunohistochemistry and immunoelectron microscopy in 8 PD and 4 DLB autopsy cases. The proportions of VAPB-negative neurons in the substantia nigra in PD and in the temporal cortex in DLB were significantly higher than those in 5 controls. In PD, the incidence of α-Syn inclusions in VAPB-negative neurons was significantly higher (77.4%) than in VAPB-positive neurons (1.6%) in the substantia nigra. In DLB, the incidence of α-Syn inclusions in VAPB-negative neurons was also significantly higher (65.3%) than in VAPB-positive neurons (2.8%) in the temporal cortex. Immunoelectron microscopy revealed that α-Syn and VAPB were localized to filamentous structures of Lewy bodies (LBs). However, only a few vesicular structures labeled with anti-α-Syn were observed within LBs. These findings suggest that reduction of VAPB is involved in the disease processes of PD and DLB, although vesicular structures may not directly contribute to the formation of LBs.

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  • Epilepsy surgery without lipoma removal for temporal lobe epilepsy associated with lipoma in the Sylvian fissure. International journal

    Kazuki Nomura, Hiroharu Suzuki, Yasushi Iimura, Takumi Mitsuhashi, Samantha Tamrakar, Tetsuya Ueda, Kazuki Nishioka, Keiko Fusegi, Mari Tada, Madoka Nakajima, Akiyoshi Kakita, Hidenori Sugano

    Acta neurochirurgica   165 ( 1 )   265 - 269   2022.8

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    Epileptic seizure is the common symptom associated with lipomas in the Sylvian fissure (Sylvian lipomas). Removal of these lipomas carries risks of hemorrhage and brain damage. We report a surgical strategy of not removing the lipoma in a case of intractable temporal lobe epilepsy associated with Sylvian lipoma. We performed anterior temporal lobectomy with preservation of the pia mater of the Sylvian fissure and achieved seizure freedom. Focal cortical dysplasia type 1 of the epileptic neocortex adjacent to the Sylvian lipoma was pathologically diagnosed. We recommend our surgical procedure in similar cases to avoid complications and achieve adequate seizure control.

    DOI: 10.1007/s00701-022-05330-7

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  • ヒトてんかん焦点組織における興奮・抑制不均衡の病態病理学的基盤

    小笠原 輝, 中島 光子, 才津 浩智, 竹林 浩秀, 福多 真史, 伊藤 陽祐, 柿田 明美, 北浦 弘樹

    てんかん研究   40 ( 2 )   423 - 423   2022.8

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  • Pathological substrate of memory impairment in multiple system atrophy. International journal

    Yasuo Miki, Kunikazu Tanji, Kana Shinnai, Makoto T Tanaka, Firat Altay, Sandrine C Foti, Catherine Strand, Takanori Sasaki, Tomoya Kon, Shuji Shimoyama, Tomonori Furukawa, Haruo Nishijima, Hiromi Yamazaki, Yasmine T Asi, Conceição Bettencourt, Zane Jaunmuktane, Mari Tada, Fumiaki Mori, Hiroki Mizukami, Masahiko Tomiyama, Hilal A Lashuel, Tammaryn Lashley, Akiyoshi Kakita, Helen Ling, Andrew J Lees, Janice L Holton, Thomas T Warner, Koichi Wakabayashi

    Neuropathology and applied neurobiology   48 ( 7 )   e12844   2022.7

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    AIMS: Synaptic dysfunction in Parkinson's disease is caused by propagation of pathogenic α-synuclein between neurons. Previously, in multiple system atrophy (MSA), pathologically characterised by ectopic deposition of abnormal α-synuclein predominantly in oligodendrocytes, we demonstrated that the occurrence of memory impairment was associated with the number of α-synuclein-positive neuronal cytoplasmic inclusions (NCIs) in the hippocampus. In the present study, we aimed to investigate how abnormal α-synuclein in the hippocampus can lead to memory impairment. METHODS: We performed pathological and biochemical analyses using a mouse model of adult-onset MSA and human cases (MSA, N = 25; Parkinson's disease, N = 3; Alzheimer's disease, N = 2; normal controls, N = 11). In addition, the MSA model mice were examined behaviourally and physiologically. RESULTS: In the MSA model, inducible human α-synuclein was first expressed in oligodendrocytes and subsequently accumulated in the cytoplasm of excitatory hippocampal neurons (NCI-like structures) and their presynaptic nerve terminals with the development of memory impairment. α-Synuclein oligomers increased simultaneously in the hippocampus of the MSA model. Hippocampal dendritic spines also decreased in number, followed by suppression of long-term potentiation. Consistent with these findings obtained in the MSA model, post-mortem analysis of human MSA brain tissues showed that cases of MSA with memory impairment developed more NCIs in excitatory hippocampal neurons along with α-synuclein oligomers than those without. CONCLUSIONS: Our results provide new insights into the role of α-synuclein oligomers as a possible pathological cause of memory impairment in MSA.

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  • Periodic cycles of seizure clustering and suppression in children with epilepsy strongly suggest focal cortical dysplasia

    Yoshihiko Saito, Kenji Sugai, Masaki Iwasaki, Mahito Atobe, Noriko Sato, Akiyoshi Kakita, Yuko Saito, Taisuke Ohtsuki, Masayuki Sasaki

    Developmental Medicine &amp; Child Neurology   2022.7

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    DOI: 10.1111/dmcn.15365

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  • 【神経核内封入体病・白質脳症】脳小血管病の病理

    齋藤 理恵, 柿田 明美

    脳神経内科   97 ( 1 )   81 - 90   2022.7

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  • 【神経核内封入体病・白質脳症】ミクログリア関連疾患の病理(HDLS、NHD、ALD)

    他田 真理, 柿田 明美

    脳神経内科   97 ( 1 )   91 - 100   2022.7

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  • Praja1 RING-finger E3 ubiquitin ligase is a common suppressor of neurodegenerative disease-associated protein aggregation. International journal

    Kazuhiko Watabe, Motoko Niida-Kawaguchi, Mari Tada, Yoichiro Kato, Makiko Murata, Kunikazu Tanji, Koichi Wakabayashi, Mitsunori Yamada, Akiyoshi Kakita, Noriyuki Shibata

    Neuropathology : official journal of the Japanese Society of Neuropathology   2022.6

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    The formation of misfolded protein aggregates is one of the pathological hallmarks of neurodegenerative diseases. We have previously demonstrated the cytoplasmic aggregate formation of adenovirally expressed transactivation response DNA-binding protein of 43 kDa (TDP-43), the main constituent of neuronal cytoplasmic aggregates in cases of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD), in cultured neuronal cells under the condition of proteasome inhibition. The TDP-43 aggregate formation was markedly suppressed by co-infection of adenoviruses expressing heat shock transcription factor 1 (HSF1), a master regulator of heat shock response, and Praja1 RING-finger E3 ubiquitin ligase (PJA1) located downstream of the HSF1 pathway. In the present study, we examined other reportedly known E3 ubiquitin ligases for TDP-43, i.e. Parkin, RNF112 and RNF220, but failed to find their suppressive effects on neuronal cytoplasmic TDP-43 aggregate formation, although they all bind to TDP-43 as verified by co-immunoprecipitation. In contrast, PJA1 also binds to adenovirally expressed wild-type and mutated fused in sarcoma, superoxide dismutase 1, α-synuclein and ataxin-3, and huntingtin polyglutamine proteins in neuronal cultures and suppressed the aggregate formation of these proteins. These results suggest that PJA1 is a common sensing factor for aggregate-prone proteins to counteract their aggregation propensity, and could be a potential therapeutic target for neurodegenerative diseases that include ALS, FTLD, Parkinson's disease and polyglutamine diseases.

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  • 臨床医のための神経病理再入門 CARASIL

    齋藤 理恵, 小野寺 理, 柿田 明美

    Clinical Neuroscience   40 ( 6 )   700 - 702   2022.6

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  • 臨床医のための神経病理再入門 CARASIL

    齋藤 理恵, 小野寺 理, 柿田 明美

    Clinical Neuroscience   40 ( 6 )   700 - 702   2022.6

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  • Actin-binding protein filamin-A drives tau aggregation and contributes to progressive supranuclear palsy pathology. Reviewed International journal

    Koyo Tsujikawa, Kohei Hamanaka, Yuichi Riku, Yuki Hattori, Norikazu Hara, Yohei Iguchi, Shinsuke Ishigaki, Atsushi Hashizume, Satoko Miyatake, Satomi Mitsuhashi, Yu Miyazaki, Mayumi Kataoka, Li Jiayi, Keizo Yasui, Satoshi Kuru, Haruki Koike, Kenta Kobayashi, Naruhiko Sahara, Norio Ozaki, Mari Yoshida, Akiyoshi Kakita, Yuko Saito, Yasushi Iwasaki, Akinori Miyashita, Takeshi Iwatsubo, Takeshi Ikeuchi, Takaki Miyata, Gen Sobue, Naomichi Matsumoto, Kentaro Sahashi, Masahisa Katsuno

    Science advances   8 ( 21 )   eabm5029   2022.5

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    While amyloid-β lies upstream of tau pathology in Alzheimer's disease, key drivers for other tauopathies, including progressive supranuclear palsy (PSP), are largely unknown. Various tau mutations are known to facilitate tau aggregation, but how the nonmutated tau, which most cases with PSP share, increases its propensity to aggregate in neurons and glial cells has remained elusive. Here, we identified genetic variations and protein abundance of filamin-A in the PSP brains without tau mutations. We provided in vivo biochemical evidence that increased filamin-A levels enhance the phosphorylation and insolubility of tau through interacting actin filaments. In addition, reduction of filamin-A corrected aberrant tau levels in the culture cells from PSP cases. Moreover, transgenic mice carrying human filamin-A recapitulated tau pathology in the neurons. Our data highlight that filamin-A promotes tau aggregation, providing a potential mechanism by which filamin-A contributes to PSP pathology.

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  • The neostriatum in polyglutamine diseases: preferential decreases in large neurons in dentatorubral‐pallidoluysian atrophy and <scp>Machado‐Joseph</scp> disease and in small neurons in Huntington disease

    Kiyomitsu Oyanagi, Hiroshi Shimizu, Mitsunori Yamada, Akiyoshi Kakita

    Neuropathology   2022.5

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    DOI: 10.1111/neup.12811

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  • 小児・AYA世代のヒストン遺伝子変異びまん性神経膠腫症例の後方視的検討

    塚本 佳広, 高橋 陽彦, 温 城太郎, 小倉 良介, 棗田 学, 岡本 浩一郎, 大石 誠, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   39 ( Suppl. )   100 - 100   2022.5

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  • 脳腫瘍研究のcutting edge-先端画像、実験/分子病理、デジタル病理- 髄芽腫におけるGLI3 single cell RNAシーケンス解析 細胞レベルから見えて来たこと

    棗田 学, 宮下 聡, 宮原 弘明, 高橋 晴彦, 塚本 佳広, 大石 誠, 吉村 淳一, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   39 ( Suppl. )   072 - 072   2022.5

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  • Elevation of EGR1/zif268, a Neural Activity Marker, in the Auditory Cortex of Patients with Schizophrenia and its Animal Model

    Yuriko Iwakura, Ryoka Kawahara-Miki, Satoshi Kida, Hidekazu Sotoyama, Ramil Gabdulkhaev, Hitoshi Takahashi, Yasuto Kunii, Mizuki Hino, Atsuko Nagaoka, Ryuta Izumi, Risa Shishido, Toshiyuki Someya, Hirooki Yabe, Akiyoshi Kakita, Hiroyuki Nawa

    Neurochemical Research   2022.4

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    DOI: 10.1007/s11064-022-03599-9

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  • Independent distribution between tauopathy secondary to subacute sclerotic panencephalitis and measles virus: An immunohistochemical analysis in autopsy cases including cases treated with aggressive antiviral therapies. International journal

    Hiroaki Miyahara, Akio Akagi, Yuichi Riku, Jun Sone, Yasushi Otsuka, Motoko Sakai, Satoshi Kuru, Masato Hasegawa, Mari Yoshida, Akiyoshi Kakita, Yasushi Iwasaki

    Brain pathology (Zurich, Switzerland)   32 ( 6 )   e13069   2022.4

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    Subacute sclerotic panencephalitis (SSPE) is a refractory neurological disorder after exposure to measles virus. Recently, SSPE cases have been treated with antiviral therapies, but data on the efficacy are inconclusive. Abnormal tau accumulation has been reported in the brain tissue of SSPE cases, but there are few reports in which this is amply discussed. Five autopsied cases diagnosed as definite SSPE were included in this study. The subject age or disease duration ranged from 7.6 to 40.9 years old or from 0.5 to 20.8 years, respectively. Cases 3 and 4 had been treated with antiviral therapies. All evaluated cases showed marked brain atrophy with cerebral ventricle dilatation; additionally, marked demyelination with fibrillary gliosis were observed in the cerebral white matter. The brainstem, cerebellum, and spinal cord were relatively preserved. Immunoreactivity (IR) against measles virus was seen in the brainstem tegmentum, neocortex, and/or limbic cortex of the untreated cases but was rarely seen in the two treated cases. Activated microglia were broadly observed from the cerebrum to the spinal cord and had no meaningful difference among cases. Neurofibrillary tangles characterized by a combination of 3- and 4-repeat tau were observed mainly in the oculomotor nuclei, locus coeruleus, and limbic cortex. IR against phosphorylated tau was seen mainly in the cingulate gyrus, oculomotor nuclei, and pontine tegmentum, and tended to be observed frequently in cases with long disease durations but also tended to decrease along with neuronal loss, as in Case 5, which had the longest disease duration. Since the distribution of phosphorylated tau was independent from that of measles virus, the tauopathy following SSPE was inferred to be the result of diffuse brain inflammation triggered by measles rather than a direct result of measles virus. Moreover, antiviral therapies seemed to suppress measles virus but not the progression of tauopathy.

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  • Brain TDP-43 pathology in corticobasal degeneration: Topographical correlation with neuronal loss. International journal

    Makoto Sainouchi, Mari Tada, Yusran Ady Fitrah, Norikazu Hara, Kou Tanaka, Jiro Idezuka, Izumi Aida, Takashi Nakajima, Akinori Miyashita, Kohei Akazawa, Takeshi Ikeuchi, Osamu Onodera, Akiyoshi Kakita

    Neuropathology and applied neurobiology   48 ( 3 )   e12786   2022.4

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    AIMS: Neuronal and glial inclusions comprising transactive response DNA-binding protein of 43 kDa (TDP-43) have been identified in the brains of patients with corticobasal degeneration (CBD), and a possible correlation between the presence of these inclusions and clinical phenotypes has been speculated. However, the significance of TDP-43 pathology in the pathomechanism of CBD has remained unclear. Here, we investigated the topographical relationship between TDP-43 inclusions and neuronal loss in CBD. METHODS: We estimated semi-quantitatively neuronal loss and TDP-43 pathology in the form of neuronal cytoplasmic inclusions (NCIs), astrocytic inclusions (AIs), oligodendroglial cytoplasmic inclusions (GCIs), and dystrophic neurites in 22 CNS regions in 10 patients with CBD. Then, the degree of correlation between the severity of neuronal loss and the quantity of each type of TDP-43 inclusion was assessed. We also investigated tau pathology in a similar manner. RESULTS: TDP-43 pathology was evident in nine patients. The putamen and globus pallidus were the regions most frequently affected (80%). NCIs were the most prominent form, and their quantity was significantly correlated with the severity of neuronal loss in more than half of the regions examined. The quantities of TDP-43 NCIs and tau NCIs were correlated in only a few regions. The number of regions where the quantities of TDP-43 AIs and GCIs were correlated with the severity of neuronal loss was apparently small in comparison with that of NCIs. CONCLUSIONS: TDP-43 alterations in neurons, not closely associated with tau pathology, may be involved in the pathomechanism underlying neuronal loss in CBD. There was a significant topographical correlation between neuronal cytoplasmic aggregation of TDP-43 and neuronal loss in CBD, suggesting that TDP-43 protein aberration might be associated with neuronal degeneration in CBD. There was no close correlation between the burden of TDP-43 and that of tau in neurons.

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  • Fibrodysplasia ossificans progressiva: Histopathological implications of aberrant bone morphogenic protein signalling for CNS dysgenesis

    Hidetomo Tanaka, Hiroshi Shimizu, Yosuke Yonemochi, Tetsuo Ozawa, Yasuko Toyoshima, Takashi Nakajima, Akiyoshi Kakita

    Neuropathology and Applied Neurobiology   2022.3

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    DOI: 10.1111/nan.12805

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  • Endogenous human retrovirus-K is not increased in the affected tissues of Japanese ALS patients. International journal

    Tomohiko Ishihara, Akihide Koyama, Yuya Hatano, Ryoko Takeuchi, Yuka Koike, Taisuke Kato, Mari Tada, Akiyoshi Kakita, Osamu Onodera

    Neuroscience research   178   78 - 82   2022.2

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    Activation of human endogenous retrovirus-K (HERV-K) is one of the proposed risk factors for amyotrophic lateral sclerosis (ALS). The HERV-K envelope protein has been reported to show neurotoxicity, and development of therapy with reverse transcriptase inhibitors is being investigated. On the other hand, some reports have failed to show HERV-K activation in ALS. In this study, we analyzed the expression of HERV-K mRNA in the motor cortex and spinal cord of 15 Japanese patients with sporadic ALS and 19 controls using reverse transcriptase droplet digital PCR. This revealed no significant increase of HERV-K expression in ALS-affected tissues, suggesting that the association between ALS and HERV-K remains questionable.

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  • Burden of seizures and comorbidities in patients with epilepsy: a survey based on the tertiary hospital-based Epilepsy Syndrome Registry in Japan. International journal

    Yushi Inoue, Shin-Ichiro Hamano, Masaharu Hayashi, Hiroshi Sakuma, Shinichi Hirose, Atsushi Ishii, Ryoko Honda, Akio Ikeda, Katsumi Imai, Kazutaka Jin, Akiko Kada, Akiyoshi Kakita, Mitsuhiro Kato, Kensuke Kawai, Tamihiro Kawakami, Katsuhiro Kobayashi, Toyojiro Matsuishi, Takeshi Matsuo, Shin Nabatame, Nobuhiko Okamoto, Susumu Ito, Akihisa Okumura, Akiko Saito, Hideaki Shiraishi, Hiroshi Shirozu, Takashi Saito, Hidenori Sugano, Yukitoshi Takahashi, Hitoshi Yamamoto, Tetsuhiro Fukuyama, Ichiro Kuki

    Epileptic disorders : international epilepsy journal with videotape   24 ( 1 )   82 - 94   2022.2

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    OBJECTIVE: To examine the current medical and psychosocial status of patients with epilepsy, aiming to facilitate appropriate application of the Intractable/Rare Diseases Act of Japan. METHODS: By analysing the cross-sectional data of patients registered in the tertiary hospital-based Epilepsy Syndrome Registry of Japan, we investigated the proportion of patients who met the severity criteria as defined by the Act (seizure frequency of at least once a month, or presence of intellectual/neurological/psychiatric symptoms, or both) and whether there are candidate syndrome/diseases to be added to the existing list in the Act. RESULTS: In total, 2,209 patients were registered. After excluding self-limited/idiopathic epilepsies, 1,851 of 2,110 patients (87.7%) met the severity criteria. The patients were classified into eight main epilepsy syndromes (594 patients), 20 groups based on aetiology (1,078 patients), and three groups without known aetiology (427 patients). Most of the groups classified by syndrome or aetiology had high proportions of patients satisfying the severity criteria (>90%), but some groups had relatively low proportions (<80%) resulting from favourable outcome of surgical therapy. Several small groups with known syndrome/aetiology await detailed analysis based on a sufficiently large enough number of patients registered, some of whom may potentially be added to the list of the Act. SIGNIFICANCE: The registry provides data to examine the usefulness of the severity criteria and list of diseases that are operationally defined by the Act. Most epilepsy patients with various syndromes/diseases and aetiology groups are covered by the Act but some are not, and the list of designated syndromes/diseases should be complemented by further amendments, as suggested by future research.

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  • Sirolimus for epileptic seizures associated with focal cortical dysplasia type II. International journal

    Mitsuhiro Kato, Akiko Kada, Hideaki Shiraishi, Jun Tohyama, Eiji Nakagawa, Yukitoshi Takahashi, Tomoyuki Akiyama, Akiyoshi Kakita, Noriko Miyake, Atsushi Fujita, Akiko M Saito, Yushi Inoue

    Annals of clinical and translational neurology   9 ( 2 )   181 - 192   2022.2

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    OBJECTIVE: To determine whether sirolimus, a mechanistic target of rapamycin (mTOR) inhibitor, reduces epileptic seizures associated with focal cortical dysplasia (FCD) type II. METHODS: Sixteen patients (aged 6-57 years) with FCD type II received sirolimus at an initial dose of 1 or 2 mg/day based on body weight (FCDS-01). In 15 patients, the dose was adjusted to achieve target trough ranges of 5-15 ng/mL, followed by a 12-week maintenance therapy period. The primary endpoint was a lower focal seizure frequency during the maintenance therapy period. Further, we also conducted a prospective cohort study (RES-FCD) in which 60 patients with FCD type II were included as an external control group. RESULTS: The focal seizure frequency reduced by 25% in all patients during the maintenance therapy period and by a median value of 17%, 28%, and 23% during the 1-4-, 5-8-, and 9-12-week periods. The response rate was 33%. The focal seizure frequency in the external control group reduced by 0.5%. However, the background characteristics of external and sirolimus-treated groups differed. Adverse events were consistent with those of mTOR inhibitors reported previously. The blood KL-6 level was elevated over time. INTERPRETATION: The reduction of focal seizures did not meet the predetermined level of statistical significance. The safety profile of the drug was tolerable. The potential for a reduction of focal seizures over time merit further investigations.

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  • 臨床医のための神経病理再入門 小脳・脳幹梗塞

    佐藤 朋江, 齊ノ内 信, 齋藤 理恵, 柿田 明美

    Clinical Neuroscience   40 ( 2 )   148 - 150   2022.2

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  • Familial idiopathic basal ganglia calcification with a heterozygous missense variant (c. 902C >T/p. P307L ) in SLC20A2 showing widespread cerebrovascular lesions

    Kenji Sakai, Chiho Ishida, Koji Hayashi, Naotaka Tsuji, Takayuki Kannon, Kazuyoshi Hosomichi, Nobuyuki Takei, Akiyoshi Kakita, Atsushi Tajima, Masahito Yamada

    Neuropathology   2022.1

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    DOI: 10.1111/neup.12781

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  • USP10 inhibits aberrant cytoplasmic aggregation of TDP-43 by promoting stress granule clearance. International journal

    Masahiko Takahashi, Hiroki Kitaura, Akiyoshi Kakita, Taichi Kakihana, Yoshinori Katsuragi, Osamu Onodera, Yuriko Iwakura, Hiroyuki Nawa, Masaaki Komatsu, Masahiro Fujii

    Molecular and cellular biology   42 ( 3 )   MCB0039321   2022.1

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    TDP-43 is a causative factor of amyotrophic lateral sclerosis (ALS). Cytoplasmic TDP-43 aggregates in neurons are a hallmark pathology of ALS. Under various stress conditions, TDP-43 localizes sequentially to two cytoplasmic protein aggregates: stress granules (SGs) first, and then aggresomes. Accumulating evidence suggests that delayed clearance of TDP-43-positive SGs is associated with pathological TDP-43 aggregates in ALS. We found that USP10 promotes the clearance of TDP-43-positive SGs in cells treated with proteasome inhibitor, thereby promoting the formation of TDP-43-positive aggresomes, and the depletion of USP10 increases the amount of insoluble TDP-35, a cleaved product of TDP-43, in the cytoplasm. TDP-35 interacted with USP10 in an RNA-binding dependent manner; however, impaired RNA-binding of TDP-35 reduced the localization in SGs and aggresomes and induced USP10-negative TDP-35 aggregates. Immunohistochemistry showed that most of the cytoplasmic TDP-43/TDP-35-aggregates in the neurons of ALS patients were USP10-negative. Our findings suggest that USP10 inhibits aberrant aggregation of TDP-43/TDP-35 in the cytoplasm of neuronal cells by promoting the clearance of TDP-43/TDP-35-positive SGs and facilitating the formation of TDP-43/TDP-35-positive aggresomes.

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  • EGF Downregulates Presynaptic Maturation and Suppresses Synapse Formation In Vitro and In Vivo. International journal

    Nobuyuki Takei, Daisaku Yokomaku, Takaho Yamada, Tadasato Nagano, Akiyoshi Kakita, Hisaaki Namba, Tatsuo Ushiki, Hitoshi Takahashi, Hiroyuki Nawa

    Neurochemical research   2022.1

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    Neuronal differentiation, maturation, and synapse formation are regulated by various growth factors. Here we show that epidermal growth factor (EGF) negatively regulates presynaptic maturation and synapse formation. In cortical neurons, EGF maintained axon elongation and reduced the sizes of growth cones in culture. Furthermore, EGF decreased the levels of presynaptic molecules and number of presynaptic puncta, suggesting that EGF inhibits neuronal maturation. The reduction of synaptic sites is confirmed by the decreased frequencies of miniature EPSCs. In vivo analysis revealed that while peripherally administrated EGF decreased the levels of presynaptic molecules and numbers of synaptophysin-positive puncta in the prefrontal cortices of neonatal rats, EGF receptor inhibitors upregulated these indexes, suggesting that endogenous EGF receptor ligands suppress presynaptic maturation. Electron microscopy further revealed that EGF decreased the numbers, but not the sizes, of synaptic structures in vivo. These findings suggest that endogenous EGF and/or other EGF receptor ligands negatively modulates presynaptic maturation and synapse formation.

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  • Meningoencephalocele in the Lateral Sphenoid Sinus Showing Malformation of Cortical Development: A Case Report.

    Taro Sato, Tetsuya Hiraishi, Mari Tada, Manabu Natsumeda, Jotaro On, Haruhiko Takahashi, Taiki Saito, Noritaka Okubo, Makoto Oishi, Akiyoshi Kakita, Yukihiko Fujii

    NMC case report journal   9   281 - 287   2022

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    Meningoencephalocele in the lateral sphenoid sinus (SS) has been determined to be a rare entity often detected by cerebrospinal fluid (CSF) rhinorrhea. To date, the pathology of meningoencephalocele in the lateral SS has remained to be unclear in many cases. In this study, we report on a case of a 72-year-old woman with an arteriovenous malformation who presented with CSF rhinorrhea. Radiologic investigations revealed a left temporal meningoencephalocele in the lateral SS. We removed the meningoencephalocele and performed skull base repair, after which the CSF rhinorrhea resolved. Pathological examination showed congenital cortical abnormalities with dysmorphic neurons in various shapes and acquired chronic tissue alterations including fibrillary gliosis and scattered Rosenthal fibers. These findings may further aid in understanding the etiopathogenesis of meningoencephalocele in the lateral SS.

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  • Cytosolic dsDNA of mitochondrial origin induces cytotoxicity and neurodegeneration in cellular and zebrafish models of Parkinson’s disease

    Hideaki Matsui, Junko Ito, Noriko Matsui, Tamayo Uechi, Osamu Onodera, Akiyoshi Kakita

    Nature Communications   12 ( 1 )   2021.12

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    <title>Abstract</title>Mitochondrial dysfunction and lysosomal dysfunction have been implicated in Parkinson’s disease (PD), but the links between these dysfunctions in PD pathogenesis are still largely unknown. Here we report that cytosolic dsDNA of mitochondrial origin escaping from lysosomal degradation was shown to induce cytotoxicity in cultured cells and PD phenotypes in vivo. The depletion of PINK1, GBA and/or ATP13A2 causes increases in cytosolic dsDNA of mitochondrial origin and induces type I interferon (IFN) responses and cell death in cultured cell lines. These phenotypes are rescued by the overexpression of DNase II, a lysosomal DNase that degrades discarded mitochondrial DNA, or the depletion of IFI16, which acts as a sensor for cytosolic dsDNA of mitochondrial origin. Reducing the abundance of cytosolic dsDNA by overexpressing human DNase II ameliorates movement disorders and dopaminergic cell loss in gba mutant PD model zebrafish. Furthermore, IFI16 and cytosolic dsDNA puncta of mitochondrial origin accumulate in the brain of patients with PD. These results support a common causative role for the cytosolic leakage of mitochondrial DNA in PD pathogenesis.

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  • 【ブレインバンク/死後脳研究】統合失調症死後脳におけるタンパク定量解析-ALDH4A1とその発現に影響する遺伝子多型

    長岡 敦子, 國井 泰人, 日野 瑞城, 泉 竜太, 宍戸 理紗, 齊ノ内 信, 柿田 明美, 矢部 博興

    日本生物学的精神医学会誌   32 ( 4 )   186 - 190   2021.12

  • Parkinson's disease and parkinsonism: Clinicopathological discrepancies on diagnosis in three patients. International journal

    Yasuko Toyoshima, Hitoshi Takahashi, Shinnichi Katada, Naoyuki Kojima, Mari Tada, Takashi Tani, Ryoko Koike, Takanori Nozawa, Izumi Aida, Takashi Nakajima, Osamu Onodera, Akiyoshi Kakita

    Neuropathology : official journal of the Japanese Society of Neuropathology   41 ( 6 )   450 - 456   2021.12

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    Parkinson's disease (PD) is one of the most common neurodegenerative disorders. The cardinal neuropathological features of PD include selective and progressive loss of pigmented neurons in the substantia nigra, deficiencies in dopaminergic signaling in the striatum, and occurrence of phosphorylated α-synuclein-identified Lewy bodies in the nervous system. Parkinsonism, the clinical presentation of movement disorders seen in PD, is a feature shared commonly by other pathologically distinct neurodegenerative diseases, such as progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and multiple system atrophy (MSA). Consequently, it is sometimes difficult to distinguish PD from such parkinsonism-related neurological disorders. In addition, parkinsonism is not always a feature of certain neurodegenerative diseases, and it can sometimes develop as a result of various forms of drug intoxication or cerebrovascular disease. Here, we describe the clinicopathological features of three patients (cases 1, 2, and 3) diagnosed as having PSP, MSA, and PD, respectively, in each of whom the postmortem histopathological diagnosis differed from the final clinical diagnosis. Neuropathologically, they had suffered from coexistent disorders: PD, MSA, and argyrophilic grain disease (case 1); PD (case 2); and vascular parkinsonism (case 3). The variety of patients showing features of parkinsonism underlines the importance of careful long-term follow up followed by postmortem neuropathological evaluation.

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  • Deep learning-based diagnosis of temporal lobe epilepsy associated with hippocampal sclerosis: An MRI study. International journal

    Yosuke Ito, Masafumi Fukuda, Hitoshi Matsuzawa, Hiroshi Masuda, Yu Kobayashi, Naoya Hasegawa, Hiroki Kitaura, Akiyoshi Kakita, Yukihiko Fujii

    Epilepsy research   178   106815 - 106815   2021.12

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    PURPOSE: The currently available indicators-sensitivity and specificity of expert radiological evaluation of MRIs-to identify mesial temporal lobe epilepsy (MTLE) associated with hippocampal sclerosis (HS) are deficient, as they cannot be easily assessed. We developed and investigated the use of a novel convolutional neural network trained on preoperative MRIs to aid diagnosis of these conditions. SUBJECTS AND METHODS: We enrolled 141 individuals: 85 with clinically diagnosed mesial temporal lobe epilepsy (MTLE) and hippocampal sclerosis International League Against Epilepsy (HS ILAE) type 1 who had undergone anterior temporal lobe hippocampectomy were assigned to the MTLE-HS group, and 56 epilepsy clinic outpatients diagnosed as nonepileptic were assigned to the normal group. We fine-tuned a modified CNN (mCNN) to classify the fully connected layers of ImageNet-pretrained VGG16 network models into the MTLE-HS and control groups. MTLE-HS was diagnosed using MRI both by the fine-tuned mCNN and epilepsy specialists. Their performances were compared. RESULTS: The fine-tuned mCNN achieved excellent diagnostic performance, including 91.1% [85%, 96%] mean sensitivity and 83.5% [75%, 91%] mean specificity. The area under the resulting receiver operating characteristic curve was 0.94 [0.90, 0.98] (DeLong's method). Expert interpretation of the same image data achieved a mean sensitivity of 73.1% [65%, 82%] and specificity of 66.3% [50%, 82%]. These confidence intervals were located entirely under the receiver operating characteristic curve of the fine-tuned mCNN. CONCLUSIONS: Deep learning-based diagnosis of MTLE-HS from preoperative MR images using our fine-tuned mCNN achieved a performance superior to the visual interpretation by epilepsy specialists. Our model could serve as a useful preoperative diagnostic tool for ascertaining hippocampal atrophy in patients with MTLE.

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  • 【ブレインバンク/死後脳研究】統合失調症死後脳におけるタンパク定量解析-ALDH4A1とその発現に影響する遺伝子多型

    長岡 敦子, 國井 泰人, 日野 瑞城, 泉 竜太, 宍戸 理紗, 齊ノ内 信, 柿田 明美, 矢部 博興

    日本生物学的精神医学会誌   32 ( 4 )   186 - 190   2021.12

  • Detection of 2-Hydroxyglutarate by 3.0-Tesla Magnetic Resonance Spectroscopy in Gliomas with Rare IDH Mutations: Making Sense of "False-Positive" Cases. International journal

    Manabu Natsumeda, Hironaka Igarashi, Ramil Gabdulkhaev, Haruhiko Takahashi, Kunio Motohashi, Ryosuke Ogura, Jun Watanabe, Yoshihiro Tsukamoto, Kouichirou Okamoto, Akiyoshi Kakita, Tsutomu Nakada, Yukihiko Fujii

    Diagnostics (Basel, Switzerland)   11 ( 11 )   2021.11

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    We have previously published a study on the reliable detection of 2-hydroxyglutarate (2HG) in lower-grade gliomas by magnetic resonance spectroscopy (MRS). In this short article, we re-evaluated five glioma cases originally assessed as isocitrate dehydrogenase (IDH) wildtype, which showed a high accumulation of 2HG, and were thought to be false-positives. A new primer was used for the detection of IDH2 mutation by Sanger sequencing. Adequate tissue for DNA analysis was available in 4 out of 5 cases. We found rare IDH2 mutations in two cases, with IDH2 R172W mutation in one case and IDH2 R172K mutation in another case. Both cases had very small mutant peaks, suggesting that the tumor volume was low in the tumor samples. Thus, the specificity of MRS for detecting IDH1/2 mutations was higher (81.3%) than that originally reported (72.2%). The detection of 2HG by MRS can aid in the diagnosis of rare, non-IDH1-R132H IDH1 and IDH2 mutations in gliomas.

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  • Candesartan prevents arteriopathy progression in cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy model. Reviewed International journal

    Taisuke Kato, Ri-Ichiroh Manabe, Hironaka Igarashi, Fuyuki Kametani, Sachiko Hirokawa, Yumi Sekine, Natsumi Fujita, Satoshi Saito, Yusuke Kawashima, Yuya Hatano, Shoichiro Ando, Hiroaki Nozaki, Akihiro Sugai, Masahiro Uemura, Masaki Fukunaga, Toshiya Sato, Akihide Koyama, Rie Saito, Atsushi Sugie, Yasuko Toyoshima, Hirotoshi Kawata, Shigeo Murayama, Masaki Matsumoto, Akiyoshi Kakita, Masato Hasegawa, Masafumi Ihara, Masato Kanazawa, Masatoyo Nishizawa, Shoji Tsuji, Osamu Onodera

    The Journal of clinical investigation   131 ( 22 )   2021.11

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    Cerebral small vessel disease (CSVD) causes dementia and gait disturbance due to arteriopathy. Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) is a hereditary form of CSVD caused by loss of high-temperature requirement A1 (HTRA1) serine protease activity. In CARASIL, arteriopathy causes intimal thickening, smooth muscle cell (SMC) degeneration, elastic lamina splitting, and vasodilation. The molecular mechanisms were proposed to involve the accumulation of matrisome proteins as substrates or abnormalities in transforming growth factor β (TGF-β) signaling. Here, we show that HTRA1-/- mice exhibited features of CARASIL-associated arteriopathy: intimal thickening, abnormal elastic lamina, and vasodilation. In addition, the mice exhibited reduced distensibility of the cerebral arteries and blood flow in the cerebral cortex. In the thickened intima, matrisome proteins, including the hub protein fibronectin (FN) and latent TGF-β binding protein 4 (LTBP-4), which are substrates of HTRA1, accumulated. Candesartan treatment alleviated matrisome protein accumulation and normalized the vascular distensibility and cerebral blood flow. Furthermore, candesartan reduced the mRNA expression of Fn1, Ltbp-4, and Adamtsl2, which are involved in forming the extracellular matrix network. Our results indicate that these accumulated matrisome proteins may be potential therapeutic targets for arteriopathy in CARASIL.

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  • Autoimmune glial fibrillary acidic protein astrocytopathy resembling isolated central nervous system lymphomatoid granulomatosis. International journal

    Akio Kimura, Shinei Kato, Akira Takekoshi, Nobuaki Yoshikura, Narufumi Yanagida, Hiroshi Kitaguchi, Daisuke Akiyama, Hiroshi Shimizu, Akiyoshi Kakita, Takayoshi Shimohata

    Journal of neuroimmunology   361   577748 - 577748   2021.10

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    We report two patients with meningoencephalomyelitis without evidence of extra central nervous system (CNS) involvement. Brain MRI showed linear perivascular radial gadolinium enhancement patterns and spinal cord MRI showed longitudinal extensive T2-hyperintensity lesions. Pathological findings from brain biopsies were angiocentric T-cell predominant lymphoid infiltrates that lacked Epstein-Barr virus-positive atypical B cells. The patients were initially suspected to have isolated CNS-lymphomatoid granulomatosis (LYG). Thereafter, glial fibrillary acidic protein (GFAP)-immunoglobulin G were detected in their cerebrospinal fluid. This finding suggested autoimmune GFAP astrocytopathy. We speculate there is a link between isolated CNS-LYG and autoimmune GFAP astrocytopathy.

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  • 各種タウオパチーにおける線維形成タウの翻訳後修飾の解析

    亀谷 富由樹, 吉田 眞理, 松原 知康, 村山 茂雄, 齊藤 祐子, 河上 緒, 女屋 光基, 田中 英智, 柿田 明美, 長谷川 成人

    Dementia Japan   35 ( 4 )   651 - 651   2021.10

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  • 認知症のゲノム医療 APOEの遺伝型とミスセンスレアバリアント:臨床応用への可能性

    宮下 哲典, 原 範和, 春日 健作, 菊地 正隆, 尾崎 浩一, 新飯田 俊平, 他田 真理, 柿田 明美, 池内 健

    Dementia Japan   35 ( 4 )   585 - 585   2021.10

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  • ヒト剖検脳による神経疾患横断的なレアバリアント解析 APOE

    宮下 哲典, 他田 真理, 原 範和, 長谷川 舞衣, 月江 珠緒, Lixin Liu, Bin Zhu, Yusran Ady Fitrah, 春日 健作, 菊地 正隆, 柿田 明美, 池内 健

    Dementia Japan   35 ( 4 )   650 - 650   2021.10

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  • 加齢と関連したDNA脱メチル化がTDP-43量の自己調節機構を障害する

    小池 佑佳, 須貝 章弘, 原 範和, 伊藤 絢子, 横関 明男, 石原 智彦, 山岸 拓磨, 坪口 晋太朗, 他田 真理, 池内 健, 柿田 明美, 小野寺 理

    Dementia Japan   35 ( 4 )   610 - 610   2021.10

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  • Alzheimer's Aβ assembly binds sodium pump and blocks endothelial NOS activity via ROS-PKC pathway in brain vascular endothelial cells. International journal

    Tomoya Sasahara, Kaori Satomura, Mari Tada, Akiyoshi Kakita, Minako Hoshi

    iScience   24 ( 9 )   102936 - 102936   2021.9

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    Amyloid β-protein (Aβ) may contribute to worsening of Alzheimer's disease (AD) through vascular dysfunction, but the molecular mechanism involved is unknown. Using ex vivo blood vessels and primary endothelial cells from human brain microvessels, we show that patient-derived Aβ assemblies, termed amylospheroids (ASPD), exist on the microvascular surface in patients' brains and inhibit vasorelaxation through binding to the α3 subunit of sodium, potassium-ATPase (NAKα3) in caveolae on endothelial cells. Interestingly, NAKα3 is also the toxic target of ASPD in neurons. ASPD-NAKα3 interaction elicits neurodegeneration through calcium overload in neurons, while the same interaction suppresses vasorelaxation by increasing the inactive form of endothelial nitric oxide synthase (eNOS) in endothelial cells via mitochondrial ROS and protein kinase C, independently of the physiological relaxation system. Thus, ASPD may contribute to both neuronal and vascular pathologies through binding to NAKα3. Therefore, blocking the ASPD-NAKα3 interaction may be a useful target for AD therapy.

    DOI: 10.1016/j.isci.2021.102936

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  • Hemiplegic-type ALS: clinicopathological features of two autopsied patients. International journal

    Makoto Sainouchi, Hidetomo Tanaka, Hiroshi Shimizu, Takuya Mashima, Takao Fukushima, Yuya Hatano, Tomohiko Ishihara, Kunihiko Makino, Osamu Onodera, Akiyoshi Kakita

    Journal of neurology, neurosurgery, and psychiatry   92 ( 9 )   1014 - 1016   2021.9

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  • Dysregulation of DPYSL2 expression by mTOR signaling in schizophrenia: Multi-level study of postmortem brain

    Ryuta Izumi, Mizuki Hino, Atsuko Nagaoka, Risa Shishido, Akiyoshi Kakita, Mikio Hoshino, Yasuto Kunii, Hirooki Yabe

    Neuroscience Research   2021.9

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    DOI: 10.1016/j.neures.2021.09.004

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  • Current medico-psycho-social conditions of patients with West syndrome in Japan. International journal

    Shinsaku Yoshitomi, Shin-Ichiro Hamano, Masaharu Hayashi, Hiroshi Sakuma, Shinichi Hirose, Atsushi Ishii, Ryoko Honda, Akio Ikeda, Katsumi Imai, Kazutaka Jin, Akiko Kada, Akiyoshi Kakita, Mitsuhiro Kato, Kensuke Kawai, Tamihiro Kawakami, Katsuhiro Kobayashi, Toyojiro Matsuishi, Takeshi Matsuo, Shin Nabatame, Nobuhiko Okamoto, Susumu Ito, Akihisa Okumura, Akiko Saito, Hideaki Shiraishi, Hiroshi Shirozu, Takashi Saito, Hidenori Sugano, Yukitoshi Takahashi, Hitoshi Yamamoto, Tetsuhiro Fukuyama, Ichiro Kuki, Yushi Inoue

    Epileptic disorders : international epilepsy journal with videotape   23 ( 4 )   579 - 589   2021.8

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    OBJECTIVE: To unveil current medical and psychosocial conditions of patients with West syndrome in Japan. METHODS: A cross-sectional analysis was performed in patients with West syndrome registered in the Rare Epilepsy Syndrome Registry (RES-R) of Japan. Furthermore, new-onset patients registered in the RES-R were observed prospectively and their outcomes after one and two years of follow-up were compared with data at onset. RESULTS: For the cross-sectional study, 303 patients with West syndrome were included. Seizures (such as spasms, tonic seizures and focal seizures) occurred daily in 69.3% of the patients at registration. Seizure frequency of less than one per year was observed in cases of unknown etiology (22.6%), genetic etiology (23.8%) and malformation of cortical development (MCD; 19.1%). Neurological findings were absent in 37.0%, but a high rate of abnormality was seen in patients with Aicardi syndrome, hypoxic-ischemic encephalopathy (HIE), genetic etiology and MCD other than focal cortical dysplasia, accompanied by a >50% rate of bedridden patients. Abnormal EEG was found in 96.7%, and CT/MRI was abnormal in 62.7%. Treatments included antiepileptic drug therapy (94.3%), hormonal therapy (72.6%), diet therapy (8.3%) and surgery (15.8%). Intellectual/developmental delay was present in 88.4%, and was more severe in patients with Aicardi syndrome, genetic etiology and HIE. Autism spectrum disorder was found in 13.5%. For the longitudinal study, 27 new-onset West syndrome patients were included. The follow-up study revealed improved seizure status after two years in 66.7%, but worsened developmental status in 55.6%, with overall improvement in 51.9%. SIGNIFICANCE: The study reveals the challenging neurological, physical and developmental aspects, as well as intractable seizures, in patients with West syndrome. More than a half of the children showed developmental delay after onset, even though seizures were reduced during the course of the disease.

    DOI: 10.1684/epd.2021.1301

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  • Evidence for Altered Phosphoinositide Signaling-Associated Molecules in the Postmortem Prefrontal Cortex of Patients with Schizophrenia. International journal

    Yasuto Kunii, Junya Matsumoto, Ryuta Izumi, Atsuko Nagaoka, Mizuki Hino, Risa Shishido, Makoto Sainouchi, Hiroyasu Akatsu, Yoshio Hashizume, Akiyoshi Kakita, Hirooki Yabe

    International journal of molecular sciences   22 ( 15 )   2021.7

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    Phosphoinositides (PIs) play important roles in the structure and function of the brain. Associations between PIs and the pathophysiology of schizophrenia have been studied. However, the significance of the PI metabolic pathway in the pathology of schizophrenia is unknown. We examined the expression of PI signaling-associated proteins in the postmortem brain of schizophrenia patients. Protein expression levels of phosphatidylinositol 4-phosphate 5-kinase type-1 gamma (PIP5K1C), phosphatidylinositol 4-kinase alpha (PIK4CA, also known as PIK4A), phosphatase and tensin homolog deleted from chromosome 10 (PTEN), protein kinase B (Akt), and glycogen synthase kinase 3β (GSK3β) were measured using enzyme-linked immunosorbent assays and multiplex fluorescent bead-based immunoassays of the prefrontal cortex (PFC) of postmortem samples from 23 schizophrenia patients and 47 normal controls. We also examined the association between PIK4CA expression and its genetic variants in the same brain samples. PIK4CA expression was lower, whereas Akt expression was higher, in the PFC of schizophrenia patients than in that of controls; PIP5K1C, PTEN, and GSK3β expression was not different. No single-nucleotide polymorphism significantly affected protein expression. We identified molecules involved in the pathology of schizophrenia via this lipid metabolic pathway. These results suggest that PIK4CA is involved in the mechanism underlying the pathogenesis of schizophrenia and is a potential novel therapeutic target.

    DOI: 10.3390/ijms22158280

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  • Reactive astrocytes contribute to epileptogenesis in patients with cavernous angioma. International journal

    Hiroki Kitaura, Tetsuya Hiraishi, Yosuke Itoh, Makoto Oishi, Yukihiko Fujii, Masafumi Fukuda, Akiyoshi Kakita

    Epilepsy research   176   106732 - 106732   2021.7

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    OBJECTIVE: Patients with cavernous angioma (CA) often suffer from severe epilepsy, and surgical resection is often performed to attenuate these epileptic seizures. Several studies have suggested that surgical removal of the surrounding hemosiderin-pigmented tissues adjacent to CA achieves better seizure control than restricted lesionectomy. Pathological examination of the resected foci reveals not only hemosiderin pigmentation but also various degrees of inflammatory change, such as hemosiderin-laden macrophages, gliosis and fibrosis. However, there is some controversy regarding the epileptogenic potential of these regions due to the uncertain nature of the mechanisms contributing to these histopathological changes. METHODS: To investigate the correlations between neuron hyperexcitability and evident pathological changes, we performed ex vivo flavoprotein fluorescence imaging using surgically resected epileptogenic foci surrounding CA. The mirror surfaces of the tissues used for the physiological experiment were also subjected to morphological examination. RESULTS: Hemosiderin-laden macrophages and many gemistocytic astrocytes were observed in the area adjacent to CA, where horizontal spreading excitations were detected significantly more frequently. Outside these areas, we found fine granular iron deposits and only a few fibrillary astrocytes, and weakly propagating excitations were detected. Furthermore, areas of enhanced activation were more clearly correlated with the glial proliferation index than with iron deposition. CONCLUSION: These results suggest that the epileptogenesis in patients with CA may be based on a biological process, such as alteration of glial function, rather than direct chemical reactions involving iron deposition.

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  • Role of VAPB and vesicular profiles in α-synuclein aggregates in multiple system atrophy. International journal

    Fumiaki Mori, Yasuo Miki, Kunikazu Tanji, Tomoya Kon, Masahiko Tomiyama, Akiyoshi Kakita, Koichi Wakabayashi

    Brain pathology (Zurich, Switzerland)   31 ( 6 )   e13001   2021.7

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    The pathological hallmark of multiple system atrophy (MSA) is fibrillary aggregates of α-synuclein (α-Syn) in the cytoplasm and nucleus of both oligodendrocytes and neurons. In neurons, α-Syn localizes to the cytosolic and membrane compartments, including the synaptic vesicles, mitochondria, and endoplasmic reticulum (ER). α-Syn binds to vesicle-associated membrane protein-binding protein B (VAPB) in the ER membrane. Overexpression of wild-type and familial Parkinson's disease mutant α-Syn perturbs the association between the ER and mitochondria, leading to ER stress and ultimately neurodegeneration. We examined brains from MSA patients (n = 7) and control subjects (n = 5) using immunohistochemistry and immunoelectron microscopy with antibodies against VAPB and phosphorylated α-Syn. In controls, the cytoplasm of neurons and glial cells was positive for VAPB, whereas in MSA lesions VAPB immunoreactivity was decreased. The proportion of VAPB-negative neurons in the pontine nucleus was significantly higher in MSA (13.6%) than in controls (0.6%). The incidence of cytoplasmic inclusions in VAPB-negative neurons was significantly higher (42.2%) than that in VAPB-positive neurons (3.6%); 67.2% of inclusion-bearing oligodendrocytes and 51.1% of inclusion-containing neurons were negative for VAPB. Immunoelectron microscopy revealed that α-Syn and VAPB were localized to granulofilamentous structures in the cytoplasm of oligodendrocytes and neurons. Many vesicular structures labeled with anti-α-Syn were also observed within the granulofilamentous structures in the cytoplasm and nucleus of both oligodendrocytes and neurons. These findings suggest that, in MSA, reduction of VAPB is involved in the disease process and that vesicular structures are associated with inclusion formation.

    DOI: 10.1111/bpa.13001

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  • Predicting BRAF V600E mutation in glioblastoma: utility of radiographic features.

    Manabu Natsumeda, Michael Chang, Ramil Gabdulkhaev, Haruhiko Takahashi, Yoshihiro Tsukamoto, Yu Kanemaru, Masayasu Okada, Makoto Oishi, Kouichirou Okamoto, Fausto J Rodriguez, Akiyoshi Kakita, Yukihiko Fujii, Karisa C Schreck

    Brain tumor pathology   38 ( 3 )   228 - 233   2021.7

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    Detection of BRAF V600E mutation in glioblastomas (GBMs) is important because of potential therapeutic implications. Still, the relative paucity of these mutations makes molecular detection in all GBMs controversial. In the present study, we analyzed clinical, radiographic and pathologic features of 12 BRAF V600E-mutant GBMs and 12 matched controls from 2 institutions. We found that a majority of BRAF V600E-mutant GBMs displayed a combination of well-circumscribed lesions, large cystic components with thin walls and solid cortical component on MRI, but with some overlap with matched BRAF wildtype controls (p = 0.069). BRAF V600E-mutant GBMs were also apt to gross total resection (83% vs 17%, p = 0.016) and morphologically displayed epithelioid features (83% vs 0%, p < 0.0001). Identification of these clinical, radiographic, and pathologic characteristics should prompt testing for BRAF V600E in IDH-wildtype GBM.

    DOI: 10.1007/s10014-021-00407-0

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  • Less-invasive diagnosis of disseminated epithelioid glioblastoma harboring BRAF V600E mutation by cerebrospinal fluid analysis-A case report. International journal

    Manabu Natsumeda, Yu Kanemaru, Yukie Kawaguchi, Hajime Umezu, Akiyoshi Kakita, Yukihiko Fujii

    Clinical case reports   9 ( 7 )   e04551   2021.7

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    Spinal dissemination in epithelioid glioblastoma can be diagnosed by cerebrospinal fluid cytology and liquid biopsy to detect BRAF V600E mutation.

    DOI: 10.1002/ccr3.4551

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  • 多系統萎縮症(MSA-P)の臨床経過をとり、病理学的にMSA-OPCA typeとパーキンソン病の合併が示唆された一例

    長谷川 有香, 竹島 明, 中村 航世, 青山 あずさ, 黒羽 泰子, 高橋 哲哉, 松原 奈絵, 他田 真理, 柿田 明美, 小池 亮子

    パーキンソン病・運動障害疾患コングレスプログラム・抄録集   15回   98 - 98   2021.7

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  • Correction to: A novel splicing variant of ANXA11 in a patient with amyotrophic lateral sclerosis: histologic and biochemical features. International journal

    Makoto Sainouchi, Yuya Hatano, Mari Tada, Tomohiko Ishihara, Shoichiro Ando, Taisuke Kato, Jun Tokunaga, Gaku Ito, Hiroaki Miyahara, Yasuko Toyoshima, Akio Yokoseki, Tetsutaro Ozawa, Kohei Akazawa, Osamu Onodera, Akiyoshi Kakita

    Acta neuropathologica communications   9 ( 1 )   115 - 115   2021.6

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  • Long Spinal Cord Lesions Caused by Venous Congestive Myelopathy Associated with Intravascular Large B-cell Lymphoma.

    Takeshi Miura, Shoji Saito, Rie Saito, Tomohiro Iwasaki, Naomi Mezaki, Tomoe Sato, Yoichi Ajioka, Akiyoshi Kakita, Takuya Mashima

    Internal medicine (Tokyo, Japan)   2021.6

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    Intravascular large B-cell lymphoma (IVLBCL) is a subtype of B-cell lymphoma, characterized by lymphoma cell proliferation within small blood vessels. We herein describe a rare case with long spinal cord lesions caused by venous congestive myelopathy associated with IVLBCL. An 81-year-old man presented with paraplegia of the lower limbs and sensory disturbances. Magnetic resonance imaging revealed intramedullary longitudinal T2-hyperintensity lesions in the thoracic cords. The patient died three months after disease onset, and a neuropathological analysis revealed predominantly atypical B-lymphocytes located sparsely in the veins of the spinal cord. IVLBCL should be considered in the differential diagnoses of long spinal cord lesions.

    DOI: 10.2169/internalmedicine.6717-20

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  • A novel splicing variant of ANXA11 in a patient with amyotrophic lateral sclerosis: histologic and biochemical features. International journal

    Makoto Sainouchi, Yuya Hatano, Mari Tada, Tomohiko Ishihara, Shoichiro Ando, Taisuke Kato, Jun Tokunaga, Gaku Ito, Hiroaki Miyahara, Yasuko Toyoshima, Akio Yokoseki, Tetsutaro Ozawa, Kohei Akazawa, Osamu Onodera, Akiyoshi Kakita

    Acta neuropathologica communications   9 ( 1 )   106 - 106   2021.6

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  • 小児脳腫瘍の新展開 髄芽腫におけるGLI3発現および役割の解明 完結編

    棗田 学, 宮原 弘明, 吉村 淳一, 塚本 佳広, 大石 誠, エバーハート・チャールズ, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   38 ( Suppl. )   058 - 058   2021.5

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  • 悪性神経膠腫におけるテモゾロミド療法前後のミスマッチ修復蛋白発現の検討

    山田 史織, 棗田 学, 高橋 陽彦, 安藤 和弘, 温 城太郎, 塚本 佳広, 岡田 正康, 大石 誠, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   38 ( Suppl. )   076 - 076   2021.5

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  • 脳腫瘍遺伝子異常の画像診断 IDH変異型神経膠腫における3T-MRSを用いた2HGの検出

    棗田 学, 五十嵐 博中, 本橋 邦夫, 塚本 佳広, 小倉 良介, 岡本 浩一郎, 大石 誠, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   38 ( Suppl. )   059 - 059   2021.5

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  • GH産生下垂体腺腫に対するソマトスタチンアナログの効果とソマトスタチン受容体発現分類の検討

    岡田 正康, 米岡 有一郎, 大石 誠, 平石 哲也, 佐野 正和, 棗田 学, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   38 ( Suppl. )   094 - 094   2021.5

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  • High grade astrocytomaに準じて治療したprimary anaplastic pleomorphic xanthoastrocytomaの4症例の検討

    塚本 佳広, 棗田 学, 温 城太郎, 小倉 良介, 清水 宏, 岡本 浩一郎, 大石 誠, 藤井 幸彦, 柿田 明美

    Brain Tumor Pathology   38 ( Suppl. )   078 - 078   2021.5

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  • 髄膜腫摘出術の7年後に発生した局所浸潤性・再発性fibromatosisの一例

    温 城太郎, 清水 宏, 齋藤 理恵, 渋谷 航平, 棗田 学, 平石 哲也, 佐野 正和, 梅津 哉, 藤井 幸彦, 柿田 明美

    Brain Tumor Pathology   38 ( Suppl. )   121 - 121   2021.5

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  • Betaine ameliorates schizophrenic traits by functionally compensating for KIF3-based CRMP2 transport. International journal

    Shogo Yoshihara, Xuguang Jiang, Momo Morikawa, Tadayuki Ogawa, Sotaro Ichinose, Hirooki Yabe, Akiyoshi Kakita, Manabu Toyoshima, Yasuto Kunii, Takeo Yoshikawa, Yosuke Tanaka, Nobutaka Hirokawa

    Cell reports   35 ( 2 )   108971 - 108971   2021.4

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    In schizophrenia (SCZ), neurons in the brain tend to undergo gross morphological changes, but the related molecular mechanism remains largely elusive. Using Kif3b+/- mice as a model with SCZ-like behaviors, we found that a high-betaine diet can significantly alleviate schizophrenic traits related to neuronal morphogenesis and behaviors. According to a deficiency in the transport of collapsin response mediator protein 2 (CRMP2) by the KIF3 motor, we identified a significant reduction in lamellipodial dynamics in developing Kif3b+/- neurons as a cause of neurite hyperbranching. Betaine administration significantly decreases CRMP2 carbonylation, which enhances the F-actin bundling needed for proper lamellipodial dynamics and microtubule exclusion and may thus functionally compensate for KIF3 deficiency. Because the KIF3 expression levels tend to be downregulated in the human prefrontal cortex of the postmortem brains of SCZ patients, this mechanism may partly participate in human SCZ pathogenesis, which we hypothesize could be alleviated by betaine administration.

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  • Low Detection Rate of H3K27M Mutations in Cerebrospinal Fluid Obtained from Lumbar Puncture in Newly Diagnosed Diffuse Midline Gliomas. International journal

    Jotaro On, Manabu Natsumeda, Jun Watanabe, Shoji Saito, Yu Kanemaru, Hideaki Abe, Yoshihiro Tsukamoto, Masayasu Okada, Makoto Oishi, Junichi Yoshimura, Akiyoshi Kakita, Yukihiko Fujii

    Diagnostics (Basel, Switzerland)   11 ( 4 )   2021.4

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    Recent studies have suggested the feasibility of detecting H3K27M mutations in the cerebrospinal fluid of diffuse midline glioma (DMG) patients. However, cerebrospinal fluid from patients in these studies were collected mainly during biopsy, ventriculo-peritoneal shunt procedures or postmortem. We assessed circulating tumor DNA (ctDNA) extracted from cerebrospinal fluid (CSF) and plasma in a series of 12 radiographically suspected and/or pathologically confirmed diffuse midline glioma patients and assessed for H3F3A K27M mutation using digital droplet PCR. In 10 patients, CSF was obtained by lumbar puncture at presentation. A definitive detection of H3F3A K27M mutation was achieved in only one case (10%); H3F3A K27M mutation was suspected in three other cases (30%). H3F3A K27M mutation was detected in two patients in CSF obtained by ventricular tap during a ventriculo-peritoneal shunt for obstructive hydrocephalus. Cases in which a definitive assessment was possible (definite H3F3A K27M or definite H3F3A wildtype) tended to be younger (median 7.5 years vs. 40.5 years; p = 0.07) and have a higher concentration of CSF protein (median 123 mg/dL vs. 27.5 mg/dL; p = 0.21) compared to nondefinite cases. Low proliferation and apoptotic rates seemed to be characteristics of DMG unfavorable for liquid biopsy. More advanced lesions with necrosis and evidence of dissemination were unlikely to be candidates for lumbar puncture due to the fear of exacerbating obstructive hydrocephalus. Methods to safely sample CSF and a more sensitive detection of ctDNA are necessary for reliable liquid biopsy of DMG at presentation.

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  • Topoisomerase IIβ immunoreactivity (IR) co-localizes with neuronal marker-IR but not glial fibrillary acidic protein-IR in GLI3-positive medulloblastomas: an immunohistochemical analysis of 124 medulloblastomas from the Japan Children's Cancer Group.

    Hiroaki Miyahara, Manabu Natsumeda, Yonehiro Kanemura, Kai Yamasaki, Yuichi Riku, Akio Akagi, Wataru Oohashi, Tomoko Shofuda, Ema Yoshioka, Yuya Sato, Takashi Taga, Yuki Naruke, Ryo Ando, Daiichiro Hasegawa, Makiko Yoshida, Tsukasa Sakaida, Naoki Okada, Hiroyoshi Watanabe, Michio Ozeki, Yoshiki Arakawa, Junichi Yoshimura, Yukihiko Fujii, Souichi Suenobu, Kenji Ihara, Junichi Hara, Akiyoshi Kakita, Mari Yoshida, Yasushi Iwasaki

    Brain tumor pathology   38 ( 2 )   109 - 121   2021.4

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    We previously reported observing GLI3 in medulloblastomas expressing neuronal markers (NM) and/or glial fibrillary acidic protein (GFAP). Furthermore, patients with medulloblastomas expressing NM or GFAP tended to show favorable or poor prognosis, respectively. In the present study, we focused on the role of topoisomerase IIβ (TOP2β) as a possible regulator for neuronal differentiation in medulloblastomas and examined the pathological roles of GLI3, NM, GFAP, and TOP2β expressions in a larger population. We divided 124 medulloblastomas into three groups (NM-/GFAP-, NM +/GFAP-, and GFAP +) based on their immunoreactivity (IR) against NM and GFAP. The relationship among GLI3, NM, GFAP, and TOP2β was evaluated using fluorescent immunostaining and a publicly available single-cell RNA sequencing dataset. In total, 87, 30, and 7 medulloblastomas were classified as NM-/GFAP-, NM + /GFAP-, and GFAP +, and showed intermediate, good, and poor prognoses, respectively. GLI3-IR was frequently observed in NM +/GFAP-  and GFAP + , and TOP2β-IR was frequently observed only in NM +/GFAP-  medulloblastomas. In fluorescent immunostaining, TOP2β-IR was mostly co-localized with NeuN-IR but not with GFAP-IR. In single-cell RNA sequencing, TOP2β expression was elevated in CMAS/DCX-positive, but not in GFAP-positive, cells. NM-IR and GFAP-IR are important for estimating the prognosis of patients with medulloblastoma; hence they should be assessed in clinical practice.

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  • Genetic Variations and Neuropathologic Features of Patients With PRKN Mutations

    Naohiko Seike, Akio Yokoseki, Ryoko Takeuchi, Kento Saito, Hiroaki Miyahara, Akinori Miyashita, Tetsuhiko Ikeda, Izumi Aida, Takashi Nakajima, Masato Kanazawa, Masatoshi Wakabayashi, Yasuko Toyoshima, Hitoshi Takahashi, Riki Matsumoto, Tatsushi Toda, Osamu Onodera, Atsushi Ishikawa, Takeshi Ikeuchi, Akiyoshi Kakita

    Movement Disorders   36 ( 7 )   1634 - 1643   2021.2

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    DOI: 10.1002/mds.28521

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  • 高度な両下肢痙性を呈したレビー小体病の剖検例

    黒羽 泰子, 長谷川 有香, 高橋 哲哉, 松原 奈絵, 石黒 敬信, 田中 英智, 柿田 明美, 小池 亮子

    パーキンソン病・運動障害疾患コングレスプログラム・抄録集   14回   118 - 118   2021.2

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  • 高齢発症多系統萎縮症の臨床病理学的検討

    荻根沢 真也, 今野 卓哉, 清水 宏, 他田 真理, 柿田 明美, 小野寺 理

    パーキンソン病・運動障害疾患コングレスプログラム・抄録集   14回   112 - 112   2021.2

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  • Novel tankyrase inhibitors suppress TDP-43 aggregate formation. International journal

    Kunikazu Tanji, Fumiaki Mori, Fumiyuki Shirai, Takehiro Fukami, Hiroyuki Seimiya, Jun Utsumi, Akiyoshi Kakita, Koichi Wakabayashi

    Biochemical and biophysical research communications   537   85 - 92   2021.1

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    Transactive response DNA-binding protein of 43 kDa (TDP-43) abnormally forms aggregates in certain subtypes of frontotemporal lobar degeneration (FTLD) and in amyotrophic lateral sclerosis (ALS). The pathological forms of TDP-43 have reported to be associated with poly(ADP-ribose) (PAR), which regulates the properties of these aggregates. A recent study has indicated that tankyrase, a member of the PAR polymerase (PARP) family, regulates pathological TDP-43 formation under conditions of stress, and tankyrase inhibitors suppress TDP-43 aggregate formation and cytotoxicity. Since we reported the development of tankyrase inhibitors that are more specific than conventional inhibitors, in this study, we examined their effects on the formation of TDP-43 aggregates in cultured cells. Time-lapse imaging showed that TDP-43 aggregates appeared in the nucleus within 30 min of treatment with sodium arsenite. Several tankyrase inhibitors suppressed the formation of aggregates and decreased the levels of the tankyrase protein. Immunohistochemical studies demonstrated that tankyrase was localized to neuronal cytoplasmic inclusions in the spinal cords of patients with ALS. Moreover, the tankyrase protein levels were significantly higher in the brains of patients with FTLD than in the brains of control subjects. These findings suggest that the inhibition of tankyrase activity protects against TDP-43 toxicity. Tankyrase inhibitors may be a potential treatment to suppress the progression of TDP-43 proteinopathies.

    DOI: 10.1016/j.bbrc.2020.12.037

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  • GLI3 Is Associated With Neuronal Differentiation in SHH-Activated and WNT-Activated Medulloblastoma. International journal

    Manabu Natsumeda, Hiroaki Miyahara, Junichi Yoshimura, Satoshi Nakata, Takanori Nozawa, Junko Ito, Yu Kanemaru, Jun Watanabe, Yoshihiro Tsukamoto, Masayasu Okada, Makoto Oishi, Junko Hirato, Takafumi Wataya, Sama Ahsan, Kensuke Tateishi, Tetsuya Yamamoto, Fausto J Rodriguez, Hitoshi Takahashi, Volker Hovestadt, Mario L Suva, Michael D Taylor, Charles G Eberhart, Yukihiko Fujii, Akiyoshi Kakita

    Journal of neuropathology and experimental neurology   80 ( 2 )   129 - 136   2021.1

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    Glioma-associated oncogene homolog 3 (GLI3), whose main function is to inhibit GLI1, has been associated with neuronal differentiation in medulloblastoma. However, it is not clear what molecular subtype(s) show increased GLI3 expression. GLI3 levels were assessed by immunohistochemistry in 2 independent cohorts, including a total of 88 cases, and found to be high in both WNT- and SHH-activated medulloblastoma. Analysis of bulk mRNA expression data and single cell RNA sequencing studies confirmed that GLI1 and GLI3 are highly expressed in SHH-activated medulloblastoma, whereas GLI3 but not GLI1 is highly expressed in WNT-activated medulloblastoma. Immunohistochemical analysis has shown that GLI3 is expressed inside the neuronal differentiated nodules of SHH-activated medulloblastoma, whereas GLI1/2 are expressed in desmoplastic areas. In contrast, GLI3 is diffusely expressed in WNT-activated medulloblastoma, whereas GLI1 is suppressed. Our data suggest that GLI3 may be a master regulator of neuronal differentiation and morphology in these subgroups.

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  • Age-related demethylation of the TDP-43 autoregulatory region in the human motor cortex

    Yuka Koike, Akihiro Sugai, Norikazu Hara, Junko Ito, Akio Yokoseki, Tomohiko Ishihara, Takuma Yamagishi, Shintaro Tsuboguchi, Mari Tada, Takeshi Ikeuchi, Akiyoshi Kakita, Osamu Onodera

    2021.1

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    <title>Abstract</title>In amyotrophic lateral sclerosis (ALS), TAR DNA-binding protein 43 (TDP-43) forms aggregates in the motor cortex of the aging brain. This aggregate formation may be triggered by the increase in TDP-43 levels with aging. However, the amount of TDP-43 is autoregulated by the alternative splicing of the <italic>TARDBP</italic> 3’UTR, and its relationship with aging remains unresolved. Since DNA methylation is altered during aging, we hypothesized that 3’UTR methylation is also altered in the aging motor cortex, disrupting this autoregulatory system and increasing TDP-43 levels. We found that DNA demethylation in the autoregulatory region of TDP-43 reduced alternative splicing and increased TDP-43 expression. Furthermore, in the human motor cortex, we found that this region was demethylated with age and that the expression of TDP-43 increased. The dysregulation of TDP-43 autoregulation by age-related DNA demethylation in the motor cortex may explain the contribution of aging and system selectivity in ALS.

    DOI: 10.1101/2021.01.13.426599

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  • Detailed Postmortem Profiling of Inflammatory Mediators Expression Revealed Post-inflammatory Alternation in the Superior Temporal Gyrus of Schizophrenia. International journal

    Ryuta Izumi, Mizuki Hino, Akira Wada, Atsuko Nagaoka, Takashi Kawamura, Tsutomu Mori, Makoto Sainouchi, Akiyoshi Kakita, Kiyoto Kasai, Yasuto Kunii, Hirooki Yabe

    Frontiers in psychiatry   12   653821 - 653821   2021

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    Recent studies have lent support to the possibility that inflammation is associated with the pathology of schizophrenia. In the study of measurement of inflammatory mediators, which are markers of inflammation, elevated inflammatory cytokine levels in the brain and blood have been reported in patients with schizophrenia. Several postmortem brain studies have also reported changes in the expression of inflammatory cytokines. However, it is not clear how these elevated inflammatory cytokines interact with other inflammatory mediators, and their association with the pathology of schizophrenia. We comprehensively investigated the expression of 30 inflammatory mediators in the superior temporal gyrus (STG) of 24 patients with schizophrenia and 26 controls using a multiplex method. Overall, inflammatory mediator expression in the STG was mostly unchanged. However, the expression of interleukin (IL)1-α and interferon-gamma-inducible protein (IP)-10 was decreased [IL-1α, median (IQR), 0.51 (0.37-0.70) vs. 0.87 (0.47-1.23), p = 0.01; IP-10, 13.99 (8.00-36.64) vs. 30.29 (10.23-134.73), p = 0.05], whereas that of IFN-α was increased [2.34 (1.84-4.48) vs. 1.94 (1.39-2.36), p = 0.04] in schizophrenia, although these alterations did not remain significant after multiple testing. Clustering based on inflammatory mediator expression pattern and analysis of upstream transcription factors using pathway analysis revealed that the suppression of IL-1α and IP-10 protein expression may be induced by regulation of a common upstream pathway. Neuroinflammation is important in understanding the biology of schizophrenia. While neuroimaging has been previously used, direct observation to determine the expression of inflammatory mediators is necessary. In this study, we identified protein changes, previously unreported, using comprehensive protein analysis in STG. These results provide insight into post-inflammatory alternation in chronic schizophrenia.

    DOI: 10.3389/fpsyt.2021.653821

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  • Serotonin/5-HT1A Signaling in the Neurovascular Unit Regulates Endothelial CLDN5 Expression. International journal

    Kotaro Sugimoto, Naoki Ichikawa-Tomikawa, Keisuke Nishiura, Yasuto Kunii, Yasuteru Sano, Fumitaka Shimizu, Akiyoshi Kakita, Takashi Kanda, Tetsuya Imura, Hideki Chiba

    International journal of molecular sciences   22 ( 1 )   2020.12

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    We previously reported that site-selective claudin-5 (CLDN5) breakdown and protein kinase A (PKA) activation are observed in brain microvessels of schizophrenia, but the underlying molecular basis remains unknown. The 5-HT1 receptors decline the intracellular cAMP levels and inactivate the major downstream PKA, and the 5-HT1A receptor is a promising target for schizophrenia. Therefore, we elucidated the involvement of serotonin/5-HT1A signaling in the endothelial CLDN5 expression. We demonstrate, by immunohistochemistry using post-mortem human brain tissue, that the 5-HT1A receptor is expressed in brain microvascular endothelial cells (BMVECs) and mural cells of the normal prefrontal cortex (PFC) gray matter. We also show that PKA is aberrantly activated not only in BMVECs but also in mural cells of the schizophrenic PFC. We subsequently revealed that the endothelial cell-pericyte tube-like structure was formed in a novel two-dimensional co-culture of human primary BMVECs and a human brain-derived pericyte cell line, in both of which the 5-HT1A receptor was expressed. Furthermore, we disclose that the serotonin/5-HT1A signaling enhances endothelial CLDN5 expression in BMVECs under two-dimensional co-culture conditions. Our findings provide novel insights into the physiological and pathological significance of serotonin/5-HT1A signaling in the region-specific regulation of the blood-brain barrier.

    DOI: 10.3390/ijms22010254

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  • Ethnicity-Dependent Effects of Schizophrenia Risk Variants of the OLIG2 Gene on OLIG2 Transcription and White Matter Integrity. International journal

    Hiroshi Komatsu, Hikaru Takeuchi, Yoshie Kikuchi, Chiaki Ono, Zhiqian Yu, Kunio Iizuka, Yuji Takano, Yoshihisa Kakuto, Shunichi Funakoshi, Takashi Ono, Junko Ito, Yasuto Kunii, Mizuki Hino, Atsuko Nagaoka, Yasushi Iwasaki, Hidenaga Yamamori, Yuka Yasuda, Michiko Fujimoto, Hirotsugu Azechi, Noriko Kudo, Ryota Hashimoto, Hirooki Yabe, Mari Yoshida, Yuko Saito, Akiyoshi Kakita, Nobuo Fuse, Ryuta Kawashima, Yasuyuki Taki, Hiroaki Tomita

    Schizophrenia bulletin   46 ( 6 )   1619 - 1628   2020.12

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    Previous studies have indicated associations between several OLIG2 gene single-nucleotide polymorphisms (SNPs) and susceptibility to schizophrenia among Caucasians. Consistent with these findings, postmortem brain and diffusion tensor imaging studies have indicated that the schizophrenia-risk-associated allele (A) in the OLIG2 SNP rs1059004 predicts lower OLIG2 gene expression in the dorsolateral prefrontal cortex (DLPFC) of schizophrenia patients and reduced white matter (WM) integrity of the corona radiata in normal brains among Caucasians. In an effort to replicate the association between this variant and WM integrity among healthy Japanese, we found that the number of A alleles was positively correlated with WM integrity in some fiber tracts, including the right posterior limb of the internal capsule, and with mean blood flow in a widespread area, including the inferior frontal operculum, orbital area, and triangular gyrus. Because the A allele affected WM integrity in opposite directions in Japanese and Caucasians, we investigated a possible association between the OLIG2 gene SNPs and the expression level of OLIG2 transcripts in postmortem DLPFCs. We evaluated rs1059004 and additional SNPs in the 5' upstream and 3' downstream regions of rs1059004 to cover the broader region of the OLIG2 gene. The 2 SNPs (rs1059004 and rs9653711) had opposite effects on OLIG2 gene expression in the DLPFC in Japanese and Caucasians. These findings suggest ethnicity-dependent opposite effects of OLIG2 gene SNPs on WM integrity and OLIG2 gene expression in the brain, which may partially explain the failures in replicating associations between genetic variants and psychiatric phenotypes among ethnicities.

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  • Proteomic profile differentiating between mesial temporal lobe epilepsy with and without hippocampal sclerosis. International journal

    Ayako Furukawa, Akiyoshi Kakita, Yoichi Chiba, Hiroki Kitaura, Yukihiko Fujii, Masafumi Fukuda, Shigeki Kameyama, Atsuyoshi Shimada

    Epilepsy research   168   106502 - 106502   2020.12

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    Hippocampal sclerosis (HS) is the most common neuropathological condition in adults with drug-resistant epilepsy and represents a critical feature in mesial temporal lobe epilepsy (MTLE) syndrome. Although epileptogenic brain tissue is associated with glutamate excitotoxicity leading to oxidative stress, the proteins that are targets of oxidative damage remain to be determined. In the present study we designed comprehensive analyses of changes in protein expression level and protein oxidation status in the hippocampus or neocortex to highlight proteins associated with excitotoxicity by comparing MTLE patients with relatively mild excitotoxicity (MTLE patients without HS, MTLE-non-HS) and those with severe excitotoxicity (MTLE patients with HS, MTLE-HS). We performed 2-dimensional fluorescence difference gel electrophoresis, 2D-oxyblot analysis, and mass spectrometric amino acid sequencing. We identified 16 proteins at 18 spots in which the protein expression levels differed between sclerotic and non-sclerotic hippocampi. In the sclerotic hippocampus, the expression levels of several synaptic proteins were decreased, and those of some glia-associated proteins increased. We confirmed histologically that all MTLE-HS cases examined exhibited severe neuronal cell loss and remarkable astrocytic gliosis in the hippocampi. In all MTLE-non-HS cases examined, neurons were spared and gliosis was unremarkable. Therefore, we consider that decreased synaptic proteins are a manifestation of loss of neuronal cell bodies and dendrites, whereas increased glia-associated proteins are a manifestation of proliferation and hypertrophy of astrocytes. These are considered to be the result of hippocampal sclerosis. In contrast, the expression level of d-3-phosphoglycerate dehydrogenase (PHGDH), an l-serine synthetic enzyme expressed exclusively by astrocytes, was decreased, and that of stathmin 1, a neurite extension-related protein expressed by neurons, was increased in the sclerotic hippocampus. These findings cannot be explained solely as the result of hippocampal sclerosis. Rather, these changes can be involved in the continuation of seizure disorders in MTLE-HS. In addition, the protein carbonylation detection, an indicator of protein oxidation caused by excitotoxicity of multiple seizures and/or status epilepticus, revealed that the carbonyl level of collapsin response mediator protein 2 (CRMP2) increased significantly in the sclerotic hippocampus. In conclusion, protein identification following profiling of protein expression levels and detection of oxidative proteins indicated potential pathognomonic protein changes. The decreased expression of PHGDH, increased expression of stathmin 1, and carbonylation of CRMP2 differentiate between MTLE with and without HS. Therefore, further investigations of PHGDH, stathmin 1 and CRMP2 are promising to study more detailed effects of excitotoxicity on epileptogenic hippocampal tissue.

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  • Astrocytes release glutamate via cystine/glutamate antiporter upregulated in response to increased oxidative stress related to sporadic amyotrophic lateral sclerosis. International journal

    Miku Kazama, Yoichiro Kato, Akiyoshi Kakita, Noriko Noguchi, Yasuomi Urano, Kenta Masui, Motoko Niida-Kawaguchi, Tomoko Yamamoto, Kazuhiko Watabe, Kazuo Kitagawa, Noriyuki Shibata

    Neuropathology : official journal of the Japanese Society of Neuropathology   40 ( 6 )   587 - 598   2020.12

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    A vast body of evidence implicates increased oxidative stress and extracellular glutamate accumulation in the pathomechanism of sporadic amyotrophic lateral sclerosis (ALS). Cystine/glutamate antiporter (xCT) carries extracellular cystine uptake and intracellular glutamate release (cystine/glutamate exchange) in the presence of oxidative stress. The aim of the present study was to determine the involvement of xCT in ALS. Immunohistochemical observations in the spinal cord sections demonstrated that xCT was mainly expressed in astrocytes, with staining more intense in 12 sporadic ALS patients as compared to 12 age-matched control individuals. Western blot and densitometric analyses of the spinal cord samples revealed that the relative value of xCT/β-actin optical density ratio was significantly higher in the ALS group as compared to the control group. Next, we conducted cell culture experiments using a human astrocytoma-derived cell line (1321N1) and a mouse motor neuron/neuroblastoma hybrid cell line (NSC34). In 1321N1 cells, the normalized xCT expression levels in cell lysates were significantly increased by H2 O2 treatment. Glutamate concentrations in 1321 N1 cell culture-conditioned media were significantly elevated by H2 O2 treatment, and the H2 O2 -driven elevations were completely canceled by the xCT inhibitor erastin pretreatment. In motor neuron-differentiated NSC34 cells (NSC34d cells), both the normalized xCT expression levels in the cell lysates and glutamate concentrations in the cell-conditioned media were constant with or without H2 O2 treatment. The present results provide in vivo and in vitro evidence that astrocytes upregulate xCT expression to release glutamate in response to increased oxidative stress associated with ALS, contributing to extracellular glutamate accumulation.

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  • 放射線療法併用下でのニボルマブ投与により一定の進行抑制効果を得た小児meningeal malanomatosisの1例

    武居 慎吾, 結城 明彦, 阿部 理一郎, 太田 智慶, 棗田 学, 大石 誠, 柿田 明美

    日本皮膚悪性腫瘍学会学術大会プログラム・抄録集   36回   139 - 139   2020.12

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  • Longitudinal GluCEST MRI Changes and Cerebral Blood Flow in 5xFAD Mice

    Hironaka Igarashi, Satoshi Ueki, Hiroki Kitaura, Tae Kera, Ken Ohno, Masaki Ohkubo, Mika Terumitsu-Tsujita, Akiyoshi Kakita, Ingrid L Kwee

    Contrast Media & Molecular Imaging   2020   1 - 12   2020.11

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    Many of the focal neurological symptoms associated with Alzheimer’s disease (AD) are due to synaptic loss. Glutamate chemical exchange saturation transfer (GluCEST) magnetic resonance imaging (MRI) is a candidate method to assess synaptic dysfunction. We assessed chronological changes in GluCEST in a 5xFAD mouse model of AD, comparing Glucest effects and regional cerebral blood flow (CBF). GluCEST effects and CBF in 5xFAD mice aged 1–15 months and their littermates (WT) were measured. Neurite orientation dispersion and density imaging (NODDI) MRI reflecting dendritic/axonal density was also measured and compared with GluCEST in 7-month-old mice. While regional CBF’s decrease began at 7 months, GluCEST-reduction effects preceded hypoperfusion of the temporal cortex and hippocampus. While longitudinal 5xFAD mouse measurements revealed a correlation between the regional GluCEST effects and CBF, a generalized linear mixed model revealed statistically different correlations in cortical and basal brain regions. Further, NODDI-derived neurite density correlated with GluCEST effects in the parietal cortex, but not in the hippocampus, thereby revealing regional differences in pathophysiological mechanisms. Finally, GluCEST’s effects correlated with regional synaptophysin. These results demonstrate that GluCEST can reflect subtle synaptic changes and may be a potential imaging method for AD diagnosis as well as serve as a biomarker of AD progression.

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  • Progressive supranuclear palsy: Neuropathology of patients with a short disease duration due to unexpected death

    Lu Zhang, Yasuko Toyoshima, Akari Takeshima, Hiroshi Shimizu, Itsuro Tomita, Osamu Onodera, Hitoshi Takahashi, Akiyoshi Kakita

    NEUROPATHOLOGY   41 ( 3 )   174 - 182   2020.11

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    DOI: 10.1111/neup.12707

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  • ALS剖検例に関するテキストマイニングとエキソーム分析を用いたALSの新規候補遺伝子の探索(Search for new candidate genes for ALS by textmining and exome analysis of autopsy cases)

    Hatano Yuya, Ishihara Tomohiko, Yokoseki Akio, Tada Mari, Kakita Akiyoshi, Okuda Shujiro, Onodera Osamu

    臨床神経学   60 ( Suppl. )   S324 - S324   2020.11

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  • 散発性ALSの137症例における剖検物のエキソーム分析(Exome analysis in 137 autopsied sporadic ALS cases)

    Ishihara Tomohiko, Hatano Yuya, Yokoseki Akio, Tada Mari, Nakajima Takashi, Koike Ryoko, Kakita Akiyoshi, Onodera Osamu

    臨床神経学   60 ( Suppl. )   S309 - S309   2020.11

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  • Imaging α-synuclein pathologies in animal models and patients with Parkinson’s and related diseases

    Hironobu Endo, Maiko Ono, Yuhei Takado, Kiwamu Matsuoka, Manami Takahashi, Kenji Tagai, Yuko Kataoka, Kosei Hirata, Keisuke Takahata, Chie Seki, Naomi Kokubo, Masayuki Fujinaga, Wakana Mori, Yuji Nagai, Koki Mimura, Katsushi Kumata, Tatsuya Kikuchi, Aki Shimozawa, Sushil K. Mishra, Yoshiki Yamaguchi, Hiroshi Shimizu, Akiyoshi Kakita, Hiroyuki Takuwa, Hitoshi Shinotoh, Hitoshi Shimada, Yasuyuki Kimura, Masanori Ichise, Tetsuya Suhara, Takafumi Minamimoto, Naruhiko Sahara, Kazunori Kawamura, Ming-Rong Zhang, Masato Hasegawa, Makoto Higuchi

    2020.10

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    SUMMARY

    Deposition of α-synuclein fibrils is implicated in Parkinson’s disease (PD) and dementia with Lewy bodies (DLB), whilein vivodetection of α-synuclein pathologies in these illnesses has been challenging. Here, we have developed a small-molecule ligand, C05-05, for visualizing α-synuclein deposits in the brains of living subjects.In vivooptical and positron emission tomography (PET) imaging of mouse and marmoset models demonstrated that C05-05 captured a dynamic propagation of fibrillogenesis along neural pathways followed by disruptions of these structures. High-affinity binding of<sup>18</sup>F-C05-05 to α-synuclein aggregates in human brain tissues was also proven byin vitroassays. Notably, PET-detectable<sup>18</sup>F-C05-05 signals were intensified in the midbrains of PD and DLB patients as compared to healthy controls, providing the first demonstration of visualizing α-synuclein pathologies in these illnesses. Collectively, we propose a new imaging technology offering neuropathology-based translational assessments of PD and allied disorders towards diagnostic and therapeutic research and development.

    DOI: 10.1101/2020.10.23.349860

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  • Toward allele-specific targeting therapy and pharmacodynamic marker for spinocerebellar ataxia type 3

    Mercedes Prudencio, Hector Garcia-Moreno, Karen R. Jansen-West, Rana Hanna AL-Shaikh, Tania F. Gendron, Michael G. Heckman, Matthew R. Spiegel, Yari Carlomagno, Lillian M. Daughrity, Yuping Song, Judith A. Dunmore, Natalie Byron, Björn Oskarsson, Katharine A. Nicholson, Nathan P. Staff, Sorina Gorcenco, Andreas Puschmann, João Lemos, Cristina Januário, Mark S. LeDoux, Joseph H. Friedman, James Polke, Robin Labrum, Vikram Shakkottai, Hayley S. McLoughlin, Henry L. Paulson, Takuya Konno, Osamu Onodera, Takeshi Ikeuchi, Mari Tada, Akiyoshi Kakita, John D. Fryer, Christin Karremo, Inês Gomes, John N. Caviness, Mark R. Pittelkow, Jan Aasly, Ronald F. Pfeiffer, Venka Veerappan, Eric R. Eggenberger, William D. Freeman, Josephine F. Huang, Ryan J. Uitti, Klaas J. Wierenga, Iris V. Marin Collazo, Philip W. Tipton, Jay A. van Gerpen, Marka van Blitterswijk, Guojun Bu, Zbigniew K. Wszolek, Paola Giunti, Leonard Petrucelli

    Science Translational Medicine   12 ( 566 )   2020.10

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    DOI: 10.1126/scitranslmed.abb7086

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  • ANCA関連脊髄肥厚性硬膜炎の臨床免疫病理学的検討

    中島 章博, 佐治 越爾, 清水 宏, 豊島 靖子, 岡本 浩一郎, 若杉 尚宏, 柳村 文寛, 柳川 香織, 柿田 明美, 小野寺 理, 河内 泉

    神経免疫学   25 ( 1 )   134 - 134   2020.10

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  • ヒト死後脳、ヒト培養細胞におけるAPOEの遺伝子発現解析

    Lixin Liu, 宮下 哲典, 村上 涼太, 原 範和, 菊地 正隆, Bin Zhu, 樋口 陽, Yusran Adyfitrah, 月江 珠緒, 長谷川 舞衣, 春日 健作, 赤津 裕康, 橋詰 良夫, 柿田 明美, 村山 繁雄, 池内 健

    Dementia Japan   34 ( 4 )   521 - 521   2020.10

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  • ヒト死後脳に由来するDNA、RNAの品質管理

    長谷川 舞衣, 宮下 哲典, 春日 健作, 原 範和, 月江 珠緒, 齋藤 祐子, 赤津 裕康, 橋詰 良夫, 柿田 明美, 吉田 眞理, 村山 繁雄, 池内 健

    Dementia Japan   34 ( 4 )   525 - 525   2020.10

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  • ヒト死後脳に由来するDNA、RNAの品質管理

    長谷川 舞衣, 宮下 哲典, 春日 健作, 原 範和, 月江 珠緒, 齋藤 祐子, 赤津 裕康, 橋詰 良夫, 柿田 明美, 吉田 眞理, 村山 繁雄, 池内 健

    Dementia Japan   34 ( 4 )   525 - 525   2020.10

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  • Toward allele-specific targeting therapy and pharmacodynamic marker for spinocerebellar ataxia type 3

    Mercedes Prudencio, Hector Garcia-Moreno, Karen R. Jansen-West, Rana Hanna AL-Shaikh, Tania F. Gendron, Michael G. Heckman, Matthew R. Spiegel, Yari Carlomagno, Lillian M. Daughrity, Yuping Song, Judith A. Dunmore, Natalie Byron, Bjorn Oskarsson, Katharine A. Nicholson, Nathan P. Staff, Sorina Gorcenco, Andreas Puschmann, Joao Lemos, Cristina Januario, Mark S. LeDoux, Joseph H. Friedman, James Polke, Robin Labrum, Vikram Shakkottai, Hayley S. McLoughlin, Henry L. Paulson, Takuya Konno, Osamu Onodera, Takeshi Ikeuchi, Mari Tada, Akiyoshi Kakita, John D. Fryer, Christin Karremo, Ines Gomes, John N. Caviness, Mark R. Pittelkow, Jan Aasly, Ronald F. Pfeiffer, Venka Veerappan, Eric R. Eggenberger, William D. Freeman, Josephine F. Huang, Ryan J. Uitti, Klaas J. Wierenga, Iris V. Marin Collazo, Philip W. Tipton, Jay A. van Gerpen, Marka van Blitterswijk, Guojun Bu, Zbigniew K. Wszolek, Paola Giunti, Leonard Petrucelli

    SCIENCE TRANSLATIONAL MEDICINE   12 ( 566 )   2020.10

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  • ANCA関連脊髄肥厚性硬膜炎の臨床免疫病理学的検討

    中島 章博, 佐治 越爾, 清水 宏, 豊島 靖子, 岡本 浩一郎, 若杉 尚宏, 柳村 文寛, 柳川 香織, 柿田 明美, 小野寺 理, 河内 泉

    神経免疫学   25 ( 1 )   134 - 134   2020.10

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  • 本邦の孤発性ALSにおけるAPOE2の認知症への影響の検討

    畠野 雄也, 石原 智彦, 他田 真理, 柿田 明美, 小野寺 理

    Dementia Japan   34 ( 4 )   521 - 521   2020.10

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  • Methylmercury exposure during the vulnerable window of the cerebrum in postnatal developing rats

    Mineshi Sakamoto, Akiyoshi Kakita, Kazuo Sakai, Satomi Kameo, Megumi Yamamoto, Masaaki Nakamura

    Environmental Research   188   2020.9

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    DOI: 10.1016/j.envres.2020.109776

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  • 統合失調症脳病態における脂質シグナル伝達の意義 死後脳研究

    國井 泰人, 松本 純弥, 泉 竜太, 長岡 敦子, 日野 瑞城, 赤津 裕康, 橋詰 良夫, 齊ノ内 信, 柿田 明美

    精神神経学雑誌   ( 2020特別号 )   S307 - S307   2020.9

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  • 【良性成人型家族性ミオクローヌスてんかん】良性成人型家族性ミオクローヌスてんかんの神経病理

    齊ノ内 信, Ramil Gabdulkhaev, 小野寺 理, 柿田 明美

    脳神経内科   93 ( 3 )   305 - 309   2020.9

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  • 統合失調症脳病態における脂質シグナル伝達の意義 死後脳研究

    國井 泰人, 松本 純弥, 泉 竜太, 長岡 敦子, 日野 瑞城, 赤津 裕康, 橋詰 良夫, 齊ノ内 信, 柿田 明美

    精神神経学雑誌   ( 2020特別号 )   S307 - S307   2020.9

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  • 【良性成人型家族性ミオクローヌスてんかん】良性成人型家族性ミオクローヌスてんかんの神経病理

    齊ノ内 信, Ramil Gabdulkhaev, 小野寺 理, 柿田 明美

    脳神経内科   93 ( 3 )   305 - 309   2020.9

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  • Novel CHP1 mutation in autosomal-recessive cerebellar ataxia: autopsy features of two siblings. Reviewed International journal

    Rie Saito, Norikazu Hara, Mari Tada, Yoshiaki Honma, Akinori Miyashita, Osamu Onodera, Takeshi Ikeuchi, Akiyoshi Kakita

    Acta neuropathologica communications   8 ( 1 )   134 - 134   2020.8

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  • 側頭葉に主座を持つH3K27M変異陽性の退形成性星細胞腫の一例

    塚本 佳広, 棗田 学, 大倉 良太, 太田 智慶, 温 城太郎, 齋藤 祥二, 岡本 浩一郎, 大石 誠, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   37 ( Suppl. )   134 - 134   2020.8

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  • 脳腫瘍の遺伝子診断とゲノム医療2 ゲノム医療を想定したBRAF V600E変異を有する脳腫瘍の臨床病理像

    棗田 学, 金丸 優, 齋藤 祥二, 塚本 佳広, 岡田 正康, 大石 誠, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   37 ( Suppl. )   076 - 076   2020.8

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  • Topoisomerase IIβは髄芽腫細胞の神経分化を誘導する

    宮原 弘明, 棗田 学, 吉村 淳一, 藤井 幸彦, 柿田 明美, 岩崎 靖, 吉田 眞理

    Brain Tumor Pathology   37 ( Suppl. )   104 - 104   2020.8

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  • GHホルモンは頭蓋咽頭腫の増大に寄与したか? GH産生下垂体腺腫と頭蓋咽頭腫が併存した一例から

    岡田 正康, 米岡 有一郎, 棗田 学, 大石 誠, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   37 ( Suppl. )   094 - 094   2020.8

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  • Praja1 RING-finger E3 ubiquitin ligase suppresses neuronal cytoplasmic TDP-43 aggregate formation. Reviewed International journal

    Kazuhiko Watabe, Yoichiro Kato, Miho Sakuma, Makiko Murata, Motoko Niida-Kawaguchi, Taro Takemura, Nobutaka Hanagata, Mari Tada, Akiyoshi Kakita, Noriyuki Shibata

    Neuropathology : official journal of the Japanese Society of Neuropathology   40 ( 6 )   570 - 586   2020.7

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    Transactivation response DNA-binding protein of 43 kDa (TDP-43) is a major constituent of cytoplasmic aggregates in neuronal and glial cells in cases of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). We have previously shown neuronal cytoplasmic aggregate formation induced by recombinant adenoviruses expressing human wild-type and C-terminal fragment (CTF) TDP-43 under the condition of proteasome inhibition in vitro and in vivo. In the present study, we demonstrated that the formation of the adenoviral TDP-43 aggregates was markedly suppressed in rat neural stem cell-derived neuronal cells by co-infection of an adenovirus expressing heat shock transcription factor 1 (HSF1), a master regulator of heat shock response. We performed DNA microarray analysis and searched several candidate molecules, located downstream of HSF1, which counteract TDP-43 aggregate formation. Among these, we identified Praja 1 RING-finger E3 ubiquitin ligase (PJA1) as a suppressor of phosphorylation and aggregate formation of TDP-43. Co-immunoprecipitation assay revealed that PJA1 binds to CTF TDP-43 and the E2-conjugating enzyme UBE2E3. PJA1 also suppressed formation of cytoplasmic phosphorylated TDP-43 aggregates in mouse facial motor neurons in vivo. Furthermore, phosphorylated TDP-43 aggregates were detected in PJA1-immunoreactive human ALS motor neurons. These results indicate that PJA1 is one of the principal E3 ubiquitin ligases for TDP-43 to counteract its aggregation propensity and could be a potential therapeutic target for ALS and FTLD.

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  • Clinical and pathological features affecting cardiac sympathetic denervation in autopsy-confirmed dementia with Lewy bodies

    M. Takahashi, T. Uchihara, M. Yoshida, K. Wakabayashi, A. Kakita, H. Takahashi, S. Toru, S. Orimo

    European Journal of Neurology   27 ( 7 )   1155 - 1163   2020.7

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    DOI: 10.1111/ene.14240

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  • MicroRNA-5572 Is a Novel MicroRNA-Regulating SLC30A3 in Sporadic Amyotrophic Lateral Sclerosis. Reviewed International journal

    Hisaka Kurita, Saori Yabe, Tomoyuki Ueda, Masatoshi Inden, Akiyoshi Kakita, Isao Hozumi

    International journal of molecular sciences   21 ( 12 )   2020.6

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    Amyotrophic lateral sclerosis (ALS) is a progressive degenerative disease caused by the loss of motor neurons. Although the pathogenesis of sporadic ALS (sALS) remains unclear, it has recently been suggested that disorders of microRNA (miRNA) may be involved in neurodegenerative conditions. The purpose of this study was to investigate miRNA levels in sALS and the target genes of miRNA. Microarray and real-time RT-PCR analyses revealed significantly-decreased levels of miR-139-5p and significantly increased levels of miR-5572 in the spinal cords of sALS patients compared with those in controls. We then focused on miR-5572, which has not been reported in ALS, and determined its target gene. By using TargetScan, we predicted SLC30A3 as the candidate target gene of miR-5572. In a previous study, we found decreased SLC30A3 levels in the spinal cords of sALS patients. We revealed that SLC30A3 was regulated by miR-5572. Taken together, these results demonstrate that the level of novel miRNA miR-5572 is increased in sALS and that SLC30A3 is one of the target genes regulated by miR-5572.

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  • Oculopharyngodistal myopathy with coexisting histology of systemic neuronal intranuclear inclusion disease: Clinicopathologic features of an autopsied patient harboring CGG repeat expansions in LRP12. Reviewed International journal

    Rie Saito, Hiroshi Shimizu, Takeshi Miura, Norikazu Hara, Naomi Mezaki, Yo Higuchi, Akinori Miyashita, Izumi Kawachi, Kazuhiro Sanpei, Yoshiaki Honma, Osamu Onodera, Takeshi Ikeuchi, Akiyoshi Kakita

    Acta neuropathologica communications   8 ( 1 )   75 - 75   2020.6

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  • Expression of the ghrelin/growth hormone secretagogue receptor axis and its functional role in promoting tumor growth in primary central nervous system lymphomas Reviewed

    Hiroko Muta, Yasuo Sugita, Takuya Furuta, Yuki Shiimura, Koichi Ohshima, Kazutaka Nakashima, Kensaku Sato, Motohiro Morioka, Hideyuki Abe, Takanori Nozawa, Yukihiko Fujii, Akiyoshi Kakita

    Neuropathology   40 ( 3 )   232 - 239   2020.6

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    DOI: 10.1111/neup.12634

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  • Author Correction: Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer's disease. International journal

    Yingyue Zhou, Wilbur M Song, Prabhakar S Andhey, Amanda Swain, Tyler Levy, Kelly R Miller, Pietro L Poliani, Manuela Cominelli, Shikha Grover, Susan Gilfillan, Marina Cella, Tyler K Ulland, Konstantin Zaitsev, Akinori Miyashita, Takeshi Ikeuchi, Makoto Sainouchi, Akiyoshi Kakita, David A Bennett, Julie A Schneider, Michael R Nichols, Sean A Beausoleil, Jason D Ulrich, David M Holtzman, Maxim N Artyomov, Marco Colonna

    Nature medicine   26 ( 6 )   981 - 981   2020.6

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    An amendment to this paper has been published and can be accessed via a link at the top of the paper.

    DOI: 10.1038/s41591-020-0922-4

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  • Versatile whole-organ/body staining and imaging based on electrolyte-gel properties of biological tissues. Reviewed International journal

    Etsuo A Susaki, Chika Shimizu, Akihiro Kuno, Kazuki Tainaka, Xiang Li, Kengo Nishi, Ken Morishima, Hiroaki Ono, Koji L Ode, Yuki Saeki, Kazunari Miyamichi, Kaoru Isa, Chihiro Yokoyama, Hiroki Kitaura, Masako Ikemura, Tetsuo Ushiku, Yoshihiro Shimizu, Takashi Saito, Takaomi C Saido, Masashi Fukayama, Hirotaka Onoe, Kazushige Touhara, Tadashi Isa, Akiyoshi Kakita, Mitsuhiro Shibayama, Hiroki R Ueda

    Nature communications   11 ( 1 )   1982 - 1982   2020.4

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    Whole-organ/body three-dimensional (3D) staining and imaging have been enduring challenges in histology. By dissecting the complex physicochemical environment of the staining system, we developed a highly optimized 3D staining imaging pipeline based on CUBIC. Based on our precise characterization of biological tissues as an electrolyte gel, we experimentally evaluated broad 3D staining conditions by using an artificial tissue-mimicking material. The combination of optimized conditions allows a bottom-up design of a superior 3D staining protocol that can uniformly label whole adult mouse brains, an adult marmoset brain hemisphere, an ~1 cm3 tissue block of a postmortem adult human cerebellum, and an entire infant marmoset body with dozens of antibodies and cell-impermeant nuclear stains. The whole-organ 3D images collected by light-sheet microscopy are used for computational analyses and whole-organ comparison analysis between species. This pipeline, named CUBIC-HistoVIsion, thus offers advanced opportunities for organ- and organism-scale histological analysis of multicellular systems.

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  • 【まれな感染症-ウイルス,細菌,寄生虫,輸入感染症-】脳神経領域のまれな感染症 画像診断のポイント Reviewed

    岡本 浩一郎, 高橋 陽彦, 鈴木 倫明, 小野寺 理, 柿田 明美, 阿部 博史

    臨床放射線   65 ( 4 )   317 - 324   2020.4

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  • Soluble iron accumulation induces microglial glutamate release in the spinal cord of sporadic amyotrophic lateral sclerosis. Reviewed International journal

    Motoko Niida-Kawaguchi, Akiyoshi Kakita, Noriko Noguchi, Miku Kazama, Kenta Masui, Yoichiro Kato, Tomoko Yamamoto, Tatsuo Sawada, Kazuo Kitagawa, Kazuhiko Watabe, Noriyuki Shibata

    Neuropathology : official journal of the Japanese Society of Neuropathology   40 ( 2 )   152 - 166   2020.4

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    Previous studies on sporadic amyotrophic lateral sclerosis (SALS) demonstrated iron accumulation in the spinal cord and increased glutamate concentration in the cerebrospinal fluid. To clarify the relationship between the two phenomena, we first performed quantitative and morphological analyses of substances related to iron and glutamate metabolism using spinal cords obtained at autopsy from 12 SALS patients and 12 age-matched control subjects. Soluble iron content determined by the Ferrozine method as well as ferritin (Ft) and glutaminase C (GLS-C) expression levels on Western blots were significantly higher in the SALS group than in the control group, while ferroportin (FPN) levels on Western blots were significantly reduced in the SALS group as compared to the control group. There was no significant difference in aconitase 1 (ACO1) and tumor necrosis factor-alpha (TNFα)-converting enzyme (TACE) levels on Western blots between the two groups. Immunohistochemically, Ft, ACO1, TACE, TNFα, and GLS-C were proven to be selectively expressed in microglia. Immunoreactivities for FPN and hepcidin were localized in neuronal and glial cells. Based on these observations, it is predicted that soluble iron may stimulate microglial glutamate release. To address this issue, cell culture experiments were carried out on a microglial cell line (BV-2). Treatment of BV-2 cells with ferric ammonium citrate (FAC) brought about significant increases in intracellular soluble iron and Ft expression levels and conditioned medium glutamate and TNFα concentrations. Glutamate concentration was also significantly increased in conditioned media of TNFα-treated BV-2 cells. While the FAC-driven increases in glutamate and TNFα release were completely canceled by pretreatment with ACO1 and TACE inhibitors, respectively, the TNFα-driven increase in glutamate release was completely canceled by GLS-C inhibitor pretreatment. Moreover, treatment of BV-2 cells with hepcidin resulted in a significant reduction in FPN expression levels on Western blots of the intracellular total protein extracts. The present results provide in vivo and in vitro evidence that microglial glutamate release in SALS spinal cords is enhanced by intracellular soluble iron accumulation-induced activation of ACO1 and TACE and by increased extracellular TNFα-stimulated GLS-C upregulation, and suggest a positive feedback mechanism to maintain increased intracellular soluble iron levels, involving TNFα, hepcidin, and FPN.

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  • ALDH4A1 expression levels are elevated in postmortem brains of patients with schizophrenia and are associated with genetic variants in enzymes related to proline metabolism

    Atsuko Nagaoka, Yasuto Kunii, Mizuki Hino, Ryuta Izumi, Chisato Nagashima, Akari Takeshima, Makoto Sainouchi, Hiroyuki Nawa, Akiyoshi Kakita, Hirooki Yabe

    Journal of Psychiatric Research   123   119 - 127   2020.4

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  • 【まれな感染症-ウイルス,細菌,寄生虫,輸入感染症-】脳神経領域のまれな感染症 画像診断のポイント

    岡本 浩一郎, 高橋 陽彦, 鈴木 倫明, 小野寺 理, 柿田 明美, 阿部 博史

    臨床放射線   65 ( 4 )   317 - 324   2020.4

  • [Amyloid β-related angiitis presenting extensive brain involvement without detection of hemorrhagic lesions: A case report]. Reviewed

    Yuya Hatano, Akihiro Sugai, Takuma Yamagishi, Akihiro Nakajima, Akiyoshi Kakita, Osamu Onodera

    Rinsho shinkeigaku = Clinical neurology   60 ( 3 )   187 - 192   2020.3

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    In amyloid β-related angiitis, cortical or subcortical microbleeding or cortical superficial siderosis supports clinical diagnosis. However, here we present a 75-year-old female case of amyloid β-related angiitis that did not initially show these lesions. The patient developed right homonymous hemianopia and aphasia, and subsequently became comatose. Her brain lesions progressed extensively from the left occipital lobe to the bilateral cerebral hemispheres, with diffused leptomeningeal lesions and scattered DWI high-intensity lesions. After pathological diagnosis, steroid treatment improved her symptoms as well as imaging findings. No hemorrhagic lesions were detected in the T2*-weighted imaging performed before treatment. However, susceptibility-weighted imaging performed after treatment showed a number of lesions with microbleeding. The clinical features of amyloid β-related angiitis that do not show hemorrhagic lesions at onset should be investigated for rapid therapeutic intervention in the future.

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  • A homogeneously enhancing mass evolving into multiple hemorrhagic and necrotic lesions in amoebic encephalitis with necrotizing vasculitis. International journal

    Tomoaki Suzuki, Kouichirou Okamoto, Nobuyuki Genkai, Akiyoshi Kakita, Hiroshi Abe

    Clinical imaging   60 ( 1 )   48 - 52   2020.3

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    BACKGROUND: Granulomatous amoebic encephalitis (GAE) is a rare and mostly fatal disease. Without specific symptoms, laboratory findings, or radiologic characteristics, establishing a correct diagnosis is challenging. In many cases of GAE, multiple ring-enhancing lesions with perifocal edema are observed on magnetic resonance imaging (MRI); a solitary and homogeneously enhancing mass masquerading as a malignant lymphoma that evolved into multiple hemorrhagic and necrotic lesions has rarely been reported in GAE. CASE DESCRIPTION: An immunocompetent 68-year-old man presented with transient right hemiparesis due to epilepsy. MRI revealed a well- and homogeneously enhancing mass with perifocal edema and restricted diffusion in the left parietal subcortical region. As malignant lymphoma was suspected based on MRI findings and an elevated β2-microglobulin level in the cerebrospinal fluid, an open biopsy was performed; the pathological diagnosis was inconclusive but suggested a granulomatous disease. Although steroid therapy was administrated, subsequently the mass lesion gradually enlarged. After a second surgery for removal of the mass lesion, multiple hemorrhagic and necrotic lesions developed at the primary site and additionally in the brainstem. The patient entered a comatose state and died 3 months after admission. Histopathological examination and polymerase chain reaction analysis of the specimen revealed posthumously GAE caused by Balamuthia mandrillaris with necrotizing vasculitis. CONCLUSION: A solitary mass lesion initially mimicked a malignant lymphoma, and subsequently evolved into multiple hemorrhagic and necrotic lesions detected on T2*-weighted and susceptibility-weighted imaging. Such serial changes noted on MRI seem characteristic and suggestive of necrotizing vasculitis of GAE.

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  • 出血性病変が検出されずに広範な脳病変に至ったアミロイドβ関連血管炎の1例

    畠野 雄也, 須貝 章弘, 山岸 拓磨, 中島 章博, 柿田 明美, 小野寺 理

    臨床神経学   60 ( 3 )   187 - 192   2020.3

  • 胃管潰瘍の左房穿孔による大脳空気塞栓症の一剖検例

    中原 亜紗, 橋立 英樹, 勇 亜衣子, 他田 正義, 佐藤 晶, 柿田 明美, 渋谷 宏行

    日本病理学会会誌   109 ( 1 )   383 - 383   2020.3

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  • Amyotrophic Lateral Sclerosis with Pallidonigroluysian Degeneration: A Clinicopathological Study. Reviewed International journal

    Junko Ito, Hiroshi Shimizu, Kentaro Ohta, Jiro Idezuka, Hajime Tanaka, Hiroshi Kondo, Takashi Nakajima, Hitoshi Takahashi, Kohei Akazawa, Osamu Onodera, Akiyoshi Kakita

    Annals of neurology   87 ( 2 )   302 - 312   2020.2

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    OBJECTIVE: The pallidonigroluysian (PNL) system, the primary component of corticosubcortical circuits, is generally spared in amyotrophic lateral sclerosis (ALS). We evaluated the clinicopathological features of an unusual form of ALS with PNL degeneration (PNLD) and assessed whether ALS with PNLD represents a distinct ALS subtype. METHODS: From a cohort of 97 autopsied cases of sporadic ALS with phosphorylated 43kDa TAR DNA-binding protein (TDP-43) inclusions, we selected those with PNLD and analyzed their clinicopathological features. RESULTS: Eleven cases (11%) that showed PNLD were divided into 2 subtypes depending on the lesion distribution: (1) extensive type (n = 6), showing widespread TDP-43 pathology and multisystem degeneration, both involving the PNL system; and (2) limited type (n = 5), showing selective PNL and motor system involvement, thus being unclassifiable in terms of Brettschneider's staging or Nishihira's typing of ALS. The limited type showed a younger age at onset and predominant PNLD that accounted for the early development of extrapyramidal signs. The limited type exhibited the heaviest pathology in the subthalamus and external globus pallidus, suggesting that TDP-43 inclusions propagated via indirect or hyperdirect pathways, unlike ALS without PNLD, where the direct pathway is considered to convey TDP-43 aggregates from the cerebral cortex to the substantia nigra. INTERPRETATION: The PNL system can be involved in the disease process of ALS, either nonselectively as part of multisystem degeneration, or selectively. ALS with selective involvement of the PNL and motor systems exhibits unique clinicopathological features and TDP-43 propagation routes, thus representing a distinct subtype of ALS. ANN NEUROL 2020;87:302-312.

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  • MGMT Expression Contributes to Temozolomide Resistance in H3K27M-Mutant Diffuse Midline Gliomas Reviewed International journal

    Hideaki Abe, Manabu Natsumeda, Masayasu Okada, Jun Watanabe, Yoshihiro Tsukamoto, Yu Kanemaru, Junichi Yoshimura, Makoto Oishi, Rintaro Hashizume, Akiyoshi Kakita, Yukihiko Fujii

    Frontiers in Oncology   9   1568 - 1568   2020.1

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    DOI: 10.3389/fonc.2019.01568

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  • Skull diploë is rich in aquaporin-4 Reviewed

    Yuji Suzuki, Hiroki Kitaura, Yukimi Nakamura, Akiyoshi Kakita, Vincent J. Huber, Nicholas Capozzoli, Ingrid L. Kwee, Tsutomu Nakada

    Heliyon   6 ( 1 )   e03259 - e03259   2020.1

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    DOI: 10.1016/j.heliyon.2020.e03259

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  • Rare Brain Metastasis From a Pancreatobiliary Subtype of Intraductal Papillary Mucinous Neoplasm. Reviewed International journal

    Yoshihisa Arao, Kenya Kamimura, Masatoshi Ikemi, Kazunao Hayashi, Masayuki Takaki, Shunsaku Takahashi, Satoshi Seino, Hiroyuki Abe, Shintaro Tsuboguchi, Yutaka Otsu, Kazuhiro Sanpei, Junji Kohisa, Shuhei Kondo, Yusuke Tani, Junko Ito, Yasuko Toyoshima, Akiyoshi Kakita, Yoichi Ajioka, Shuji Terai

    Pancreas   49 ( 1 )   e8-e11 - e11   2020.1

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  • Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer's disease. Reviewed International journal

    Yingyue Zhou, Wilbur M Song, Prabhakar S Andhey, Amanda Swain, Tyler Levy, Kelly R Miller, Pietro L Poliani, Manuela Cominelli, Shikha Grover, Susan Gilfillan, Marina Cella, Tyler K Ulland, Konstantin Zaitsev, Akinori Miyashita, Takeshi Ikeuchi, Makoto Sainouchi, Akiyoshi Kakita, David A Bennett, Julie A Schneider, Michael R Nichols, Sean A Beausoleil, Jason D Ulrich, David M Holtzman, Maxim N Artyomov, Marco Colonna

    Nature medicine   26 ( 1 )   131 - 142   2020.1

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    Glia have been implicated in Alzheimer's disease (AD) pathogenesis. Variants of the microglia receptor triggering receptor expressed on myeloid cells 2 (TREM2) increase AD risk, and activation of disease-associated microglia (DAM) is dependent on TREM2 in mouse models of AD. We surveyed gene-expression changes associated with AD pathology and TREM2 in 5XFAD mice and in human AD by single-nucleus RNA sequencing. We confirmed the presence of Trem2-dependent DAM and identified a previously undiscovered Serpina3n+C4b+ reactive oligodendrocyte population in mice. Interestingly, remarkably different glial phenotypes were evident in human AD. Microglia signature was reminiscent of IRF8-driven reactive microglia in peripheral-nerve injury. Oligodendrocyte signatures suggested impaired axonal myelination and metabolic adaptation to neuronal degeneration. Astrocyte profiles indicated weakened metabolic coordination with neurons. Notably, the reactive phenotype of microglia was less evident in TREM2-R47H and TREM2-R62H carriers than in non-carriers, demonstrating a TREM2 requirement in both mouse and human AD, despite the marked species-specific differences.

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  • Identification of VGF nerve growth factor inducible-producing cells in human spinal cords and expression change in patients with amyotrophic lateral sclerosis. Reviewed International journal

    Yasuhiro Noda, Miruto Tanaka, Shinsuke Nakamura, Junko Ito, Akiyoshi Kakita, Hideaki Hara, Masamitsu Shimazawa

    International journal of medical sciences   17 ( 4 )   480 - 489   2020

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    Amyotrophic lateral sclerosis (ALS) is a serious disease characterized by the degeneration of motor neurons resulting in muscle weakness and paralysis. The neuroendocrine polypeptide VGF is localized in the central nervous system and peripheral endocrine neurons and is cleaved into several polypeptides with multiple functions. Previous studies revealed that VGF was decreased in the cerebrospinal fluid of ALS model mice and sporadic ALS patients. However, it is unknown which cells supply VGF in the spinal cord and a detailed localization is lacking. In this study, we evaluated the VGF-producing cells and protein localization using in situ hybridization and immunostaining in the spinal cords of ALS and control patients. VGF mRNA was localized both in the dorsal and anterior horns of the spinal cords. Moreover, in the anterior horn, VGF mRNA co-localized with a neurofilament heavy chain, which is a motor neuron marker, and VGF mRNA-positive motor neurons were decreased in the spinal cords of ALS patients. We revealed that VGF protein level was decreased in the anterior horn of ALS patients; however, the expression level of VGF protein was not changed in the posterior horn or white matter. Furthermore, the expression level of VGF protein was conserved in ALS patients with long-term survival. These results reveal that VGF is mainly supplied by human motor neurons, and suggest that VGF expression changes may be involved in ALS pathology.

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  • Comparison of Common and Disease-Specific Post-translational Modifications of Pathological Tau Associated With a Wide Range of Tauopathies. International journal

    Fuyuki Kametani, Mari Yoshida, Tomoyasu Matsubara, Shigeo Murayama, Yuko Saito, Ito Kawakami, Mitsumoto Onaya, Hidetomo Tanaka, Akiyoshi Kakita, Andrew C Robinson, David M A Mann, Masato Hasegawa

    Frontiers in neuroscience   14   581936 - 581936   2020

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    Tauopathies are the most common type of neurodegenerative proteinopathy, being characterized by cytoplasmic aggregates of hyperphosphorylated tau protein. The formation and morphologies of these tau inclusions, the distribution of the lesions and related metabolic changes in cytoplasm differ among different tauopathies. The aim of this study was to examine whether there are differences in the post-translational modifications (PTMs) in the pathological tau proteins. We analyzed sarkosyl-insoluble pathological tau proteins prepared from brains of patients with Alzheimer's disease, Pick's disease, progressive supranuclear palsy, corticobasal degeneration, globular glial tauopathy, and frontotemporal dementia and parkinsonisms linked to chromosome 17 with tau inclusions using liquid chromatography mass spectrometry. In pathological tau proteins associated with a wide range of tauopathies, 170 PTMs in total were identified including new PTMs. Among them, common PTMs were localized in the N- and C-terminal flanking regions of the microtubule binding repeats and PTMs, which were considered to be disease-specific, were found in microtubule binding repeats forming filament core. These suggested that the differences in PTMs reflected the differences in tau filament core structures in each disease.

    DOI: 10.3389/fnins.2020.581936

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  • Fatal Progressive Meningoencephalitis Diagnosed in Two Members of a Family With X-Linked Agammaglobulinemia. International journal

    Yasushi Kasahara, Masaru Imamura, Chansu Shin, Hiroshi Shimizu, Jirou Utsumi, Ryosuke Hosokai, Haruko Iwabuchi, Takayuki Takachi, Akiyoshi Kakita, Hirokazu Kanegane, Akihiko Saitoh, Chihaya Imai

    Frontiers in pediatrics   8   579 - 579   2020

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    Chronic enteroviral meningoencephalitis is a well-known complication in patients with X-linked agammaglobulinemia (XLA). However, progressive neurodegenerative disorders or chronic neuroinflammatory diseases with no causative microorganisms have been recognized as rare central nervous system (CNS) complications in XLA. We herein report a family in which two of three members with XLA had developed progressive meningoencephalitis with an unknown etiology. A 15-month-old male infant presented with left-sided ptosis. Initially, the family denied any family history of inherited diseases, but later disclosed a family history of agammaglobulinemia previously diagnosed in two family members. In the early 1980s, one of the elder brothers of the index patient's mother who had been treated with intramuscular immunoglobulin [or later intravenous immunoglobulin (IVIG)] for agammaglobulinemia deceased at 10 years of age after showing progressive neurological deterioration during the last several years of his life. The index patient was diagnosed with XLA caused by Bruton tyrosine kinase deficiency (654delG; Val219Leufs*9), and chronic meningoencephalitis with an unknown infectious etiology. Magnetic resonance imaging of the brain demonstrated inflammatory changes in the basal ganglia, hypothalamus, midbrain, and pons, with multiple nodular lesions with ring enhancement, which showed impressive amelioration after the initiation of IVIG replacement therapy. Pleocytosis, which was characterized by an increase in CD4-positive and CD8-positive T cells expressing an activation marker and an elevation in inflammatory cytokines in the cerebrospinal fluid, was identified. No microorganism was identified as a cause of CNS complications. He thereafter developed brain infarction at 19 months of age and fatal status epilepticus at 5 years of age, despite regular IVIG with high trough levels and regular intraventricular immunoglobulin administration. The etiology of this rare CNS complication in XLA is currently unknown. Previous studies have suggested a possible association of IVIG, which was clearly denied in our index case because of the demonstration of his neurological disorder at presentation. In the future, extensive and unbiased molecular methods to detect causative microorganisms, as well as to investigate the possible role of autoimmunity are needed to clarify the etiology of CNS complications.

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  • Reciprocal connectivity between secondary auditory cortical field and amygdala in mice. Reviewed International journal

    Hiroaki Tsukano, Xubin Hou, Masao Horie, Hiroki Kitaura, Nana Nishio, Ryuichi Hishida, Kuniyuki Takahashi, Akiyoshi Kakita, Hirohide Takebayashi, Sayaka Sugiyama, Katsuei Shibuki

    Scientific reports   9 ( 1 )   19610 - 19610   2019.12

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    Recent studies have examined the feedback pathway from the amygdala to the auditory cortex in conjunction with the feedforward pathway from the auditory cortex to the amygdala. However, these connections have not been fully characterized. Here, to visualize the comprehensive connectivity between the auditory cortex and amygdala, we injected cholera toxin subunit b (CTB), a bidirectional tracer, into multiple subfields in the mouse auditory cortex after identifying the location of these subfields using flavoprotein fluorescence imaging. After injecting CTB into the secondary auditory field (A2), we found densely innervated CTB-positive axon terminals that were mainly located in the lateral amygdala (La), and slight innervations in other divisions such as the basal amygdala. Moreover, we found a large number of retrogradely-stained CTB-positive neurons in La after injecting CTB into A2. When injecting CTB into the primary auditory cortex (A1), a small number of CTB-positive neurons and axons were visualized in the amygdala. Finally, we found a near complete absence of connections between the other auditory cortical fields and the amygdala. These data suggest that reciprocal connections between A2 and La are main conduits for communication between the auditory cortex and amygdala in mice.

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  • Neuromyelitis optica spectrum disorder with massive basal ganglia involvement: a case report. Reviewed

    Ohara S, Miyahira TA, Oguchi K, Takei YI, Yanagimura F, Kawachi I, Oyanagi K, Kakita A

    BMC neurology   19 ( 1 )   351   2019.12

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    Abstract

    Background

    Occurrence of basal ganglia involvement in neuromyelitis optica spectrum disorders (NMOSD) has rarely been reported and none documented pathologically.

    Case presentation

    A 73-year-old female was clinically diagnosed with a NMOSD based on the clinical and radiological features and positive serum autoantibodies to AQP4. One month before her death, she became acutely ill with disturbed consciousness and right hemiparesis, and was diagnosed and treated as having basal ganglia infarction based on the brain CT. She made a partial recovery but later died from heart failure. At autopsy, the corresponding basal ganglia process revealed a large fresh area of necrosis. Histologically, several pathological signatures of NMOSD could be recognized in the lesion, including inflammatory cell infiltrations by B and T lymphocytes, perivascular complement and fibrinogen deposition, and the appearance of numerous phagocytosed corpora amylacea within the infiltrating macrophages.

    Conclusions

    The present case illustrates that basal ganglia may be directly involved in the pathological processes of NMOSD, although the possibility of modification of the lesions by superimposed regional ischemia could not be excluded.

    DOI: 10.1186/s12883-019-1580-3

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    Other Link: http://link.springer.com/article/10.1186/s12883-019-1580-3/fulltext.html

  • 外科的介入を受けていない症候性もやもや病の1剖検例

    齋藤 祥二, 齋藤 理恵, 中原 亜紗, 長谷川 仁, 田口 貴博, 上村 昌寛, 本多 忠幸, 伊藤 靖, 小野寺 理, 梅津 哉, 藤井 幸彦, 柿田 明美

    新潟医学会雑誌   133 ( 11-12 )   389 - 389   2019.12

  • Excess hydrogen sulfide and polysulfides production underlies a schizophrenia pathophysiology. International journal

    Masayuki Ide, Tetsuo Ohnishi, Manabu Toyoshima, Shabeesh Balan, Motoko Maekawa, Chie Shimamoto-Mitsuyama, Yoshimi Iwayama, Hisako Ohba, Akiko Watanabe, Takashi Ishii, Norihiro Shibuya, Yuka Kimura, Yasuko Hisano, Yui Murata, Tomonori Hara, Momo Morikawa, Kenji Hashimoto, Yayoi Nozaki, Tomoko Toyota, Yuina Wada, Yosuke Tanaka, Tadafumi Kato, Akinori Nishi, Shigeyoshi Fujisawa, Hideyuki Okano, Masanari Itokawa, Nobutaka Hirokawa, Yasuto Kunii, Akiyoshi Kakita, Hirooki Yabe, Kazuya Iwamoto, Kohji Meno, Takuya Katagiri, Brian Dean, Kazuhiko Uchida, Hideo Kimura, Takeo Yoshikawa

    EMBO molecular medicine   11 ( 12 )   e10695   2019.12

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    Mice with the C3H background show greater behavioral propensity for schizophrenia, including lower prepulse inhibition (PPI), than C57BL/6 (B6) mice. To characterize as-yet-unknown pathophysiologies of schizophrenia, we undertook proteomics analysis of the brain in these strains, and detected elevated levels of Mpst, a hydrogen sulfide (H2 S)/polysulfide-producing enzyme, and greater sulfide deposition in C3H than B6 mice. Mpst-deficient mice exhibited improved PPI with reduced storage sulfide levels, while Mpst-transgenic (Tg) mice showed deteriorated PPI, suggesting that "sulfide stress" may be linked to PPI impairment. Analysis of human samples demonstrated that the H2 S/polysulfides production system is upregulated in schizophrenia. Mechanistically, the Mpst-Tg brain revealed dampened energy metabolism, while maternal immune activation model mice showed upregulation of genes for H2 S/polysulfides production along with typical antioxidative genes, partly via epigenetic modifications. These results suggest that inflammatory/oxidative insults in early brain development result in upregulated H2 S/polysulfides production as an antioxidative response, which in turn cause deficits in bioenergetic processes. Collectively, this study presents a novel aspect of the neurodevelopmental theory for schizophrenia, unraveling a role of excess H2 S/polysulfides production.

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  • 外科的介入を受けていない症候性もやもや病の1剖検例

    齋藤 祥二, 齋藤 理恵, 中原 亜紗, 長谷川 仁, 田口 貴博, 上村 昌寛, 本多 忠幸, 伊藤 靖, 小野寺 理, 梅津 哉, 藤井 幸彦, 柿田 明美

    新潟医学会雑誌   133 ( 11-12 )   389 - 389   2019.12

  • TAF15が主要に蓄積したFET病理を伴う筋萎縮性側索硬化症 剖検例の臨床病理学的特徴(Amsotrophic lateral sclerosis with TAF15-predominant FET pathology: clinicopathologic features of an autopsied patient)

    Cui Bo, Tada Mari, Hatano Yuya, Takeshima Akari, Ishihara Tomohiko, Sugai Akihiro, Tokutake Takayoshi, Kanazawa Masato, Onodera Osamu, Kakita Akiyoshi

    新潟医学会雑誌   133 ( 11-12 )   391 - 391   2019.12

  • すべてがわかる白質病変の画像と病理 遺伝性白質脳症 病理から見た病態形成

    他田 真理, 柿田 明美

    臨床神経学   59 ( Suppl. )   S73 - S73   2019.11

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  • Phosphorylated TDP-43 aggregates in skeletal and cardiac muscle are a marker of myogenic degeneration in amyotrophic lateral sclerosis and various conditions. Reviewed International journal

    Fumiaki Mori, Mari Tada, Tomoya Kon, Yasuo Miki, Kunikazu Tanji, Hidekachi Kurotaki, Masahiko Tomiyama, Tomohiko Ishihara, Osamu Onodera, Akiyoshi Kakita, Koichi Wakabayashi

    Acta neuropathologica communications   7 ( 1 )   165 - 165   2019.10

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    BACKGROUND: Amyotrophic lateral sclerosis (ALS) is characterized pathologically by the occurrence of phosphorylated TDP-43 (pTDP-43)-immunoreactive neuronal and glial inclusions in the central nervous system. Recent studies have shown that pTDP-43 aggregates also occur in the skeletal muscles in a certain proportion of ALS patients. AIM: The aim of this study was to clarify the distribution and incidence of pTDP-43 aggregates in the skeletal and cardiac muscles of patients with ALS, and also those of patients with neuromuscular diseases (NMDs) and non-NMDs. MATERIAL AND METHODS: Five regions of muscle (tongue, cervical muscle, diaphragm, iliopsoas muscle and heart) were examined histologically and immunohistochemically in patients with ALS (n = 30), NMDs (n = 13) and non-NMDs (n = 7). RESULTS: Two types of pTDP-43 aggregates were distinguishable morphologically: dense filamentous and short linear inclusions. These inclusions were found in at least one of the five muscle regions in all 30 cases of ALS; skeletal muscles in 28 cases and myocardium in 12. pTDP-43 aggregates were also found in 9 of 13 patients with NMDs, including myositis, muscular dystrophy and mitochondrial myopathy, as well as in 3 of 7 patients with non-NMDs. In ALS, pTDP-43 aggregates were most frequent in the diaphragm (19 cases). The mean density of pTDP-43 aggregates in ALS was significantly higher than that in NMDs and non-NMDs. In contiguous sections stained with hematoxylin and eosin and anti-pTDP-43, muscle fibers with dense filamentous inclusions demonstrated single-fiber atrophy with vacuolar degeneration. CONCLUSION: The present findings indicate that pTDP-43 aggregates in skeletal and cardiac muscle are a myogenic pathological marker in multiple diseases including ALS.

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  • Differential protein expression of DARPP-32 versus Calcineurin in the prefrontal cortex and nucleus accumbens in schizophrenia and bipolar disorder. Reviewed International journal

    Yasuto Kunii, Mizuki Hino, Junya Matsumoto, Atsuko Nagaoka, Hiroyuki Nawa, Akiyoshi Kakita, Hiroyasu Akatsu, Yoshio Hashizume, Hirooki Yabe

    Scientific reports   9 ( 1 )   14877 - 14877   2019.10

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    Dopamine- and cAMP-regulated phosphoprotein of molecular weight 32 kDa (DARPP-32) integrates dopaminergic signaling into that of several other neurotransmitters. Calcineurin (CaN), located downstream of dopaminergic pathways, inactivates DARPP-32 by dephosphorylation. Despite several studies have examined their expression levels of gene and protein in postmortem patients' brains, they rendered inconsistent results. In this study, protein expression levels of DARPP-32 and CaN were measured by enzyme-linked immunosorbent assay (ELISA) in the prefrontal cortex (PFC), and nucleus accumbens (NAc) of 49 postmortem samples from subjects with schizophrenia, bipolar disorder, and normal controls. We also examined the association between this expression and genetic variants of 8 dopaminergic system-associated molecules for 55 SNPs in the same postmortem samples. In the PFC of patients with schizophrenia, levels of DARPP-32 were significantly decreased, while those of CaN tended to increase. In the NAc, both of DARPP-32 and CaN showed no significant alternations in patients with schizophrenia or bipolar disorder. Further analysis of the correlation of DARPP-32 and CaN expressions, we found that positive correlations in controls and schizophrenia in PFC, and schizophrenia in NAc. In PFC, the expression ratio of DARPP-32/CaN were significantly lower in schizophrenia than controls. We also found that several of the aforementioned SNPs may predict protein expression, one of which was confirmed in a second independent sample set. This differential expression of DARPP-32 and CaN may reflect potential molecular mechanisms underlying the pathogenesis of schizophrenia and bipolar disorder, or differences between these two major psychiatric diseases.

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  • Glial pathology in a novel spontaneous mutant mouse of the Eif2b5 gene: a vanishing white matter disease model. Reviewed International journal

    Mika Terumitsu-Tsujita, Hiroki Kitaura, Ikuo Miura, Yuji Kiyama, Fumiko Goto, Yoshiko Muraki, Shiho Ominato, Norikazu Hara, Anna Simankova, Norihisa Bizen, Kazuhiro Kashiwagi, Takuhiro Ito, Yasuko Toyoshima, Akiyoshi Kakita, Toshiya Manabe, Shigeharu Wakana, Hirohide Takebayashi, Hironaka Igarashi

    Journal of neurochemistry   154 ( 1 )   25 - 40   2019.10

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    Vanishing white matter disease (VWM) is an autosomal recessive neurological disorder caused by mutation(s) in any subunit of eukaryotic translation initiation factor 2B (eIF2B), an activator of translation initiation factor eIF2. VWM occurs with mutation of the genes encoding eIF2B subunits (EIF2B1, EIF2B2, EIF2B3, EIF2B4, and EIF2B5). However, little is known regarding the underlying pathogenetic mechanisms or how to treat patients with VWM. Here we describe the identification and detailed analysis of a new spontaneous mutant mouse harboring a point mutation in the Eif2b5 gene (p.Ile98Met). Homozygous Eif2b5I98M mutant mice exhibited a small body, abnormal gait, male and female infertility, epileptic seizures, and a shortened lifespan. Biochemical analyses indicated that the mutant eIF2B protein with the Eif2b5I98M mutation decreased guanine nucleotide exchange activity on eIF2, and the level of the endoplasmic reticulum stress marker activating transcription factor 4 was elevated in the 1-month-old Eif2b5I98M brain. Histological analyses indicated up-regulated glial fibrillary acidic protein immunoreactivity in the astrocytes of the Eif2b5I98M forebrain and translocation of Bergmann glia in the Eif2b5I98M cerebellum, as well as increased mRNA expression of an endoplasmic reticulum stress marker, C/EBP homologous protein. Disruption of myelin and clustering of oligodendrocyte progenitor cells were also indicated in the white matter of the Eif2b5I98M spinal cord at 8 months old. Our data show that Eif2b5I98M mutants are a good model for understanding VWM pathogenesis and therapy development.

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  • ヒト死後脳におけるAPP・APOEの遺伝子発現解析 Reviewed

    Lixin Liu, 宮下 哲典, 村上 涼太, Bin Zhu, 原 範和, 菊地 正隆, 月江 珠緒, 樋口 陽, 春日 健作, 中谷 明弘, 赤津 裕康, 柿田 明美, 村山 繁雄, 池内 健

    Dementia Japan   33 ( 4 )   519 - 519   2019.10

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  • TΔΠ-43 プロテイノパチー (1) 前頭側頭葉変性症 (FTLD) Reviewed

    他田 真理, 柿田 明美

    病理と臨床   37 ( 9 )   2019.9

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    連載 –変性疾患のみかた–

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  • G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10. Reviewed International journal

    Anisimov S, Takahashi M, Kakihana T, Katsuragi Y, Kitaura H, Zhang L, Kakita A, Fujii M

    Scientific reports   9 ( 1 )   12896 - 12896   2019.9

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    The aberrant accumulation of ubiquitinated protein aggregates in cells plays a critical role in the pathogenesis of several degenerative diseases, including Parkinson disease (PD) and cystic fibrosis (CF). In this study, we found that Ras GTPase-activating protein-binding protein 1 (G3BP1) inhibits ubiquitinated protein aggregations induced by p62 and USP10 in cultured cells. p62 is a ubiquitin receptor, and p62 and its binding partner USP10 have been shown to augment ubiquitinated protein aggregation. G3BP1 interacted with p62 and USP10 and inhibited p62/USP10-induced protein aggregation. The G3BP1 inhibition of protein aggregations targeted two aggregation-prone proteins, α-synuclein and CFTR-ΔF508, which are causative factors of PD and CF, respectively. G3BP1 depletion increased the amounts of ubiquitinated α-synuclein and CFTR-ΔF508 protein. A proteasome reporter indicated that G3BP1 depletion inhibits the proteasome activity. We herein present evidence that G3BP1, p62 and USP10 together control ubiquitinated protein toxicity by controlling both ubiquitination and aggregation. Taken together, these results suggest that G3BP1, p62 and USP10 could be therapeutic targets for ubiquitinated protein aggregation disorders, including PD and CF.

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  • Neurite orientation dispersion and density imagingによる皮質形成異常の可視化

    伊藤 陽祐, 松澤 等, 福多 真史, 増田 浩, 白水 洋史, 村井 志乃, 北浦 弘樹, 柿田 明美, 藤井 幸彦

    てんかん研究   37 ( 2 )   617 - 617   2019.9

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  • Rapid chemical clearing of white matter in post-mortem human brain by 1,2-hexanediol delipidation. Reviewed

    Inoue M, Saito R, Kakita A, Tainaka K

    Bioorganic Medicinal Chem Lett   29 ( 15 )   1886 - 1890   2019.8

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    DOI: 10.1016/j.bmcl.2019.05.049.

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  • USP10 is a critical factor for Tau-positive stress granule formation in neuronal cells. Reviewed International journal

    Svetlana Piatnitskaia, Masahiko Takahashi, Hiroki Kitaura, Yoshinori Katsuragi, Taichi Kakihana, Lu Zhang, Akiyoshi Kakita, Yuriko Iwakura, Hiroyuki Nawa, Takeshi Miura, Takeshi Ikeuchi, Toshifumi Hara, Masahiro Fujii

    Scientific reports   9 ( 1 )   10591 - 10591   2019.7

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    Tau aggregates in neurons of brain lesions is a hallmark pathology of tauopathies, including Alzheimer's disease (AD). Recent studies suggest that the RNA-binding protein TIA1 initiates Tau aggregation by inducing the formation of stress granules (SGs) containing Tau. SGs are stress-inducible cytoplasmic protein aggregates containing many RNA-binding proteins that has been implicated as an initial site of multiple pathogenic protein aggregates in several neurodegenerative diseases. In this study, we found that ubiquitin-specific protease 10 (USP10) is a critical factor for the formation of Tau/TIA1/USP10-positive SGs. Proteasome inhibition or TIA1-overexpression in HT22 neuronal cells induced the formation of TIA1/Tau-positive SGs, and the formations were severely attenuated by depletion of USP10. In addition, the overexpression of USP10 without stress stimuli in HT22 cells induced TIA1/Tau/USP10-positive SGs in a deubiquitinase-independent manner. In AD brain lesions, USP10 was colocalized with Tau aggregates in the cell body of neurons. The present findings suggest that USP10 plays a key role in the initiation of pathogenic Tau aggregation in AD through SG formation.

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  • A mouse model of adult-onset multiple system atrophy. Reviewed International journal

    Kunikazu Tanji, Yasuo Miki, Fumiaki Mori, Yoshikazu Nikaido, Hidemi Narita, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    Neurobiology of disease   127   339 - 349   2019.7

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    Multiple system atrophy (MSA) is an adult-onset neurodegenerative disorder clinically characterized by autonomic failure in addition to various combinations of symptoms of parkinsonism, cerebellar ataxia, and pyramidal dysfunction. Despite extensive research, the mechanisms underlying the progression of MSA remain unknown. Animal models of human diseases that recapitulate their clinical, biochemical and pathological features are indispensable for increasing our understanding of their underlying molecular mechanisms, which allows preclinical studies to be advanced. Because the onset of MSA occurs in middle age, an animal model that first manifests abnormal protein aggregates in adulthood would be most appropriate. We therefore used the Cre-loxP system to express inducible α-synuclein (Syn), a major component of the pathological hallmark of MSA, to generate a mouse model of MSA. Beginning in adulthood, these MSA model mice express excessive levels of Syn in oligodendrocytes, resulting in abnormal Syn accumulation and modifications similar to those observed in human MSA pathology. Additionally, MSA model mice exhibit some clinical features of MSA, including decreased motor activity. These findings suggest that this new mouse model of MSA represents a useful tool for analyzing the pathophysiological alterations that underlie the progression of this disease.

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  • Dramatic response of BRAF V600E-mutant epithelioid glioblastoma to combination therapy with BRAF and MEK inhibitor: establishment and xenograft of a cell line to predict clinical efficacy. Reviewed International journal

    Kanemaru Y, Natsumeda M, Okada M, Saito R, Kobayashi D, Eda T, Watanabe J, Saito S, Tsukamoto Y, Oishi M, Saito H, Nagahashi M, Sasaki T, Hashizume R, Aoyama H, Wakai T, Kakita A, Fujii Y

    Acta neuropathologica communications   7 ( 1 )   119 - 119   2019.7

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    Epithelioid glioblastoma is a rare aggressive variant of glioblastoma (GBM) characterized by a dismal prognosis of about 6 months and frequent leptomeningeal dissemination. A recent study has revealed that 50% of epithelioid GBMs harbor three genetic alterations - BRAF V600E mutation, TERT promoter mutations, and homozygous deletions of CDKN2A/2B. Emerging evidence support the effectiveness of targeted therapies for brain tumors with BRAF V600E mutation. Here we describe a dramatic radiographical response to combined therapy with BRAF and MEK inhibitors in a patient with epithelioid GBM harboring BRAF V600E mutation, characterized by thick spinal dissemination. From relapsed tumor procured at autopsy, we established a cell line retaining the BRAF V600E mutation, TERT promoter mutation and CDKN2A/2B loss. Intracranial implantation of these cells into mice resulted in tumors closely resembling the original, characterized by epithelioid tumor cells and dissemination, and invasion into the perivascular spaces. We then confirmed the efficacy of treatment with BRAF and MEK inhibitor both in vitro and in vivo. Epithelioid GBM with BRAF V600E mutation can be considered a good treatment indication for precision medicine, and this patient-derived cell line should be useful for prediction of the tumor response and clarification of its biological characteristics.

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  • 統合失調症患者の脳内ゲノムにおけるコピー数変異の評価

    坂井 美和子, 渡部 雄一郎, 染矢 俊幸, 荒木 一明, 澁谷 雅子, 新里 和弘, 大島 健一, 國井 泰人, 矢部 博興, 松本 純弥, 和田 明, 日野 瑞城, 橋本 健志, 菱本 明豊, 北村 登, 入谷 修司, 白川 治, 前田 潔, 宮下 哲典, 丹羽 真一, 高橋 均, 柿田 明美, 桑野 良三, 那波 宏之

    精神神経学雑誌   ( 2019特別号 )   S603 - S603   2019.6

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  • 統合失調症患者における脳内コンドロイチン硫酸鎖の変化

    湯川 尊行, 岩倉 百合子, 武井 延之, 斎藤 摩美, 渡部 雄一郎, 豊岡 和彦, 五十嵐 道弘, 新里 和弘, 大島 健一, 國井 泰人, 矢部 博興, 松本 純弥, 和田 明, 日野 瑞城, 入谷 修司, 丹羽 真一, 竹内 亮子, 高橋 均, 柿田 明美, 染矢 俊幸, 那波 宏之

    精神神経学雑誌   ( 2019特別号 )   S410 - S410   2019.6

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  • パーキンソン病、筋萎縮性側索硬化症、進行性核上性麻痺の合併を認めた高齢女性剖検例 Reviewed

    田中 英智, 清水 宏, 豊島 靖子, 若林 允甫, 柿田 明美

    The Kitakanto Medical Journal   69 ( 2 )   170 - 170   2019.5

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  • An autopsy case of peliosis hepatis with X-linked myotubular myopathy. Reviewed International journal

    Kazuhisa Funayama, Hiroshi Shimizu, Hidetomo Tanaka, Izumi Kawachi, Ichizo Nishino, Kou Matsui, Naoya Takahashi, Akihide Koyama, Rieka Katsuragi-Go, Ryoko Higuchi, Takashi Aoyama, Hiraku Watanabe, Akiyoshi Kakita, Hisakazu Takatsuka

    Legal medicine (Tokyo, Japan)   38   77 - 82   2019.5

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    This report describes the autopsy case of a 4-year-old boy who died from hepatic hemorrhage and rupture caused by peliosis hepatis with X-linked myotubular myopathy. Peliosis hepatis is characterized by multiple blood-filled cavities of various sizes in the liver, which occurs in chronic wasting disease or with the use of specific drugs. X-linked myotubular myopathy is one of the most serious types of congenital myopathies, in which an affected male infant typically presents with severe hypotonia and respiratory distress immediately after birth. Although each disorder is rare, 12 cases of pediatric peliosis hepatis associated with X-linked myotubular myopathy have been reported, including our case. Peliosis hepatis should be considered as a cause of hepatic hemorrhage despite its low incidence, and it requires adequate gross and histological investigation for correct diagnosis.

    DOI: 10.1016/j.legalmed.2019.04.005

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  • 統合失調症として長期入院していた特発性基底核石灰化症 (Fahr病) の臨床病理学的特徴 Reviewed

    伊藤 陽, 吉田浩樹, 清水敬三, 長谷川まこと, 今野公和, 中原亜紗, 原 範和, 宮下哲典, 池内 健, 豊島靖子, 柿田明美

    精神医学   61 ( 5 )   595 - 603   2019.5

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  • DNTにおけるMLPA法を用いたFGFR1-ITD解析

    松村 望, 信澤 純人, 伊藤 絢子, 柿田 明美, 鈴木 博義, 山崎 達弥, 中里 洋一, 平戸 純子, 横尾 英明

    Brain Tumor Pathology   36 ( Suppl. )   123 - 123   2019.5

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  • High detection rate of MYD88 mutations in cerebrospinal fluid from patients with central nervous system lymphomas. Reviewed

    Watanabe J, Matsumeda M, Olada M, Kobayashi D, Kanemaru Y, Tsukamoto Y, Oishi M, Kakita A, Fujii Y

    JCO Precis Oncol,   e1 - e10   2019.4

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    DOI: 10.1200/PO.18.00308.

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  • Globular glial tauopathy Type II: Clinicopathological study of two autopsy cases. Reviewed International journal

    Hidetomo Tanaka, Shinobu Kawakatsu, Yasuko Toyoshima, Takeshi Miura, Naomi Mezaki, Atsushi Mano, Kazuhiro Sanpei, Ryota Kobayashi, Hiroshi Hayashi, Koichi Otani, Takeshi Ikeuchi, Osamu Onodera, Akiyoshi Kakita, Hitoshi Takahashi

    Neuropathology : official journal of the Japanese Society of Neuropathology   39 ( 2 )   111 - 119   2019.4

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    Globular glial tauopathies (GGTs) are four-repeat tauopathies characterized by the presence of two types of tau-positive globular glial inclusions (GGIs): globular oligodendrocytic and astrocytic inclusions (GOIs and GAIs). GGTs are classified into three different neuropathological subtypes: Types I, II and III. We report two patients with GGTs - a 76-year-old woman and a 70-year-old man - in whom the disease duration was 5 and 6 years, respectively. Both patients exhibited upper and lower motor neuron signs and involuntary movements, and the latter also had dementia with frontotemporal cerebral atrophy evident on magnetic resonance imaging. Neuropathologically, in both cases, the precentral gyrus was most severely affected, and at the gray-white matter junction there was almost complete loss of Betz cells and occurrence of GOIs and coiled bodies with numerous neuropil threads. Both patients also showed neuronal loss and GGIs (mostly GOIs) in many other central nervous system regions, including the basal ganglia. Apart from the degree of regional severity, the distribution pattern was essentially the same in both cases. However, GAIs were not conspicuous in any of the affected regions. Based on the morphology and distribution pattern of the GGIs, we diagnosed the present two patients as having GGT Type II. Electron microscopic and biochemical findings in the former were consistent with the diagnosis. Type II cases are reported to be characterized by pyramidal features reflecting predominant motor cortex and corticospinal tract degeneration. The present observations suggest that a variety of neurological features, including dementia, can occur in GGT Type II reflecting widespread degeneration beyond the motor neuron system.

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  • 経過中にBálint症候群を発症し、塩酸メフロキンとミルタザピンの併用療法により改善した進行性多巣性白質脳症の1例. Reviewed

    竹腰顕, 吉倉延亮, 小澤憲司, 生駒良和, 竹島明, 大槻美佳, 中道一生, 西條政幸, 望月清文, 柿田明美, 下畑享良

    Brain Nerve   71 ( 3 )   281 - 286   2019.3

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    DOI: 10.11477/mf.1416201256.

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  • [A Patient with Progressive Multifocal Leukoencephalopathy Who Developed Bálint Syndrome Improved by Combination Therapy Using Mefloquine and Mirtazapine]. Reviewed

    Akira Takekoshi, Nobuaki Yoshikura, Kenji Ozawa, Yoshikazu Ikoma, Junichi Kitagawa, Akari Takeshima, Mika Otsuki, Kazuo Nakamichi, Masayuki Saijo, Naoyuki Ohe, Kiyofumi Mochizuki, Akiyoshi Kakita, Takayoshi Shimohata

    Brain and nerve = Shinkei kenkyu no shinpo   71 ( 3 )   281 - 286   2019.3

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    We describe a 62-year-old man who developed subacute visual loss after cord blood stem cell transplantation for malignant lymphoma. Brain magnetic resonance imaging (MRI) showed bilateral hyperintense lesions in the occipital and parietal lobes. A diagnosis of progressive multifocal encephalopathy (PML) was established following brain biopsy and detection of JC virus (JCV) deoxyribonucleic acid (DNA) in the cerebrospinal fluid (CSF). He developed optic ataxia and visual inattention, and was then diagnosed as having Bálint syndrome. After he was treated with mefloquine and mirtazapine, his Bálint syndrome and, MRI findings improved and the copy number of JCV DNA in the CSF decreased. In summary, we demonstrate that patient with PML may develop Bálint syndrome and that combination therapy using mefloquine and mirtazapine may be an effective treatment. (Received August 23, 2018; Accepted November 29, 2018; Published March 1, 2019).

    DOI: 10.11477/mf.1416201256

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  • EGFRvIII is expressed in cellular areas of tumor in a subset of glioblastoma. Reviewed

    Nozawa T, Okada M, Natsumeda M, Eda T, Abe H, Tsukamoto Y, Okamoto K, Oishi M, Takahashi H, Fujii Y, Kakita A

    Neurol Med Chir   59 ( 3 )   89 - 97   2019.3

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    DOI: 10.2176/nmc.oa.2018-0078.

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  • Multiplex ligation-dependent probe amplification analysis is useful for detecting a copy number gain of the FGFR1 tyrosine kinase domain in dysembryoplastic neuroepithelial tumors. Reviewed

    Matsumura N, Nobusawa S, Ito J, Kakita A, Suzuki H, Fujii Y, Fukuda M, Iwasaki M, Nakasato N, Yominaga T, Natsume A, Mikami Y, Shinojima N, Yamazaki T, Nakazato Y, Hirato J, Yokoo H

    J Neurooncol   2019.3

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    DOI: 10.1007/s11060-019-03138-7.

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  • Retinal Vasculopathy With Cerebral Leukodystrophy: Clinicopathologic Features of an Autopsied Patient With a Heterozygous TREX 1 Mutation. Reviewed International journal

    Rie Saito, Hiroaki Nozaki, Taisuke Kato, Yasuko Toyoshima, Hajime Tanaka, Yutaka Tsubata, Tetsuo Morioka, Yoh Horikawa, Kiyomitsu Oyanagi, Takashi Morita, Osamu Onodera, Akiyoshi Kakita

    Journal of neuropathology and experimental neurology   78 ( 2 )   181 - 186   2019.2

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    Retinal vasculopathy with cerebral leukodystrophy (RVCL) is an autosomal-dominant disorder involving the cerebral, retinal, renal, and other systemic microvessels due to frameshift mutations in the TREX1 gene. Under physiological conditions, the TREX1 protein is localized in the cellular cytoplasm and perinuclear area, but translocates into the nucleus in response to oxidative DNA damage. It has been speculated that aberrant localization of the protein may be associated with systemic microangiopathy in patients with RVCL. However, cellular expression of TREX1 in the brain and visceral organs of patients with RVCL has been unclear. Here, we report the clinicopathologic features of an autopsied patient with a heterozygous T249fs mutation in TREX1. The patient showed the clinical phenotype of vasculopathy with retinopathy, nephropathy, and stroke. CT with contrast enhancement demonstrated a tumorous lesion in the subcortical white matter. Histologically, the lesion consisted of confluent foci of necrosis with calcification and fibrous thickening of small vessel walls. TREX1 immunohistochemistry demonstrated positivity in the nuclei of cells in the CNS and visceral organs, indicating aberrant localization of the truncated protein, and the expression was remarkable in oligodendrocytes within the lesion, suggesting possible involvement of the protein in the pathomechanism of vasculopathy leading to white matter degeneration.

    DOI: 10.1093/jnen/nly115

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  • Autopsy findings and clinical feature of a mild-type xeroderma pigmentosum complementation group A siblings: 40 years of follow-up Reviewed

    Masaki T, Tsujimoto M, Kitazawa R, Nakano E, Funasaka Y, Ichihashi M, Kitazawa S, Kakita A, Kanda F, Nishigori C

    J Am Acad Dermatol Case Reports   5 ( 3 )   205 - 208   2019.2

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    DOI: 10.1016/j.jdcr.2018.04.017.

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  • Sushi repeat-containing protein 1 co-accumulates with cerebrovascular Abeta deposits in cerebral amyloid angiopathy Reviewed

    Inoue Yasuteru, Ueda Mitsuharu, Tasaki Masayoshi, Takeshima Akari, Misumi Yohei, Kosaka Takayuki, Yamashita Taro, Takahashi Hitoshi, Kakita Akiyoshi, Ando Yukio

    BRAIN PATHOLOGY   29   179 - 180   2019.2

  • 病理所見を理解する基礎 - 海馬硬化 - Reviewed

    張 璐, 田中英智, 柿田明美

    てんかん研究   39 ( 3 )   664 - 666   2019.1

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  • An attempt of non-human primate modeling of schizophrenia with neonatal challenges of epidermal growth factor Reviewed

    Sakai M, Kashiwahara M, Kakita A, Nawa H

    J Addict Res Ther   2019

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  • Surgical strategy for focal cortical dysplasia based on the analysis of the spike onset and peak zones on magnetoencephalography. Reviewed

    Sergei A, Takahashi M, Katsuragi Y, Kakihana T, Kitaura H, Zhang L, Kakita A, Fujii M

    J Neurosurg   2019

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  • Investigation of betaine as a novel psychotherapyeutic for schizophrenia. Reviewed

    Ohnishi T, Balan S, Toyoshima M, Maekawa M, Ohba H, Watanabe A, Iwayama Y, Shimamoto C, Nozaki Y, Hisano Y, Esaki K, Mataga N, Hayashi-Takagi A, Kunii Y, Kakita A, Yabe H, Yoshikawa T

    EBioMedicine   2019

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    DOI: 10.1016/j.ebiom.2019.05.062.

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  • The epileptogenic zone in pharmacy-resistant temporal lobe epilepsy with amygdala enlargement. Reviewed

    Suzuki H, Sugano H, Nakajima M, Higo T, Iimura Y, Mitsuhashi T, Fusegi K, Kakita A, Otsubo H, Arai H

    Epileptic Disord   2019

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    DOI: 10.1684/epd.2019.1075.

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  • Morphological characterizeation of glial and neuronal tau pathology in globular glial tauopathy (types II and III). Reviewed

    Tanaka H, Toyoshima Y, Kawakatsu S, Ikeuchi T, Onodera O, Kakita A, Takahashi H

    Neuropathol Appl Neurobiol   2019

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  • Epigenome-wide association study of narcolepsy-affected lateral hypothalamic brain and overlapping DNA methylation profiles between narcolepsy and multiple sclerosis. Reviewed

    Shimada M, Miyagawa T, Takeshima A, Kakita A, Toyoda H, Niizato K, Oshima K, Tokunaga K, Honda M

    Sleep   2019

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  • Phosphorylated NUB1 distinguishes α-synuclein in Lewy bodies from that in glial cytoplasmic inclusions of multiple system atrophy. Reviewed

    Tanji K, Miki Y, Mori F, Kon T, Kakita A, Takahashi H, Wakabayashi K

    Brain Pathology   2019

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    DOI: 10.1111/bpa.12728.

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  • αシヌクレイノパチー (2) 多系統萎縮症 Reviewed

    齋藤 理恵, 柿田明美

    病理と臨床   2019

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    連載-変性疾患のみかた-

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  • A minimal amount of tissue-based pH measurement to improve quality control in neuropsychiatryic postmortem brain studies. Reviewed

    Ono C, Yu Z, Kikuchi Y, Kunii Y, Hino M, Matsumoto J, Nagaoka A, Ito J, Iwasaki Y, Hagihara H, Miyakawa T, Yoshida M, Saito Y, Niwa S, Yabe H, Kakita A, Tomita H

    Psychiatry Clin Neurosci   2019

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    DOI: 10.1111/pcn.12863.

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  • Comparison of circulating tumor DNA between body fluids in patients with primary central nervous system lymphoma. Reviewed

    Watanabe J, natsumeda M, kanemaru Y, Okada M, Oishi M, kakita A, Fujii Y

    Leukemia Lymphoma   2019

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  • Immunoreactivity of myelin-associated oligodendrocytic basic protein in Lewy bodies. Reviewed

    Kon T, Tanji K, Mori F, Kimura A, Kakita A, Wakabayashi K

    Neuropathology   2019

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    DOI: 10.1111/neup.12564.

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  • Podoplanin expression and IDH-wildtype status predicts venous thrombolism in patients with high-grade gliomas in early postoperative period. Reviewed

    Watanabe J, Natsumeda M, Okada M, Kanemaru Y, Tsukamoto Y, Oishi M, Kakita A, Fujii Y

    World Neurosurg   2019

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    DOI: 10.1016/j.wneu.2019.05.049.

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  • A case of cerebral amyloid angiopathy-type hereditary ATTR amyloidosis with Y69H (p.Y89H) variant displaying transient focal neurological episodes as the main symptom. Reviewed

    Yamada Y, Fukushima T, Kodama S, Shimizu H, Kakita A, Makino K, Sekijima Y

    Amyloid   2019

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    DOI: 10.1080/13506129.2019.1632829.

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  • G3BP1 inhibits ubiquitinated protein aggregations by interacting with p62 and USP10. Reviewed

    Sergei A, Takahashi M, Katsuragi Y, Kakihana T, Kitaura H, Zhang L, Kakita A, Fujii M

    Sci Rep   2019

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  • Pathologic alterations of chondroitin sulfate moiety in the postmortem hippocampus of patients with schizophrenia. Reviewed International journal

    Yukawa T, Iwakura Y, Takei N, Saito M, Watanabe Y, Toyooka K, Igarashi M, Niizato K, Ohima K, Kunii Y, Yabe H, Matsumoto J, Wada A, Hino M, Iritani S, Niwa S, Takeuchi R, Takahashi H, Kakita A, Someya T, Nawa H

    Psychiatry Res   270   940 - 946   2018.12

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    Perineuronal nets comprise chondroitin sulfate moieties and their core proteins, and their neuropathological alterations have been implicated in schizophrenia. To explore the molecular mechanism of the perineuronal net impairments in schizophrenia, we measured the immunoreactivity of chondroitin sulfate moieties, major components of perineuronal nets, in three brain regions (postmortem dorsolateral prefrontal cortex, caudate nucleus, and hippocampus) of schizophrenia patients and control subjects. Immunoblotting for chondroitin 4-sulfate and chondroitin 6-sulfate moieties revealed a significant increase in intensity of a 180 kD band of chondroitin 4-sulfate immunoreactivity in the hippocampus of patients, although we detected no significant alteration in their immunoreactivities with any other molecular sizes or in other brain regions. The levels of immunoreactivity were not correlated with postmortem interval, age, or storage time. We failed to find such an increase in a similar molecular range of the chondroitin 4-sulfate immunoreactivity in the hippocampus of the rats chronically treated with haloperidol. These results suggest that the level alteration of the chondroitin 4-sulfate moiety might contribute to the perineuronal net abnormality found in patients with schizophrenia.

    DOI: 10.1016/j.psychres.2018.10.062.

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  • ALS診断におけるAwaji基準の有用性に関する、当科剖検例での後方視的検討

    茂木 崇秀, 石原 智彦, 竹島 明, 他田 真理, 他田 正義, 柿田 明美, 小野寺 理

    臨床神経学   58 ( Suppl. )   S265 - S265   2018.12

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  • COX10変異とPMP22欠失を伴った白質脳症の一家系 臨床病理学的解析

    黒羽 泰子, 石黒 敬信, 長谷川 有香, 谷 卓, 高橋 哲哉, 松原 奈絵, 他田 真理, 河内 泉, 柿田 明美, 小野寺 理, 池内 健, 小池 亮子

    臨床神経学   58 ( Suppl. )   S327 - S327   2018.12

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  • Clinicopathologic Features of Two Patients With Sporadic Amyotrophic Lateral Sclerosis Who Maintained Communication Ability for Over 30 Years. Reviewed International journal

    Junko Ito, Tetsuro Shimada, Mari Tada, Hiroshi Shimizu, Masatoshi Wakabayashi, Akio Yokoseki, Osamu Onodera, Hitoshi Takahashi, Akiyoshi Kakita

    Journal of neuropathology and experimental neurology   77 ( 11 )   981 - 986   2018.11

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    We report the clinicopathologic features of 2 unrelated patients with sporadic amyotrophic lateral sclerosis (SALS) supported by tracheostomy and invasive ventilation (TIV) who were able to maintain communication ability for more than 30 years after disease onset. In both cases, the age at onset was younger than the mean, initially the progression of muscle weakness was consistent with that in the majority of SALS patients, and TIV became necessary several years after disease onset. Thereafter, however, their neurologic deterioration slowed and the patients were able to operate computers by facial movements for several decades. At autopsy, neuronal loss appeared to be confined to the motor neuron system. Furthermore, while Betz cells and lower motor neurons in the spinal anterior horns and hypoglossal nucleus were severely depleted, other pyramidal neurons in the motor cortex, and lower motor neurons in the other brainstem motor nuclei were retained. Neuronal and glial cytoplasmic inclusions immunoreactive for phosphorylated 43-kDa TAR DNA-binding protein (TDP-43) were evident in the CNS, but in extremely small numbers. The present patients may represent a distinct subgroup of patients with SALS who are able to maintain communication ability for an extremely long period, accompanied by very mild TDP-43 pathology.

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  • Neuronal intranuclear inclusion disease showing intranuclear inclusions in renal biopsy 12 years earlier. Reviewed International journal

    Motoki M, Nakajima H, Sato T, Tada M, Kakita A, Arawaka S

    Neurology   91 ( 19 )   884 - 886   2018.11

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    DOI: 10.1212/WNL.0000000000006480

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  • USP10 is a driver of ubiquitinated protein aggregation and aggresome formation to inhibit apoptosis. Reviewed International journal

    Takahashi M, Kitaura H, Kakita A, Kakihana T, Katsuragi Y, Nameta M, Zhang L, Iwakura Y, Nawa H, Higuchi M, Komatsu M, Fujii M

    iScience   9   433 - 450   2018.11

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    Accumulation of ubiquitinated proteins is cytotoxic, but cells inactivate these cytotoxicities by inducing aggresome formation. We found that ubiquitin-specific protease 10 (USP10) inhibits ubiquitinated protein-induced apoptosis by inducing aggresome formation. USP10 interacted with the ubiquitin receptor p62 and the interaction augmented p62-dependent ubiquitinated protein aggregation and aggresome formation, thereby cooperatively inhibiting apoptosis. We provide evidence that USP10/p62-induced protein aggregates inhibit proteasome activity, which increases the amount of ubiquitinated proteins and promotes aggresome formation. USP10 induced aggresomes containing α-synuclein, a pathogenic protein in Parkinson disease, in cultured cells. In Parkinson disease brains, USP10 was colocalized with α-synuclein in the disease-linked aggresome-like inclusion Lewy bodies, suggesting that USP10 inhibits α-synuclein-induced neurotoxicity by promoting Lewy body formation. Collectively, these findings suggest that USP10 is a critical factor to control protein aggregation, aggresome formation, and cytotoxicity in protein-aggregation-related diseases.

    DOI: 10.1016/j.isci.2018.11.006

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  • 診断が困難であった進行性核上性麻痺の剖検例 Reviewed

    田中 弘, 田中 英智, 清水 宏, 柿田 明美, 高橋 均

    新潟医学会雑誌   132 ( 10 )   368 - 368   2018.10

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  • Altered expression of glutamate transporter-1 and water channel protein aquaporin-4 in human temporal cortex with Alzheimer's disease. Reviewed

    Hoshi A, Tsunoda A, Yamamoto T, Tada M, Kakita A, Ugawa Y

    Neuropathology and applied neurobiology   44 ( 6 )   628 - 638   2018.10

  • Autophagy mediators (FOXO1, SESN3 and TSC2) in Lewy body disease and aging. Reviewed International journal

    Yasuo Miki, Kunikazu Tanji, Fumiaki Mori, Jun Utsumi, Hidenao Sasaki, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    Neuroscience letters   684   35 - 41   2018.9

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    Neurodegenerative disorders such as Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are characterized by impairment of autophagy. Cellular survival is dependent on efficient clearance of phosphorylated α-synuclein, which accumulates as fibrils in the neuronal cytoplasm as Lewy bodies (LBs). The forkhead box O 1 (FOXO1) is a member of the FOXO family that functions in various intracellular processes including regulation of autophagy. Transcriptional activation of FOXO1 has been reported to initiate autophagy by inhibiting the expression of Mechanistic Target of Rapamycin (mTOR), mediated by sestrin 3 (SESN3) and tuberous sclerosis complex 2 (TSC2). Although many autophagy-related proteins are known to be incorporated into LBs, no report has documented the involvement of these autophagy modulators (FOXO1, SESN3 and TSC2) in the pathogenesis of PD and DLB. In the present study, we performed immunostaining and Western blot analysis using the brains of normal controls and patients with PD and DLB in order to clarify the involvement of FOXO1, SESN3 and TSC2 in LBs. Our study demonstrated for the first time the presence of FOXO1, SESN3 and TSC2 in brainstem-type LBs. The expression levels of these proteins in the brain did not differ between the normal controls and patients with PD or DLB. We further utilized mice model to investigate the effect of α-synuclein overexpression on these proteins, and found that TSC2 was significantly increased in α-synuclein transgenic mice relative to wild type mice at 9 weeks of age, but not at 30 weeks of age. Together with expression data showing gradual increase of these molecules with age in wild type mice, these findings suggest that autophagy modulators are incorporated into LBs and that the expression of these proteins can be increased by various factors including aging.

    DOI: 10.1016/j.neulet.2018.06.052

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  • Astroblastoma: a distinct tumor entity characterized by alterations of the X chromosome and MN1 rearrangement Reviewed

    Takanori Hirose, Sumihito Nobusawa, Kazuhiko Sugiyama, Vishwa J. Amatya, Naomi Fujimoto, Atsushi Sasaki, Yoshiki Mikami, Akiyoshi Kakita, Shinya Tanaka, Hideaki Yokoo

    Brain Pathology   28 ( 5 )   684 - 694   2018.9

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    DOI: 10.1111/bpa.12565

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  • 日本ブレインバンクネット(JBBN)の構築とその運用

    森島 真帆, 柿田 明美, 吉田 眞理, 矢部 博興, 國井 泰人, 入谷 修司, 寺田 整司, 横田 修, 大島 健一, 田中 紀子, 井上 悠輔, 村山 繁雄, 齊藤 祐子

    Dementia Japan   32 ( 3 )   450 - 450   2018.9

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  • てんかんにて発症した海綿状血管腫の周囲脳組織のイメージング解析

    福多 真史, 北浦 弘樹, 増田 浩, 白水 洋史, 伊藤 陽祐, 東島 威史, 大石 誠, 平石 哲也, 藤井 幸彦, 柿田 明美

    てんかん研究   36 ( 2 )   433 - 433   2018.9

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  • 病理学的に同定した進行性の白質病変を認めた脳アミロイドβ関連血管炎の2症例

    北原 匠, 上村 昌博, 柳村 文博, 畠野 雄也, 須貝 章弘, 河内 泉, 柿田 明美, 小野寺 理

    Dementia Japan   32 ( 3 )   482 - 482   2018.9

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  • 自己免疫性脳炎 Neuromyelitis opticaにおけるTRPM4分子発現動態の解析

    穂苅 万李子, 佐治 越爾, 柳村 文寛, 若杉 尚宏, 柳川 香織, 豊島 靖子, 柿田 明美, 小野寺 理, 西澤 正豊, 河内 泉

    神経免疫学   23 ( 1 )   87 - 87   2018.9

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  • MS/NMO 視神経脊髄炎におけるmelanoma cell adhesion moleculeの病理学的検討

    柳村 文寛, 佐治 越爾, 若杉 尚宏, 穂苅 万李子, 柳川 香織, 豊島 靖子, 柿田 明美, 高橋 均, 小野寺 理, 河内 泉

    神経免疫学   23 ( 1 )   93 - 93   2018.9

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  • Chemical Landscape for Tissue Clearing Based on Hydrophilic Reagents. Reviewed International journal

    Kazuki Tainaka, Tatsuya C Murakami, Etsuo A Susaki, Chika Shimizu, Rie Saito, Kei Takahashi, Akiko Hayashi-Takagi, Hiroshi Sekiya, Yasunobu Arima, Satoshi Nojima, Masako Ikemura, Tetsuo Ushiku, Yoshihiro Shimizu, Masaaki Murakami, Kenji F Tanaka, Masamitsu Iino, Haruo Kasai, Toshikuni Sasaoka, Kazuto Kobayashi, Kohei Miyazono, Eiichi Morii, Tadashi Isa, Masashi Fukayama, Akiyoshi Kakita, Hiroki R Ueda

    Cell reports   24 ( 8 )   2196 - 2210   2018.8

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    We describe a strategy for developing hydrophilic chemical cocktails for tissue delipidation, decoloring, refractive index (RI) matching, and decalcification, based on comprehensive chemical profiling. More than 1,600 chemicals were screened by a high-throughput evaluation system for each chemical process. The chemical profiling revealed important chemical factors: salt-free amine with high octanol/water partition-coefficient (logP) for delipidation, N-alkylimidazole for decoloring, aromatic amide for RI matching, and protonation of phosphate ion for decalcification. The strategic integration of optimal chemical cocktails provided a series of CUBIC (clear, unobstructed brain/body imaging cocktails and computational analysis) protocols, which efficiently clear mouse organs, mouse body including bone, and even large primate and human tissues. The updated CUBIC protocols are scalable and reproducible, and they enable three-dimensional imaging of the mammalian body and large primate and human tissues. This strategy represents a future paradigm for the rational design of hydrophilic clearing cocktails that can be used for large tissues.

    DOI: 10.1016/j.celrep.2018.07.056

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  • フラビン蛍光イメージングによるてんかん原性の解析 Reviewed

    Clin Neurosci   36 ( 8 )   970 - 972   2018.8

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  • Human-specific features of spatial gene expression and regulation in eight brain regions. Reviewed

    Xu C, Li Q, Efimova O, He L, Tatsumoto S, Stepanova V, Oishi T, Udono T, Yamaguchi K, Shigenobu S, Kakita A, Nawa H, Khaitovich P, Go Y

    Genome research   28 ( 8 )   1097 - 1110   2018.8

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    DOI: 10.1101/gr.231357.117

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  • Aquaporin Positron Emission Tomography Differentiates Between Grade III and IV Human Astrocytoma. Reviewed International journal

    Yuji Suzuki, Yukihiro Nakamura, Kenichi Yamada, Satoshi Kurabe, Kouichirou Okamoto, Hiroshi Aoki, Hiroki Kitaura, Akiyoshi Kakita, Yukihiko Fujii, Vincent J Huber, Hironaka Igarashi, Ingrid L Kwee, Tsutomu Nakada

    Neurosurgery   82 ( 6 )   842 - 846   2018.6

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    BACKGROUND: Aquaporin (AQP) water channels play a significant role in mesenchymal microvascular proliferation and infiltrative growth. AQPs are highly expressed in malignant astrocytomas, and a positive correlation is observed between their expression levels and histological tumor grade. OBJECTIVE: To examine the utility of aquaporin positron emission tomography (PET) for differentiating between astrocytoma grade III and grade IV using the AQP radioligand [11C]TGN-020. METHODS: Fifteen astrocytoma patients, grade III (n = 7) and grade IV (n = 8), and 10 healthy volunteers underwent [11C]TGN-020 aquaporin PET imaging. Surgical tissues of astrocytoma patients were examined for histopathological grading using the WHO classification standard and expression of AQP1 and AQP4 immunohistochemically. RESULTS: Mean standardized uptake values of astrocytoma grade III and IV (0.51 ± 0.11 vs 1.50 ± 0.44, respectively) were higher than normal white matter (0.17 ± 0.02, P < .001) for both tumor grades. Importantly, mean standardized uptake values of astrocytoma grade IV were significantly higher than grade III (P < .01). CONCLUSION: Our study demonstrated that [11C]TGN-020 aquaporin PET imaging differentiated between astrocytoma grades III and IV. We suggest its clinical application as a noninvasive diagnostic tool would lead to advancements in the management of these malignant brain tumors.

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  • Effects of the −141C insertion/deletion polymorphism in the dopamine D2 receptor gene on the dopamine system in the striatum in patients with schizophrenia Reviewed

    Junya Matsumoto, Atsuko Nagaoka, Yasuto Kunii, Itaru Miura, Mizuki Hino, Shin-ichi Niwa, Hiroyuki Nawa, Hitoshi Takahashi, Akiyoshi Kakita, Hirooki Yabe

    Psychiatry Research   264   116 - 118   2018.6

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    DOI: 10.1016/j.psychres.2018.03.029

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  • Intractable epilepsy due to a rosette-forming glioneuronal tumor with a dysembryoplastic neuroepithelial background. Reviewed International journal

    Noriko Sumitomo, Akihiko Ishiyama, Makoto Shibuya, Eiji Nakagawa, Yu Kaneko, Akio Takahashi, Taisuke Otsuki, Akiyoshi Kakita, Yuko Saito, Noriko Sato, Kenji Sugai, Masayuki Sasaki

    Neuropathology : official journal of the Japanese Society of Neuropathology   38 ( 3 )   300 - 304   2018.6

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    A rosette-forming glioneuronal tumor (RGNT) was initially reported as an infratentorial tumor that comprised both small neurocytic rosettes and astrocytic components. However, a few studies have reported supratentorial RGNTs arising in the cerebral hemispheres. Here, we report an unusual case involving a 9-year-old boy with a supratentorial RGNT who presented with intractable epilepsy and behavioral changes. Brain MRI revealed a well-circumscribed space-occupying lesion with septae in the right inferomedial parietal lobe. Electroencephalography showed multifocal spikes over the right frontal, temporal and parietal regions. The seizure frequency decreased dramatically after tumorectomy. Histopathological examination revealed prominent neurocytic rosette formation appearing with the specific glioneuronal element of a dysembryoplastic neuroepithelial tumor (DNT). Although the pathogenesis has not been elucidated, a supratentorial RGNT presenting with epilepsy may exhibit a rosette component, which is the major feature of this tumor, against the background of a specific glioneuronal element mimicking DNT. However, RGNT arising in regions other than the fourth ventricle is rare, and the pathogenesis of epilepsy due to RGNT has not been fully elucidated. Further clinical and histological studies are required to understand the pathology underlying epilepsy caused by RGNT.

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  • Histopathologic features of an autopsied patient with cerebral small vessel disease and a heterozygous HTRA1 mutation. Reviewed International journal

    Junko Ito, Hiroaki Nozaki, Yasuko Toyoshima, Takashi Abe, Aki Sato, Hideki Hashidate, Shuichi Igarashi, Osamu Onodera, Hitoshi Takahashi, Akiyoshi Kakita

    Neuropathology : official journal of the Japanese Society of Neuropathology   38 ( 4 )   428 - 432   2018.5

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    Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) is a hereditary cerebral small vessel disease (CSVD) caused by homozygous or compound heterozygous mutations of the high temperature requirement A serine peptidase 1 gene (HTRA1). Affected patients suffer from cognitive impairment, recurrent strokes, lumbago and alopecia. Recently, clinical studies have indicated that some patients with heterozygous mutations in HTRA1 may also suffer CSVD. Here, we report the histopathologic features of an autopsied 55-year-old male patient who had shown cognitive impairment and multiple cerebral infarcts, and was found to have a heterozygous missense mutation (p.R302Q) in the HTRA1 gene. Histologically, small vessels in the brain and spinal cord showed intimal proliferation, splitting of the internal elastic lamina, and degeneration of smooth muscle cells in the tunica media. Thus, although less severe, the features were quite similar to those of patients with CARASIL, indicating that patients with heterozygous mutations develop CSVD through underlying pathomechanisms similar to those of CARASIL.

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  • 前頭側頭葉変性症の組織学的分類 Reviewed

    Brain Nerve   70 ( 5 )   501 - 516   2018.5

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    DOI: 10.11477/mf.1416201033.

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  • 限局性皮質異形成でT1強調高信号を呈した症例の検討 Reviewed

    老谷 嘉樹, 木村 有喜男, 須貝 研司, 齊藤 祐子, 池谷 直樹, 岩崎 真樹, 竹下 絵里, 本橋 裕子, 石山 昭彦, 齋藤 貴志, 小牧 宏文, 中川 栄二, 柿田 明美, 佐藤 典子, 佐々木 征行

    脳と発達   50 ( Suppl. )   S336 - S336   2018.5

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  • 遺伝性脳血管障害の神経病理 Reviewed

    神経内科   88 ( 5 )   516 - 523   2018.5

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  • Globular glial tauopathyの神経病理 Reviewed

    神経内科   88 ( 5 )   477 - 482   2018.5

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  • [Neuropathologic Subtypes of Frontotemporal Lobar Degeneration]. Reviewed

    Tada M, Kakita A

    Brain and nerve = Shinkei kenkyu no shinpo   70 ( 5 )   501 - 516   2018.5

  • Loss of Motor Neurons Innervating Cervical Muscles in Patients With Multiple System Atrophy and Dropped Head. Reviewed International journal

    Rie Saito, Mari Tada, Yasuko Toyoshima, Masatoyo Nishizawa, Osamu Onodera, Hitoshi Takahashi, Akiyoshi Kakita

    Journal of neuropathology and experimental neurology   77 ( 4 )   317 - 324   2018.4

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    We investigated whether loss of motor neurons innervating the neck muscles contributes to dropped head (DH) in multiple system atrophy (MSA). From 75 patients with autopsy-proven MSA, we retrieved 3 who had DH (MSA-DH), and examined the 4th cervical cord segments. Neurons of the medial and lateral nuclear groups (MNG and LNG) innervate the neck and shoulder muscles, respectively. We measured the area of individual neurons in the MNG and LNG, and created an area-frequency histogram. Neurons were classified as large or small based on their area, and their total numbers in the MNG and LNG were counted. In the MNG, the numbers of both total neurons and large neurons were significantly lower in MSA patients than in the controls (214.2 ± 91.4 vs 521.3 ± 74.8, p = 0.0030, and 26.2 ± 9.1 vs 88.0 ± 34.6, p = 0.020, respectively), and were significantly lower in MSA-DH than in MSA-nonDH (139.7 ± 7.6 vs 288.7 ± 74.6, p = 0.048, and 18.0 ± 4.1 vs 34.3 ± 4.1, p = 0.016, respectively). There were no differences in the LNG neuron counts between the MSA-DH and MSA-nonDH groups. Loss of cervical motor neurons may be responsible for DH in MSA.

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  • The perivascular microenvironment in Epstein–Barr virus positive primary central nervous system lymphoma: The role of programmed cell death 1 and programmed cell death ligand 1 Reviewed

    Yasuo Sugita, Takuya Furuta, Koichi Ohshima, Satoru Komaki, Junko Miyoshi, Motohiro Morioka, Hideyuki Abe, Takanori Nozawa, Yukihiko Fujii, Hitoshi Takahashi, Akiyoshi Kakita

    Neuropathology   38 ( 2 )   125 - 134   2018.4

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    DOI: 10.1111/neup.12435

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  • Reliable diagnosis of IDH-mutant glioblastoma by 2-hydroxyglutarate detection: a study by 3-T magnetic resonance spectroscopy. Reviewed International journal

    Manabu Natsumeda, Kunio Motohashi, Hironaka Igarashi, Takanori Nozawa, Hideaki Abe, Yoshihiro Tsukamoto, Ryosuke Ogura, Masayasu Okada, Tsutomu Kobayashi, Hiroshi Aoki, Hitoshi Takahashi, Akiyoshi Kakita, Kouichirou Okamoto, Tsutomu Nakada, Yukihiko Fujii

    Neurosurgical review   41 ( 2 )   641 - 647   2018.4

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    We have previously reported that reliable detection of 2-hydroxyglutarate (2HG) in isocitrate dehydrogenase (IDH)-mutant WHO grade 2 and 3 gliomas is possible utilizing 3.0-T single-voxel magnetic resonance spectroscopy (SVMRS). We set out to determine whether the same method could be applied to detect 2HG in IDH-mutant glioblastoma. Forty-four patients harboring glioblastoma underwent pre-operative MRS evaluation to detect 2HG and other metabolites. Presence of IDH-mutations was determined by IDH1 R132H immunohistochemical analysis and DNA sequencing of surgically obtained tissues. Six out of 44 (13.6%) glioblastomas were IDH-mutant. IDH-mutant glioblastoma exhibited significantly higher accumulation of 2HG (median 3.191 vs. 0.000 mM, p < 0.0001, Mann-Whitney test). A cutoff of 2HG = 0.897 mM achieved high sensitivity (100.0%) and specificity (92.59%) in determining IDH-mutation in glioblastoma. Glioblastoma with high 2HG accumulation did not have significantly longer overall survival than glioblastoma with low 2HG accumulation (p = 0.107, log-rank test). Non-invasive and reliable detection of 2HG in IDH-mutant glioblastoma was possible by 3.0-T SVMRS.

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  • Expansions of intronic TTTCA and TTTTA repeats in benign adult familial myoclonic epilepsy Reviewed

    Hiroyuki Ishiura, Koichiro Doi, Jun Mitsui, Jun Yoshimura, Miho Kawabe Matsukawa, Asao Fujiyama, Yasuko Toyoshima, Akiyoshi Kakita, Hitoshi Takahashi, Yutaka Suzuki, Sumio Sugano, Wei Qu, Kazuki Ichikawa, Hideaki Yurino, Koichiro Higasa, Shota Shibata, Aki Mitsue, Masaki Tanaka, Yaeko Ichikawa, Yuji Takahashi, Hidetoshi Date, Takashi Matsukawa, Junko Kanda, Fumiko Kusunoki Nakamoto, Mana Higashihara, Koji Abe, Ryoko Koike, Mutsuo Sasagawa, Yasuko Kuroha, Naoya Hasegawa, Norio Kanesawa, Takayuki Kondo, Takefumi Hitomi, Masayoshi Tada, Hiroki Takano, Yutaka Saito, Kazuhiro Sanpei, Osamu Onodera, Masatoyo Nishizawa, Masayuki Nakamura, Takeshi Yasuda, Yoshio Sakiyama, Mieko Otsuka, Akira Ueki, Ken Ichi Kaida, Jun Shimizu, Ritsuko Hanajima, Toshihiro Hayashi, Yasuo Terao, Satomi Inomata-Terada, Masashi Hamada, Yuichiro Shirota, Akatsuki Kubota, Yoshikazu Ugawa, Kishin Koh, Yoshihisa Takiyama, Natsumi Ohsawa-Yoshida, Shoichi Ishiura, Ryo Yamasaki, Akira Tamaoka, Hiroshi Akiyama, Taisuke Otsuki, Akira Sano, Akio Ikeda, Jun Goto, Shinichi Morishita, Shoji Tsuji

    Nature Genetics   50 ( 4 )   581 - 590   2018.4

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    DOI: 10.1038/s41588-018-0067-2

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  • YOD1 attenuates neurogenic proteotoxicity through its deubiquitinating activity. Reviewed International journal

    Kunikazu Tanji, Fumiaki Mori, Yasuo Miki, Jun Utsumi, Hidenao Sasaki, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    Neurobiology of disease   112   14 - 23   2018.4

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    Ubiquitination, a fundamental post-translational modification of intracellular proteins, is enzymatically reversed by deubiquitinase enzymes (deubiquitinases). >90 deubiquitinases have been identified. One of these enzymes, YOD1, possesses deubiquitinase activity and is similar to ovarian tumor domain-containing protein 1, which is associated with regulation of the endoplasmic reticulum (ER)-associated degradation pathway. Indeed, YOD1 is reported to be involved in the ER stress response induced by mislocalization of unfolded proteins in mammalian cells. However, it has remained unclear whether YOD1 is associated with pathophysiological conditions such as mitochondrial damage, impaired proteostasis, and neurodegeneration. We demonstrated that YOD1 possesses deubiquitinating activity and exhibits preference for K48- and K63-linked ubiquitin. Furthermore, YOD1 expression levels increased as a result of various stress conditions. We demonstrated that the neurogenic proteins that cause Huntington disease and Parkinson's disease induced upregulation of YOD1 level. We observed that YOD1 reduced disease cytotoxicity through efficient degradation of mutant proteins, whereas this activity was abolished by catalytically inactive YOD1. Additionally, YOD1 localized to Lewy bodies in Parkinson's disease patients. Collectively, these data suggest that the deubiquitinase YOD1 contributes to pathogenesis of neurodegenerative disease by decreasing ubiquitination of abnormal proteins and their subsequent degradation.

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  • Pathophysiological Characteristics Associated With Epileptogenesis in Human Hippocampal Sclerosis Reviewed

    Hiroki Kitaura, Hiroshi Shirozu, Hiroshi Masuda, Masafumi Fukuda, Yukihiko Fujii, Akiyoshi Kakita

    EBioMedicine   29   38 - 46   2018.3

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    DOI: 10.1016/j.ebiom.2018.02.013

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  • Frontoethmoidal Schwannoma with Exertional Cerebrospinal Fluid Rhinorrhea: Case Report and Review of Literature Reviewed

    Yuichiro Yoneoka, Katsuhiko Akiyama, Yasuhiro Seki, Go Hasegawa, Akiyoshi Kakita

    World Neurosurgery   111   381 - 385   2018.3

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    DOI: 10.1016/j.wneu.2018.01.015

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  • ミクログリアの組織学的特徴 Reviewed

    Clinical Neuroscience   36 ( 3 )   276 - 277   2018.3

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  • Loss of kallikrein-related peptidase 7 exacerbates amyloid pathology in Alzheimer's disease model mice. Reviewed International journal

    Kiwami Kidana, Takuya Tatebe, Kaori Ito, Norikazu Hara, Akiyoshi Kakita, Takashi Saito, Sho Takatori, Yasuyoshi Ouchi, Takeshi Ikeuchi, Mitsuhiro Makino, Takaomi C Saido, Masahiro Akishita, Takeshi Iwatsubo, Yukiko Hori, Taisuke Tomita

    EMBO molecular medicine   10 ( 3 )   2018.3

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    Deposition of amyloid-β (Aβ) as senile plaques is one of the pathological hallmarks in the brains of Alzheimer's disease (AD) patients. In addition, glial activation has been found in AD brains, although the precise pathological role of astrocytes remains unclear. Here, we identified kallikrein-related peptidase 7 (KLK7) as an astrocyte-derived Aβ degrading enzyme. Expression of KLK7 mRNA was significantly decreased in the brains of AD patients. Ablation of Klk7 exacerbated the thioflavin S-positive Aβ pathology in AD model mice. The expression of Klk7 was upregulated by Aβ treatment in the primary astrocyte, suggesting that Klk7 is homeostatically modulated by Aβ-induced responses. Finally, we found that the Food and Drug Administration-approved anti-dementia drug memantine can increase the expression of Klk7 and Aβ degradation activity specifically in the astrocytes. These data suggest that KLK7 is an important enzyme in the degradation and clearance of deposited Aβ species by astrocytes involved in the pathogenesis of AD.

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  • Biallelic Variants in CNPY3, Encoding an Endoplasmic Reticulum Chaperone, Cause Early-Onset Epileptic Encephalopathy. Reviewed International journal

    Hiroki Mutoh, Mitsuhiro Kato, Tenpei Akita, Takuma Shibata, Hiroyuki Wakamoto, Hiroko Ikeda, Hiroki Kitaura, Kazushi Aoto, Mitsuko Nakashima, Tianying Wang, Chihiro Ohba, Satoko Miyatake, Noriko Miyake, Akiyoshi Kakita, Kensuke Miyake, Atsuo Fukuda, Naomichi Matsumoto, Hirotomo Saitsu

    American journal of human genetics   102 ( 2 )   321 - 329   2018.2

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    Early-onset epileptic encephalopathies, including West syndrome (WS), are a group of neurological disorders characterized by developmental impairments and intractable seizures from early infancy. We have now identified biallelic CNPY3 variants in three individuals with WS; these include compound-heterozygous missense and frameshift variants in a family with two affected siblings (individuals 1 and 2) and a homozygous splicing variant in a consanguineous family (individual 3). All three individuals showed hippocampal malrotation. In individuals 1 and 2, electroencephalography (EEG) revealed characteristic fast waves and diffuse sharp- and slow-wave complexes. The fast waves were clinically associated with seizures. CNPY3 encodes a co-chaperone in the endoplasmic reticulum and regulates the subcellular distribution and responses of multiple Toll-like receptors. The amount of CNPY3 in lymphoblastoid cells derived from individuals 1 and 2 was severely lower than that in control cells. Cnpy3-knockout mice exhibited spastic or dystonic features under resting conditions and hyperactivity and anxiolytic behavior during the open field test. Also, their resting EEG showed enhanced activity in the fast beta frequency band (20-35 Hz), which could mimic the fast waves in individuals 1 and 2. These data suggest that CNPY3 and Cnpy3 perform essential roles in brain function in addition to known Toll-like receptor-dependent immune responses.

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  • Biallelic variants in CNPY3, which encodes an endoplasmic reticulum chaperone, cause early-onset epileptic encephalaopathy. Reviewed

    Mutoh H, Kato M, Akita T, Shibata T, Wakamoto H, Ikeda H, Kitaura H, Aoto K, Nakashima M, Wang T, Ohba C, Miyatake S, Miyake N, Kakita A, Miyake K, Fukuda A, Matsumoto N, Saitsu H

    Am J Hum Genet   102 ( 2 )   321 - 329   2018.2

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  • 髄膜播種をきたしたEpithelioid glioblastomaの1例

    金丸 優, 棗田 学, 齋藤 理恵, 野澤 孝徳, 阿部 英明, 岡本 浩一郎, 大石 誠, 藤井 幸彦, 柿田 明美, 信澤 純人

    信州医学雑誌   66 ( 1 )   104 - 105   2018.2

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  • CNS high-grade neuroepithelial tumor with BCOR internal tandem duplication(CNS HGNET-BCOR)の1例

    吉田 由佳, 中田 聡, 信澤 純人, 杉田 保雄, 岡田 雅彦, 平戸 純子, 横尾 英明, 柿田 明美

    信州医学雑誌   66 ( 1 )   103 - 104   2018.2

  • 常染色体劣性遺伝性が疑われる若年発症 緩徐進行性小脳失調症の1剖検例

    齋藤 理恵, 他田 真理, 若林 允甫, 小野寺 理, 高橋 均, 池内 健, 柿田 明美, 横尾 英明

    信州医学雑誌   66 ( 1 )   111 - 112   2018.2

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  • Immunohistochemical localization of exoribonucleases (DIS3L2 and XRN1) in intranuclear inclusion body disease. Reviewed International journal

    Fumiaki Mori, Kunikazu Tanji, Yasuo Miki, Yasuko Toyoshima, Hidenao Sasaki, Mari Yoshida, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    Neuroscience letters   662   389 - 394   2018.1

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    mRNA turnover controls gene expression under various conditions in aging and neurodegenerative diseases. Polyglutamine (polyQ) diseases and intranuclear inclusion body disease (INIBD) are neurodegenerative diseases characterized by the formation of nuclear inclusions. These inclusions are immunopositive for several proteins associated with amyotrophic lateral sclerosis. In amyotrophic lateral sclerosis, the processing of RNA from gene transcription through degradation (RNA metabolism) has been reported to be altered. We hypothesized that the proteins associated with RNA metabolism are also involved in the formation of nuclear inclusions in polyQ diseases and INIBD. 3'-5' exoribonuclease DIS3L2 and 5'-3' exoribonuclease XRN1 play critical roles in mRNA decay. Using immunohistochemistry with antibodies against DIS3L2 and XRN1, we examined the brains of patients with polyQ diseases and INIBD and normal control subjects. In controls, immunoreactivity for DIS3L2 and XRN1 was found in the neuronal cytoplasm and neuropil, respectively. In INIBD, immunoreactivity for DIS3L2 and XRN1 was present in neuronal and glial nuclear inclusions. Co-localization of ubiquitin and DIS3L2 or XRN1 was demonstrated in these inclusions. In polyQ diseases, however, nuclear inclusions were immunonegative for DIS3L2 and XRN1. These findings suggest that sequestration of exoribonucleases to nuclear inclusions may be related to the pathogenesis of INIBD.

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  • AMBRA1, a novel α-synuclein-binding protein, is implicated in the pathogenesis of multiple system atrophy. Reviewed International journal

    Yasuo Miki, Kunikazu Tanji, Fumiaki Mori, Yota Tatara, Jun Utsumi, Hidenao Sasaki, Akiyoshi Kakita, Hitoshi Takahashi, Gian Maria Fimia, Koichi Wakabayashi

    Brain pathology (Zurich, Switzerland)   28 ( 1 )   28 - 42   2018.1

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    The accumulation of abnormal α-synuclein is the major histopathological feature of Lewy body disease and multiple system atrophy (MSA), which are referred to as synucleinopathies. Cytoplasmic degradation systems, such as the autophagy-lysosome and proteasome pathways, are involved in their pathogenesis. Autophagy is tightly regulated by several upstream proteins including UNC-51-like kinase 1/2, beclin1, vacuolar protein sorting-associated protein 34 and autophagy/beclin1 regulator 1 (AMBRA1). Recently, we revealed that both cortical and brainstem-type Lewy bodies were immunopositive for several upstream proteins of autophagy. Therefore, we conducted the present study to elucidate the role of upstream proteins of autophagy in the pathogenesis of MSA. Pathological and biochemical analyses using human brain samples revealed that AMBRA1 is a component of the pathological hallmarks of MSA and upstream proteins of autophagy are impaired in the MSA brain. In vitro and in vivo analyses revealed a ninefold stronger affinity of AMBRA1 with α-synuclein phosphorylated at serine 129 compared with non-phosphorylated α-synuclein. Furthermore, a weak but significant correlation between AMBRA1 overexpression and reduction of abnormal α-synuclein was observed. Silencing AMBRA1 function caused aggregates of α-synuclein in the cytoplasm of mouse primary cultured neurons, which was simulated by the treatment of Bafilomycin, an autophagy inhibitor. Our results demonstrated for the first time that AMBRA1 is a novel hub binding protein of α-synuclein and plays a central role in the pathogenesis of MSA through the degradative dynamics of α-synuclein. These results raise the possibility that molecular modulation targeting AMBRA1 can be a promising candidate for the treatment of synucleinopathies.

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  • Comprehensive genetic characterization of rosette-forming glioneuronal tumors: independent component analysis by tissue microdissection. Reviewed International journal

    Yohei Kitamura, Takashi Komori, Makoto Shibuya, Kentaro Ohara, Yuko Saito, Saeko Hayashi, Aya Sasaki, Eiji Nakagawa, Ryosuke Tomio, Akiyoshi Kakita, Masashi Nakatsukasa, Kazunari Yoshida, Hikaru Sasaki

    Brain pathology (Zurich, Switzerland)   28 ( 1 )   87 - 93   2018.1

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    A rosette-forming glioneuronal tumor (RGNT) is a rare mixed neuronal-glial tumor characterized by biphasic architecture of glial and neurocytic components. The number of reports of genetic analyses of RGNTs is few. Additionally, the genetic background of the unique biphasic pathological characteristics of such mixed neuronal-glial tumors remains unclear. To clarify the genetic background of RGNTs, we performed separate comprehensive genetic analyses of glial and neurocytic components of five RGNTs, by tissue microdissection. Two missense mutations in FGFR1 in both components of two cases, and one mutation in PIK3CA in both components of one case, were detected. In the latter case with PIK3CA mutation, the additional FGFR1 mutation was detected only in the glial component. Moreover, the loss of chromosome 13q in only the neurocytic component was observed in one other case. Their results suggested that RGNTs, which are tumors harboring two divergent differentiations that arose from a single clone, have a diverse genetic background. Although previous studies have suggested that RGNTs and pilocytic astrocytomas (PAs) represent the same tumor entity, their results confirm that the genetic background of RGNTs is not identical to that of PA.

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  • Ectopic pituitary null cell adenoma arising from the infundibulum in the third ventricle: A successful endonasal transsphenoidal resection after long-term follow-up MR imaging – A technical note Reviewed

    Yuichiro Yoneoka, Masayasu Okada, Naoto Watanabe, Satoru Aoki, Akiyoshi Kakita, Yukihiko Fujii

    Interdisciplinary Neurosurgery: Advanced Techniques and Case Management   10   122 - 125   2017.12

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    DOI: 10.1016/j.inat.2017.08.004

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  • Third Ventricle Germ Cell Tumor Originating from the Infundibulum with Rapidly Expansive Enlargement Reviewed

    Yuichiro Yoneoka, Junichi Yoshimura, Masakazu Sano, Masayasu Okada, Akiyoshi Kakita, Yukihiko Fujii

    Pediatric Neurosurgery   53 ( 1 )   49 - 54   2017.12

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    DOI: 10.1159/000480021

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  • PKA activation and endothelial claudin-5 breakdown in the schizophrenic prefrontal cortex Reviewed

    Keisuke Nishiura, Naoki Ichikawa-Tomikawa, Kotaro Sugimoto, Yasuto Kunii, Korehito Kashiwagi, Mizuko Tanaka, Yuichi Yokoyama, Mizuki Hino, Takashi Sugino, Hirooki Yabe, Hitoshi Takahashi, Akiyoshi Kakita, Tetsuya Imura, Hideki Chiba

    ONCOTARGET   8 ( 55 )   93382 - 93391   2017.11

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  • The SMN gene copy number states in Japanese ALS patients

    Ishihara T, Toyoda S, Koyama A, Tada M, Atsuta N, Nakamura R, Tohnai G, Sone J, Izumi Y, Kaji R, Morita M, Taniguchi A, Kakita A, Sobue G, Nishizawa M, Onodera O

    JOURNAL OF THE NEUROLOGICAL SCIENCES   381   211-211   2017.10

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  • 脳アミロイドアンギオパチーの新規病態関連因子SRPX1の解析 Reviewed

    井上 泰輝, 植田 光晴, 田崎 雅義, 竹島 明, 永利 聡仁, 増田 曜章, 三隅 洋平, 小阪 崇幸, 野村 隼也, 水上 真由美, 松本 紗也加, 山下 太郎, 高橋 均, 柿田 明美, 安東 由喜雄

    Dementia Japan   31 ( 4 )   565 - 565   2017.10

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  • Sushi repeat-containing protein 1: a novel disease-associated molecule in cerebral amyloid angiopathy Reviewed

    Yasuteru Inoue, Mitsuharu Ueda, Masayoshi Tasaki, Akari Takeshima, Akihito Nagatoshi, Teruaki Masuda, Yohei Misumi, Takayuki Kosaka, Toshiya Nomura, Mayumi Mizukami, Sayaka Matsumoto, Taro Yamashita, Hitoshi Takahashi, Akiyoshi Kakita, Yukio Ando

    ACTA NEUROPATHOLOGICA   134 ( 4 )   605 - 617   2017.10

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  • Features of amygdala in patients with mesial temporal lobe epilepsy and hippocampal sclerosis: An MRI volumetric and histopathological study Reviewed

    Yoko Nakayama, Hiroshi Masuda, Hiroshi Shirozu, Yosuke Ito, Takefumi Higashijima, Hiroki Kitaura, Yukihiko Fujii, Akiyoshi Kakita, Masafumi Fukuda

    EPILEPSY RESEARCH   135   50 - 55   2017.9

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    DOI: 10.1016/j.eplepsyres.2017.05.010

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  • GPNMB ameliorates mutant TDP-43-induced motor neuron cell death Reviewed

    Yuki Nagahara, Masamitsu Shimazawa, Kazuki Ohuchi, Junko Ito, Hitoshi Takahashi, Kazuhiro Tsuruma, Akiyoshi Kakita, Hideaki Hara

    JOURNAL OF NEUROSCIENCE RESEARCH   95 ( 8 )   1647 - 1665   2017.8

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  • Alteration of mitochondrial protein PDHA1 in Lewy body disease and PARK14 Reviewed

    Yasuo Miki, Kunikazu Tanji, Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   489 ( 4 )   439 - 444   2017.8

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    DOI: 10.1016/j.bbrc.2017.05.162

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  • Striatal hypodopamine phenotypes found in transgenic mice that overexpress glial cell line-derived neurotrophic factor Reviewed

    Hidekazu Sotoyama, Yuriko Iwakura, Kanako Oda, Toshikuni Sasaoka, Nobuyuki Takei, Akiyoshi Kakita, Hideki Enomoto, Hiroyuki Nawa

    NEUROSCIENCE LETTERS   654   99 - 106   2017.7

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  • Ca2+-permeable AMPA receptors associated with epileptogenesis of hypothalamic hamartoma Reviewed

    Hiroki Kitaura, Masaki Sonoda, Sayaka Teramoto, Hiroshi Shirozu, Hiroshi Shimizu, Tadashi Kimura, Hiroshi Masuda, Yosuke Ito, Hitoshi Takahashi, Shin Kwak, Shigeki Kameyama, Akiyoshi Kakita

    EPILEPSIA   58 ( 4 )   E59 - E63   2017.4

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  • PLA2G6 accumulates in Lewy bodies in PARK14 and idiopathic Parkinson's disease Reviewed

    Yasuo Miki, Kunikazu Tanji, Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROSCIENCE LETTERS   645   40 - 45   2017.4

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  • Expression of Aquaporin 1 and Aquaporin 4 in the Temporal Neocortex of Patients with Parkinson's Disease Reviewed

    Akihiko Hoshi, Ayako Tsunoda, Mari Tada, Masatoyo Nishizawa, Yoshikazu Ugawa, Akiyoshi Kakita

    BRAIN PATHOLOGY   27 ( 2 )   160 - 168   2017.3

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  • Familial amyotrophic lateral sclerosis with an I104F mutation in the SOD1 gene: Multisystem degeneration with neurofilamentous aggregates and SOD1 inclusions Reviewed

    Haishan Jiang, Hiroshi Shimizu, Atsushi Shiga, Masami Tanaka, Osamu Onodera, Akiyoshi Kakita, Hitoshi Takahashi

    NEUROPATHOLOGY   37 ( 1 )   69 - 77   2017.2

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  • Ca2+-permeable AMPA receptors associated with epileptogenesis of hypothalamic hamartoma. Reviewed

    Kitaura H, Sonoda M, Teramoto S, Shirozu H, Shimizu H, Kimura T, Masuda H, Ito Y, Takahashi H, Kwak S, Kameyama S, Kakita A

    Epilepsia   58 ( 4 )   e59 - e63   2017.2

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  • Stable and episodic/bolus patterns of methylmercury exposure on mercury accumulation and histopathologic alterations in the nervous system Reviewed

    Mineshi Sakamoto, Akiyoshi Kakita, Jose L. Domingo, Hiroshi Yamazaki, Ricardo B. Oliveira, Sandra L. F. Sarrazin, Komyo Eto, Katsuyuki Murata

    ENVIRONMENTAL RESEARCH   152   446 - 453   2017.1

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  • Cerebral venous sinus thrombosis due to oral contraceptive use: Postmortem 3 T-MRI and autopsy findings Reviewed

    Masahiro Uemura, Yoshihiro Tsukamoto, Yasuhisa Akaiwa, Masaki Watanabe, Ayako Tazawa, Sou Kasahara, Minoru Endou, Ryosuke Ogura, Kouichirou Okamoto, Yukihiko Fujii, Tsutomu Nakada, Akiyoshi Kakita, Masatoyo Nishizawa

    Human Pathology: Case Reports   6   32 - 36   2016.12

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    DOI: 10.1016/j.ehpc.2016.01.002

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  • Globular Glial Tauopathyの臨床的特徴、自験2例と既報例との比較 Reviewed

    三浦 健, 青木 賢樹, 高嶋 修太郎, 眞野 篤, 堅田 慎一, 目崎 直実, 石黒 敬信, 石黒 舞乃, 畠野 雄也, 相川 あかね, 石澤 伸, 竹内 亮子, 田中 英智, 豊島 靖子, 春日 健作, 三瓶 一弘, 柿田 明美, 高橋 均, 池内 健, 西澤 正豊

    臨床神経学   56 ( Suppl. )   S526 - S526   2016.12

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  • MicroRNA expression profiles of multiple system atrophy from formalin-fixed paraffin-embedded samples Reviewed

    Koichi Wakabayashi, Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Shinya Tanaka, Jun Utsumi, Hidenao Sasaki

    NEUROSCIENCE LETTERS   635   117 - 122   2016.12

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  • mTORとてんかん Reviewed

    Epilepsy   10 ( 2 )   97 - 102   2016.11

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  • Decreased VEGFR2 expression and increased phosphorylated Akt1 in the prefrontal cortex of individuals with schizophrenia Reviewed

    Mizuki Hino, Yasuto Kunii, Junya Matsumoto, Akira Wada, Atsuko Nagaoka, Shin-ichi Niwa, Hitoshi Takahashi, Akiyoshi Kakita, Hiroyasu Akatsu, Yoshio Hashizume, Sakon Yamamoto, Hirooki Yabe

    JOURNAL OF PSYCHIATRIC RESEARCH   82   100 - 108   2016.11

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  • Biallelic TBCD Mutations Cause Early-Onset Neurodegenerative Encephalopathy. Reviewed International journal

    Noriko Miyake, Ryoko Fukai, Chihiro Ohba, Takahiro Chihara, Masayuki Miura, Hiroshi Shimizu, Akiyoshi Kakita, Eri Imagawa, Masaaki Shiina, Kazuhiro Ogata, Jiu Okuno-Yuguchi, Noboru Fueki, Yoshifumi Ogiso, Hiroshi Suzumura, Yoshiyuki Watabe, George Imataka, Huey Yin Leong, Aviva Fattal-Valevski, Uri Kramer, Satoko Miyatake, Mitsuhiro Kato, Nobuhiko Okamoto, Yoshinori Sato, Satomi Mitsuhashi, Ichizo Nishino, Naofumi Kaneko, Akira Nishiyama, Tomohiko Tamura, Takeshi Mizuguchi, Mitsuko Nakashima, Fumiaki Tanaka, Hirotomo Saitsu, Naomichi Matsumoto

    American journal of human genetics   99 ( 4 )   950 - 961   2016.10

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    We describe four families with affected siblings showing unique clinical features: early-onset (before 1 year of age) progressive diffuse brain atrophy with regression, postnatal microcephaly, postnatal growth retardation, muscle weakness/atrophy, and respiratory failure. By whole-exome sequencing, we identified biallelic TBCD mutations in eight affected individuals from the four families. TBCD encodes TBCD (tubulin folding co-factor D), which is one of five tubulin-specific chaperones playing a pivotal role in microtubule assembly in all cells. A total of seven mutations were found: five missense mutations, one nonsense, and one splice site mutation resulting in a frameshift. In vitro cell experiments revealed the impaired binding between most mutant TBCD proteins and ARL2, TBCE, and β-tubulin. The in vivo experiments using olfactory projection neurons in Drosophila melanogaster indicated that the TBCD mutations caused loss of function. The wide range of clinical severity seen in this neurodegenerative encephalopathy may result from the residual function of mutant TBCD proteins. Furthermore, the autopsied brain from one deceased individual showed characteristic neurodegenerative findings: cactus and somatic sprout formations in the residual Purkinje cells in the cerebellum, which are also seen in some diseases associated with mitochondrial impairment. Defects of microtubule formation caused by TBCD mutations may underlie the pathomechanism of this neurodegenerative encephalopathy.

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  • Characteristic Microglial Features in Patients with Hereditary Diffuse Leukoencephalopathy with Spheroids Reviewed

    Mari Tada, Takuya Konno, Masayoshi Tada, Toshiyuki Tezuka, Takeshi Miura, Naomi Mezaki, Ken-ichi Okazaki, Musashi Arakawa, Kyoko Itoh, Toru Yamamoto, Hideaki Yokoo, Nobuaki Yoshikura, Kenji Ishihara, Masao Horie, Hirohide Takebayashi, Yasuko Toyoshima, Makoto Naito, Osamu Onodera, Masatoyo Nishizawa, Hitoshi Takahashi, Takeshi Ikeuchi, Akiyoshi Kakita

    ANNALS OF NEUROLOGY   80 ( 4 )   554 - 565   2016.10

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  • 脳表ヘモジデリン沈着症 Reviewed

    Clinical Neuroscience   34 ( 9 )   956 - 957   2016.9

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  • Clinicopathological characteristics of patients with amyotrophic lateral sclerosis resulting in a totally locked-in state (communication Stage V). Reviewed

    Hayashi K, Mochizuki Y, Takeuchi R, Shimizu T, Nagao M, Watabe K, Arai N, Oyanagi K, Onodera O, Hayashi M, Takahashi H, Kakita A, Isozaki E

    Acta Neuropathol Commun   4   107   2016.9

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  • 髄芽腫の予後因子Gli3. Reviewed

    74 ( 7 )   292 - 297   2016.9

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  • [Gli3: a favorable prognostic factor for patients with medulloblastoma]. Reviewed

    Yoshimura J, Miyahara H, Natsumeda M, Kakita A, Fujii Y

    Nihon rinsho. Japanese journal of clinical medicine   74 Suppl 7   292 - 297   2016.9

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  • Primary central nervous system lymphomas and related diseases: Pathological characteristics and discussion of the differential diagnosis Reviewed

    Yasuo Sugita, Hiroko Muta, Koichi Ohshima, Motohiro Morioka, Yoshihiro Tsukamoto, Hitoshi Takahashi, Akiyoshi Kakita

    NEUROPATHOLOGY   36 ( 4 )   313 - 324   2016.8

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  • Familial idiopathic basal ganglia calcification: Histopathologic features of an autopsied patient with an SLC20A2 mutation Reviewed

    Tadashi Kimura, Takeshi Miura, Kenju Aoki, Shoji Saito, Hiroaki Hondo, Takuya Konno, Akio Uchiyama, Takeshi Ikeuchi, Hitoshi Takahashi, Akiyoshi Kakita

    NEUROPATHOLOGY   36 ( 4 )   365 - 371   2016.8

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  • Spinocerebellar degeneration: Discrepancies between clinical and pathological diagnoses Reviewed

    Mitsunori Yamada, Yasuko Toyoshima, Takao Makifuchi, Akiyoshi Kakita, Hitoshi Takahashi

    NEUROPATHOLOGY   36 ( 4 )   405 - 410   2016.8

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  • Significant association of cadaveric dura mater grafting with subpial A beta deposition and meningeal amyloid angiopathy Reviewed

    Tsuyoshi Hamaguchi, Yu Taniguchi, Kenji Sakai, Tetsuyuki Kitamoto, Masaki Takao, Shigeo Murayama, Yasushi Iwasaki, Mari Yoshida, Hiroshi Shimizu, Akiyoshi Kakita, Hitoshi Takahashi, Hiroyoshi Suzuki, Hironobu Naiki, Nobuo Sanjo, Hidehiro Mizusawa, Masahito Yamada

    ACTA NEUROPATHOLOGICA   132 ( 2 )   313 - 315   2016.8

  • A case of lymphomatosis cerebri mimicking inflammatory diseases Reviewed

    Takenobu Murakami, Kenji Yoshida, Mari Segawa, Akioh Yoshihara, Akihiko Hoshi, Koichiro Nakamura, Masahiro Ichikawa, Osamu Suzuki, Yuichi Yokoyama, Yasuko Toyoshima, Yoshihiro Sugiura, Hiroshi Ito, Kiyoshi Saito, Yuko Hashimoto, Akiyoshi Kakita, Hitoshi Takahashi, Yoshikazu Ugawa

    BMC NEUROLOGY   16   128   2016.8

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  • Increased neuronal and astroglial aquaporin-1 immunoreactivity in rat striatum by chemical preconditioning with 3-nitropropionic acid Reviewed

    Akihiko Hoshi, Ayako Tsunoda, Teiji Yamamoto, Mari Tada, Akiyoshi Kakita, Yoshikazu Ugawa

    NEUROSCIENCE LETTERS   626   48 - 53   2016.7

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  • Increased cytoplasmic TARDBP mRNA in affected spinal motor neurons in ALS caused by abnormal autoregulation of TDP-43 Reviewed

    Akihide Koyama, Akihiro Sugai, Taisuke Kato, Tomohiko Ishihara, Atsushi Shiga, Yasuko Toyoshima, Misaki Koyama, Takuya Konno, Sachiko Hirokawa, Akio Yokoseki, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi, Osamu Onodera

    NUCLEIC ACIDS RESEARCH   44 ( 12 )   5820 - 5836   2016.7

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  • Heterogeneity of cerebral TDP-43 pathology in sporadic amyotrophic lateral sclerosis: evidence for clinic-pathologic subtypes. Reviewed

    Takeuchi R, Tada M, Shiga A, Toyoshima Y, Konno T, Sato T, Nozaki H, Kato T, Horie M, Shimizu H, Takebayashi H, Onodera O, Nishizawa M, Kakita A, Takahashi H

    Acta Neuropathol Commun   4 ( 1 )   61   2016.6

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  • alpha-Synuclein pathology in the cranial and spinal nerves in Lewy body disease Reviewed

    Keiko Nakamura, Fumiaki Mori, Kunikazu Tanji, Yasuo Miki, Yasuko Toyoshima, Akiyoshi Kakita, Hitoshi Takahashi, Masahito Yamada, Koichi Wakabayashi

    NEUROPATHOLOGY   36 ( 3 )   262 - 269   2016.6

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  • Choreaを伴った非典型的ALSと臨床診断された、Tauopathyの一剖検例 Reviewed

    田中 英智, 豊島 靖子, 三浦 健, 三瓶 一弘, 志賀 篤, 柿田 明美, 高橋 均

    The Kitakanto Medical Journal   66 ( 2 )   175 - 175   2016.5

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  • Alteration of Upstream Autophagy-Related Proteins (ULK1, ULK2, Beclin1, VPS34 and AMBRA1) in Lewy Body Disease Reviewed

    Yasuo Miki, Kunikazu Tanji, Fumiaki Mori, Jun Utsumi, Hidenao Sasaki, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    BRAIN PATHOLOGY   26 ( 3 )   359 - 370   2016.5

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  • 当科で経験した成人テント上PNETの2例 症例報告

    塚本 佳広, 小倉 良介, 五十川 瑞穂, 青木 洋, 平石 哲也, 高尾 哲郎, 吉村 淳一, 藤井 幸彦, 高橋 均, 柿田 明美

    Brain Tumor Pathology   33 ( Suppl. )   149 - 149   2016.5

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  • Clinicopathological features in anterior visual pathway in neuromyelitis optica Reviewed

    Mariko Hokari, Akiko Yokoseki, Musashi Arakawa, Etsuji Saji, Kaori Yanagawa, Fumihiro Yanagimura, Yasuko Toyoshima, Kouichirou Okamoto, Satoshi Ueki, Tetsuhisa Hatase, Riuko Ohashi, Takeo Fukuchi, Kohei Akazawa, Mitsunori Yamada, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa, Izumi Kawachi

    ANNALS OF NEUROLOGY   79 ( 4 )   605 - 624   2016.4

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  • Accumulation of phosphorylated -synuclein in subpial and periventricular astrocytes in multiple system atrophy of long duration Reviewed

    Keiko Nakamura, Fumiaki Mori, Tomoya Kon, Kunikazu Tanji, Yasuo Miki, Masahiko Tomiyama, Hidekachi Kurotaki, Yasuko Toyoshima, Akiyoshi Kakita, Hitoshi Takahashi, Masahito Yamada, Koichi Wakabayashi

    NEUROPATHOLOGY   36 ( 2 )   157 - 167   2016.4

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    DOI: 10.1111/neup.12243

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  • Pathological and Clinical Spectrum of Progressive Supranuclear Palsy: With Special Reference to Astrocytic Tau Pathology Reviewed

    Yuichi Yokoyama, Yasuko Toyoshima, Atsushi Shiga, Mari Tada, Hideaki Kitamura, Kazuko Hasegawa, Osamu Onodera, Takeshi Ikeuchi, Toshiyuki Someya, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    BRAIN PATHOLOGY   26 ( 2 )   155 - 166   2016.3

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    DOI: 10.1111/bpa.12265

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  • Nonfunctional intra- and suprasellar tumor in a patient with visual disturbance and panhypopituitarism Reviewed

    Rie Saito, Shinya Jinguji, Yoshinori Taniguchi, Shigekazu Takeuchi, Kouichirou Okamoto, Masatoyo Nishizawa, Hitoshi Takahashi, Akiyoshi Kakita

    NEUROPATHOLOGY   36 ( 1 )   107 - 112   2016.2

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    DOI: 10.1111/neup.12236

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  • G protein-coupled receptor 26 immunoreactivity in intranuclear inclusions associated with polyglutamine and intranuclear inclusion body diseases Reviewed

    Fumiaki Mori, Kunikazu Tanji, Yasuo Miki, Yasuko Toyoshima, Mari Yoshida, Akiyoshi Kakita, Hitoshi Takahashi, Jun Utsumi, Hidenao Sasaki, Koichi Wakabayashi

    NEUROPATHOLOGY   36 ( 1 )   50 - 55   2016.2

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  • 新潟大学脳研究所の取り組み:3T MRIを用いたAiと病理解剖 Reviewed

    KAKITA Akiyoshi

    インナービジョン   31 ( 1 )   45 - 47   2016.1

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  • 病理所見を理解する基礎 Reviewed

    KAKITA Akiyoshi

    33 ( 3 )   688 - 691   2016.1

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    DOI: 10.3805/jjes.33.688

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  • Depression-like episodes in mice harboring mtDNA deletions in paraventricular thalamus Reviewed

    T. Kasahara, A. Takata, T. M. Kato, M. Kubota-Sakashita, T. Sawada, A. Kakita, H. Mizukami, D. Kaneda, K. Ozawa, T. Kato

    MOLECULAR PSYCHIATRY   21 ( 1 )   39 - 48   2016.1

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  • Globular Glial Mixed Four Repeat Tau and TDP-43 Proteinopathy with Motor Neuron Disease and Frontotemporal Dementia Reviewed

    Ryoko Takeuchi, Yasuko Toyoshima, Mari Tada, Hidetomo Tanaka, Hiroshi Shimizu, Atsushi Shiga, Takeshi Miura, Kenju Aoki, Akane Aikawa, Shin Ishizawa, Takeshi Ikeuchi, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    BRAIN PATHOLOGY   26 ( 1 )   82 - 94   2016.1

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    DOI: 10.1111/bpa.12262

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  • Globular Glial Mixed Four Repeat Tau and TDP-43 Proteinopathy with Motor Neuron Disease and Frontotemporal Dementia. Reviewed International journal

    Ryoko Takeuchi, Yasuko Toyoshima, Mari Tada, Hidetomo Tanaka, Hiroshi Shimizu, Atsushi Shiga, Takeshi Miura, Kenju Aoki, Akane Aikawa, Shin Ishizawa, Takeshi Ikeuchi, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    Brain pathology (Zurich, Switzerland)   26 ( 1 )   82 - 94   2016.1

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    Amyotrophic lateral sclerosis (ALS) may be accompanied by frontotemporal dementia (FTD). We report a case of glial mixed tau and TDP-43 proteinopathies in a Japanese patient diagnosed clinically as having ALS-D. Autopsy revealed loss of lower motor neurons and degeneration of the pyramidal tracts in the spinal cord and brain stem. The brain showed frontotemporal lobar degeneration (FTLD), the most severe neuronal loss and gliosis being evident in the precentral gyrus. Although less severe, such changes were also observed in other brain regions, including the basal ganglia and substantia nigra. AT8 immunostaining revealed that predominant occurrence of astrocytic tau lesions termed globular astrocytic inclusions (GAIs) was a feature of the affected regions. These GAIs were Gallyas-Braak negative. Neuronal and oligodendrocytic tau lesions were comparatively scarce. pS409/410 immunostaining also revealed similar neuronal and glial TDP-43 lesions. Interestingly, occasional co-localization of tau and TDP-43 was evident in the GAIs. Immunoblot analyses revealed band patterns characteristic of a 4-repeat (4R) tauopathy, corticobasal degeneration and a TDP-43 proteinopathy, ALS/FTLD-TDP Type B. No mutations were found in the MAPT or TDP-43 genes. We consider that this patient harbored a distinct, sporadic globular glial mixed 4R tau and TDP-43 proteinopathy associated with motor neuron disease and FTD.

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  • Fibromyalgia in a Patient with Cushing's Disease Accompanied by Central Hypothyroidism Reviewed

    Nobumasa Ohara, Shinichi Katada, Takaho Yamada, Naomi Mezaki, Hiroshi Suzuki, Akiko Suzuki, Osamu Hanyu, Yuichiro Yoneoka, Izumi Kawachi, Takayoshi Shimohata, Akiyoshi Kakita, Masatoyo Nishizawa, Hirohito Sone

    INTERNAL MEDICINE   55 ( 21 )   3185 - 3190   2016

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    DOI: 10.2169/internalmedicine.55.5926

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  • Pathological features of glia in adult–onset leukoencephalopathies : implication for pathomechanisms

    Kakita Akiyoshi

    Neurological Therapeutics   33 ( 5 )   S131 - S131   2016

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    DOI: 10.15082/jsnt.33.5_S131

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  • Diagnostic performance of positron emission tomography for the presurgical evaluation of patients with non-lesional intractable partial epilepsy: Comparison among 18F-FDG, 11C-Flumazenil, and 11C-Flumazenil binding potential imaging using statistical imaging analysis Reviewed

    Daisuke Komoto, Koji Iida, Toru Higaki, Yoko Kaichi, Komei Takauchi, Koji Arihiro, Akiyoshi Kakita, Yutaka Hirokawa, Kazuo Awai

    Hiroshima Journal of Medical Sciences   64 ( 4 )   51 - 57   2015.12

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  • Localization of nuclear receptor subfamily 4, group A, member 3 (NR4A3) in Lewy body disease and multiple system atrophy Reviewed

    Tomoya Kon, Yasuo Miki, Kunikazu Tanji, Fumiaki Mori, Masahiko Tomiyama, Yasuko Toyoshima, Akiyoshi Kakita, Hitoshi Takahashi, Jun Utsumi, Hidenao Sasaki, Koichi Wakabayashi

    NEUROPATHOLOGY   35 ( 6 )   503 - 509   2015.12

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    DOI: 10.1111/neup.12210

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  • Spatiotemporal gene expression trajectory in the human and non-human ape brains Reviewed

    Yasuhiro Go, Shoji Tatsumoto, Li Qian, Takao Oishi, Toshifumi Udono, Shuji Shigenobu, Akiyoshi Kakita, Hiroyuki Nawa, Philipp Khaitovich

    GENES & GENETIC SYSTEMS   90 ( 6 )   372 - 372   2015.12

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  • フラビン蛍光イメージングによるてんかん原性の解析 Reviewed

    Epilepsy   9 ( 2 )   82 - 84   2015.11

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  • Sortilin-related receptor CNS expressed 2 (SorCS2) is localized to Bunina bodies in amyotrophic lateral sclerosis Reviewed

    Fumiaki Mori, Yasuo Miki, Kunikazu Tanji, Akiyoshi Kakita, Hitoshi Takahashi, Jun Utsumi, Hidenao Sasaki, Koichi Wakabayashi

    NEUROSCIENCE LETTERS   608   6 - 11   2015.11

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    DOI: 10.1016/j.neulet.2015.09.030

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  • Characteristic expression of p57/Kip2 in balloon cells in focal cortical dysplasia Reviewed

    Tadashi Kimura, Hiroki Kitaura, Hiroshi Masuda, Shigeki Kameyama, Yuko Saito, Kenji Sugai, Taisuke Otsuki, Atsuko Nakazawa, Nobuhito Morota, Takamichi Yamamoto, Kouji Iida, Masanori Nakagawa, Toshiki Mizuno, Hitoshi Takahashi, Akiyoshi Kakita

    NEUROPATHOLOGY   35 ( 5 )   401 - 409   2015.10

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    DOI: 10.1111/neup.12199

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  • Variable expression of microglial DAP12 and TREM2 genes in Nasu-Hakola disease Reviewed

    Atsushi Sasaki, Akiyoshi Kakita, Kunihiro Yoshida, Takuya Konno, Takeshi Ikeuchi, Shintaro Hayashi, Hidenori Matsuo, Kei Shioda

    NEUROGENETICS   16 ( 4 )   265 - 276   2015.10

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    DOI: 10.1007/s10048-015-0451-3

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  • Isopentenyl diphosphate isomerase, a cholesterol synthesizing enzyme, is localized in Lewy bodies Reviewed

    Keiko Nakamura, Fumiaki Mori, Kunikazu Tanji, Yasuo Miki, Masahito Yamada, Akiyoshi Kakita, Hitoshi Takahashi, Jun Utsumi, Hidenao Sasaki, Koichi Wakabayashi

    NEUROPATHOLOGY   35 ( 5 )   432 - 440   2015.10

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    DOI: 10.1111/neup.12204

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  • Somatic Mutations in the MTOR gene cause focal cortical dysplasia type IIb Reviewed

    Mitsuko Nakashima, Hirotomo Saitsu, Nobuyuki Takei, Jun Tohyama, Mitsuhiro Kato, Hiroki Kitaura, Masaaki Shiina, Hiroshi Shirozu, Hiroshi Masuda, Keisuke Watanabe, Chihiro Ohba, Yoshinori Tsurusaki, Noriko Miyake, Yingjun Zheng, Tatsuhiro Sato, Hirohide Takebayashi, Kazuhiro Ogata, Shigeki Kameyama, Akiyoshi Kakita, Naomichi Matsumoto

    ANNALS OF NEUROLOGY   78 ( 3 )   375 - 386   2015.9

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    DOI: 10.1002/ana.24444

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  • Somatic Mutations in MTOR Cause Focal cortical dysplasia Type IIb Reviewed

    Nakashima M, Saitsu H, Takei N, Tohyama J, Kato M, Kitaura H, Shiina M, Shirouzu H, Masuda H, Watanabe K, Ohba C, Tsurusaki Y, Miyake N, Zheng YJ, Sato T, Takebayashi H, Ogata K, Kameyama S, Kakita A, Matsumoto N

    Ann. Neurol   78 ( 3 )   375 - 386   2015.9

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    DOI: 10.1002/ana.24444

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  • Quantitative correlation between cardiac MIBG uptake and remaining axons in the cardiac sympathetic nerve in Lewy body disease Reviewed

    Makoto Takahashi, Masako Ikemura, Teruaki Oka, Toshiki Uchihara, Koichi Wakabayashi, Akiyoshi Kakita, Hitoshi Takahashi, Mari Yoshida, Shuta Toru, Takayoshi Kobayashi, Satoshi Orimo

    JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY   86 ( 9 )   939 - 944   2015.9

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    DOI: 10.1136/jnnp-2015-310686

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  • Inhibitory PAS domain protein is a substrate of PINK1 and Parkin and mediates cell death in a Parkinson's disease model Reviewed

    S. Kasai, S. Torii, A. Kakita, K. Sogawa

    CELL DEATH & DISEASE   6   e1886   2015.9

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  • ファール病(家族性特発性基底核石灰化症) Reviewed

    Clin Neurosci   33 ( 8 )   862 - 863   2015.8

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  • Na, K-ATPase alpha 3 is a death target of Alzheimer patient amyloid-beta assembly Reviewed

    Takayuki Ohnishi, Masako Yanazawa, Tomoya Sasahara, Yasuki Kitamura, Hidekazu Hiroaki, Yugo Fukazawa, Isao Kii, Takashi Nishiyama, Akiyoshi Kakita, Hiroyuki Takeda, Akihide Takeuchi, Yoshie Arai, Akane Ito, Hitomi Komura, Hajime Hirao, Kaori Satomura, Masafumi Inoue, Shin-ichi Muramatsu, Ko Matsui, Mari Tada, Michio Sato, Eri Saijo, Yoshiki Shigemitsu, Satoko Sakai, Yoshitaka Umetsu, Natsuko Goda, Naomi Takino, Hitoshi Takahashi, Masatoshi Hagiwara, Tatsuya Sawasaki, Genji Iwasaki, Yu Nakamura, Yo-ichi Nabeshima, David B. Teplow, Minako Hoshi

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   112 ( 32 )   E4465 - E4474   2015.8

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    DOI: 10.1073/pnas.1421182112

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  • Involvement of inhibitory PAS domain protein in neuronal cell death in Parkinson's disease. Reviewed

    Torii S, Kasai S, Suzuki A, Todoroki Y, Yokozawa K, Yasumoto KI, Seike N, Kiyonari H, Mukumoto Y, Kakita A, Sogawa K

    Cell death discovery   1   15015   2015.8

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    DOI: 10.1038/cddiscovery.2015.15

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  • Immunohistochemical profiles of IDH1, MGMT and P53: Practical significance for prognostication of patients with diffuse gliomas Reviewed

    Ryosuke Ogura, Yoshihiro Tsukamoto, Manabu Natsumeda, Mizuho Isogawa, Hiroshi Aoki, Tsutomu Kobayashi, Seiichi Yoshida, Kouichiro Okamoto, Hitoshi Takahashi, Yukihiko Fujii, Akiyoshi Kakita

    NEUROPATHOLOGY   35 ( 4 )   324 - 335   2015.8

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    DOI: 10.1111/neup.12196

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  • Assessment of copy number variations in the brain genome of schizophrenia patients. Reviewed

    Sakai M, Watanabe Y, Someya T, Araki K, Shibuya M, Niizato K, Oshima K, Kunii Y, Yabe H, Matsumoto J, Wada A, Hino M, Hashimoto T, Hishimoto A, Kitamura N, Iritani S, Shirakawa O, Maeda K, Miyashita A, Niwa S, Takahashi H, Kakita A, Kuwano R, Nawa H

    Mol Cytogenet   8   46   2015.7

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  • てんかん外科病理に関する最新の国際分類 Reviewed

    柿田 明美

    最新医学   70 ( 6 )   1031 - 1037   2015.6

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  • Two siblings with cortical dysplasia: Clinico-electroencephalographic features Reviewed

    Tatsuya Fukasawa, Tetsuo Kubota, Tamiko Negoro, Shinsuke Maruyama, Ryoko Honda, Yuko Saito, Masayuki Itoh, Akiyoshi Kakita, Kenji Sugai, Taisuke Otsuki, Mitsuhiro Kato, Jun Natsume, Kazuyoshi Watanabe

    PEDIATRICS INTERNATIONAL   57 ( 3 )   472 - 475   2015.6

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    DOI: 10.1111/ped.12509

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  • Filamentous aggregations of phosphorylated alpha-synuclein in Schwann cells (Schwann cell cytoplasmic inclusions) in multiple system atrophy Reviewed

    Keiko Nakamura, Fumiaki Mori, Tomoya Kon, Kunikazu Tanji, Yasuo Miki, Masahiko Tomiyama, Hidekachi Kurotaki, Yasuko Toyoshima, Akiyoshi Kakita, Hitoshi Takahashi, Masahito Yamada, Koichi Wakabayashi

    ACTA NEUROPATHOLOGICA COMMUNICATIONS   3 ( 1 )   29   2015.5

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    DOI: 10.1186/s40478-015-0208-0

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  • 髄鞘病変を鑑別するポイント Reviewed

    柿田 明美

    病理と臨床   33 ( 4 )   352 - 358   2015.4

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    神経病理診断の標準化Ⅱ

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  • 胚芽異型成性神経上皮腫瘍 Dysembryoplastic neuroepithelial tumor. Reviewed

    Pathology and Clinical Medicine   33   334   2015.4

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  • 頭蓋咽頭腫 Craniopharyngioma Reviewed

    Pathology and Clinical Medicine   33   332   2015.4

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  • Variants associated with Gaucher disease in multiple system atrophy Reviewed

    Jun Mitsui, Takashi Matsukawa, Hidenao Sasaki, Ichiro Yabe, Masaaki Matsushima, Alexandra Duerr, Alexis Brice, Hiroshi Takashima, Akio Kikuchi, Masashi Aoki, Hiroyuki Ishiura, Tsutomu Yasuda, Hidetoshi Date, Budrul Ahsan, Atsushi Iwata, Jun Goto, Yaeko Ichikawa, Yasuo Nakahara, Yoshio Momose, Yuji Takahashi, Kenju Hara, Akiyoshi Kakita, Mitsunori Yamada, Hitoshi Takahashi, Osamu Onodera, Masatoyo Nishizawa, Hirohisa Watanabe, Mizuki Ito, Gen Sobue, Kinya Ishikawa, Hidehiro Mizusawa, Kazuaki Kanai, Takamichi Hattori, Satoshi Kuwabara, Kimihito Arai, Shigeru Koyano, Yoshiyuki Kuroiwa, Kazuko Hasegawa, Tatsuhiko Yuasa, Kenichi Yasui, Kenji Nakashima, Hijiri Ito, Yuishin Izumi, Ryuji Kaji, Takeo Kato, Susumu Kusunoki, Yasushi Osaki, Masahiro Horiuchi, Tomoyoshi Kondo, Shigeo Murayama, Nobutaka Hattori, Mitsutoshi Yamamoto, Miho Murata, Wataru Satake, Tatsushi Toda, Alessandro Filla, Thomas Klockgether, Ullrich Wuellner, Garth Nicholson, Sid Gilman, Caroline M. Tanner, Walter A. Kukull, Mathew B. Stern, Virginia M. -Y. Lee, John Q. Trojanowski, Eliezer Masliah, Phillip A. Low, Paola Sandroni, Laurie J. Ozelius, Tatiana Foroud, Shoji Tsuji

    ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY   2 ( 4 )   417 - 426   2015.4

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    DOI: 10.1002/acn3.185

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  • [Hip Fracture--Epidemiology, Management and Liaison Service. Osteoporosis liaison service in Japan]. Reviewed

    Suzuki A, Sekiguchi-Ueda S, Kakita A

    Clinical calcium   25 ( 4 )   559 - 563   2015.4

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  • 認知症を主症状とし、大脳皮質に変性が強調された進行性核上性麻痺の一剖検例 Reviewed

    田中 英智, 清水 宏, 豊島 靖子, 田中 弘, 田中 政春, 池内 健, 柿田 明美, 高橋 均

    信州医学雑誌   63 ( 1 )   71 - 72   2015.2

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  • Zinc Transporters ZnT3 and ZnT6 Are Downregulated in the Spinal Cords of Patients With Sporadic Amyotrophic Lateral Sclerosis Reviewed

    Masayuki Kaneko, Takao Noguchi, Saori Ikegami, Takeyuki Sakurai, Akiyoshi Kakita, Yasuko Toyoshima, Taiho Kambe, Mitsunori Yamada, Masatoshi Inden, Hideaki Hara, Kiyomitsu Oyanagi, Takashi Inuzuka, Hitoshi Takahashi, Isao Hozumi

    JOURNAL OF NEUROSCIENCE RESEARCH   93 ( 2 )   370 - 379   2015.2

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    DOI: 10.1002/jnr.23491

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  • Identification of Neurons and Glial Cells in Pathological Human Brain Sections by in situ Hybridization Method Reviewed

    128 ( 12 )   625 - 634   2014.12

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  • ALSにおけるspliceosome異常 Reviewed

    石原智彦, 柿田明美, 高橋 均, 小野寺 理, 西澤正豊

    臨床神経   54 ( 12 )   1155 - 1157   2014.12

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  • ヒトてんかん病巣におけるグリア細胞の病理組織学的所見 Reviewed

    柿田明美

    臨床神経   54 ( 12 )   1136 - 1138   2014.12

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    DOI: 10.5692/clinicalneurol.54.1136

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  • Neuromyelitis optica脊髄炎局所におけるTH1細胞の役割

    穂苅 万李子, 河内 泉, 佐治 越爾, 荒川 武蔵, 横関 明子, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊

    臨床神経学   54 ( Suppl. )   S49 - S49   2014.12

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  • MPO-ANCA関連肥厚性硬膜炎の臨床・免疫・病理学的特徴

    横関 明子, 河内 泉, 佐治 越爾, 荒川 武蔵, 穂苅 万李子, 豊島 靖子, 小阪 崇幸, 岡本 浩一郎, 武田 茂樹, 三瓶 一弘, 菊池 弘敏, 廣畑 俊成, 赤澤 宏平, 柿田 明美, 高橋 均, 西澤 正豊

    臨床神経学   54 ( Suppl. )   S25 - S25   2014.12

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  • Histopathologic features of epileptogenic brain lesions in infants and children Reviewed

    Akiyoshi Kakita

    No To Hattatsu   46 ( 6 )   413 - 417   2014.11

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  • 結節性硬化症 Reviewed

    北浦弘樹, 柿田明美

    Epilepsy   8 ( 2 )   74 - 76   2014.11

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  • Disruption of actin-binding domain-containing Dystonin protein causes dystonia musculorum in mice Reviewed

    Masao Horie, Keisuke Watanabe, Asim K. Bepari, Jun-ichiro Nashimoto, Kimi Araki, Hiromi Sano, Satomi Chiken, Atsushi Nambu, Katsuhiko Ono, Kazuhiro Ikenaka, Akiyoshi Kakita, Ken-ichi Yamamura, Hirohide Takebayashi

    EUROPEAN JOURNAL OF NEUROSCIENCE   40 ( 10 )   3458 - 3471   2014.11

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    DOI: 10.1111/ejn.12711

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  • 小児てんかん原性病巣の外科病理 Reviewed

    柿田明美

    脳と発達   46 ( 6 )   413 - 417   2014.11

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    DOI: 10.11251/ojjscn.46.413

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  • Elevated serum anti-phosphatidylcholine IgG antibodies in patients with influenza vaccination-associated optic neuritis Reviewed

    Seigo Korematsu, Hiroaki Miyahara, Akiyoshi Kakita, Tatsuro Izumi

    VACCINE   32 ( 48 )   6345 - 6348   2014.11

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    DOI: 10.1016/j.vaccine.2014.09.053

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  • C9ORF72 repeat-associated non-ATG-translated polypeptides are distributed independently of TDP-43 in a Japanese patient with c9ALS Reviewed

    T. Konno, M. Tada, A. Shiga, A. Tsujino, H. Eguchi, M. Masuda-Suzukake, M. Hasegawa, M. Nishizawa, O. Onodera, A. Kakita, H. Takahashi

    NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY   40 ( 6 )   783 - 788   2014.10

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    Ota K, Obayashi M, Ozaki K, Ichinose S, Kakita A, Tada M, Takahashi H, Ando N, Eishi Y, Mizusawa H, Ishikawa K

    Acta neuropathologica communications   2 ( 1 )   136   2014.9

  • 中枢神経系におけるリンパ濾胞構造と自己免疫病態の解析

    穂苅 万季子, 河内 泉, 横関 明子, 佐治 越爾, 柳川 香織, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊

    神経免疫学   19 ( 1 )   136 - 136   2014.9

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  • Elevated postmortem striatal t-DARPP expression in schizophrenia and associations with DRD2/ANKK1 polymorphism Reviewed

    Yasuto Kunii, Itaru Miura, Junya Matsumoto, Mizuki Hino, Akira Wada, Shin-ichi Niwa, Hiroyuki Nawa, Miwako Sakai, Toshiyuki Someya, Hitoshi Takahashi, Akiyoshi Kakita, Hirooki Yabe

    Progress in Neuro-Psychopharmacology and Biological Psychiatry   53   123 - 128   2014.8

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  • Progressive myoclonus epilepsy: extraneuronal brown pigment deposition and system neurodegeneration in the brains of Japanese patients with novel SCARB2 mutations Reviewed

    Y. -J. Fu, I. Aida, M. Tada, M. Tada, Y. Toyoshima, S. Takeda, T. Nakajima, H. Naito, M. Nishizawa, O. Onodera, A. Kakita, H. Takahashi

    NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY   40 ( 5 )   551 - 563   2014.8

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  • Bunina bodies in motor and non-motor neurons revisited: A pathological study of an ALS patient after long-term survival on a respirator Reviewed

    Tadashi Kimura, Haishan Jiang, Takuya Konno, Makiko Seto, Keisuke Iwanaga, Mitsuhiro Tsujihata, Akira Satoh, Osamu Onodera, Akiyoshi Kakita, Hitoshi Takahashi

    NEUROPATHOLOGY   34 ( 4 )   392 - 397   2014.8

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  • An autopsy case of incipient Pick's disease: Immunohistochemical profile of early-stage Pick body formation Reviewed

    Yasuo Miki, Fumiaki Mori, Kunikazu Tanji, Hidekachi Kurotaki, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROPATHOLOGY   34 ( 4 )   386 - 391   2014.8

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  • Elevated postmortem striatal t-DARPP expression in schizophrenia and associations with DRD2/ANKK1 polymorphism Reviewed

    Yasuto Kunii, Itaru Miura, Junya Matsumoto, Mizuki Hino, Akira Wada, Shin-ichi Niwa, Hiroyuki Nawa, Miwako Sakai, Toshiyuki Someya, Hitoshi Takahashi, Akiyoshi Kakita, Hirooki Yabe

    PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY   53   123 - 128   2014.8

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  • Cerebral amyloid angiopathy-related leukoencephalopathy: successful steroid treatment for neurological deficits and subcortical white matter lesions partly involving the cortical gray matter Reviewed

    Murakami T, Morimoto J, Hoshi A, Nakatani-Enomoto S, Ichikawa M, Tasaki K, Ogura R, Toyoshima Y, Kakita A, Saito K, Takahashi H, Ugawa Y

    Neurology and Clinical Neuroscience   2 ( 4 )   119 - 121   2014.7

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  • びまん性メラニン細胞増殖症,髄膜黒色腫症 Reviewed

    柿田 明美

    別冊日本臨牀 新領域別症候群シリーズ   28   307 - 310   2014.6

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  • "Gliomatosis encephali" as a novel category of brain tumors by the first autopsy case report of gliomatosis cerebelli Reviewed

    Asa Nakahara, Toshikazu Yoshida, Masanobu Yazawa, Takashi Ehara, Jun Nakayama, Akiyoshi Kakita, Ryosuke Ogura, Mika Asakawa, Emi Suzuki-Kouyama, Kiyomitsu Oyanagi

    NEUROPATHOLOGY   34 ( 3 )   295 - 303   2014.6

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  • Genes associated with the progression of neurofibrillary tangles in Alzheimer's disease Reviewed

    A. Miyashita, H. Hatsuta, M. Kikuchi, A. Nakaya, Y. Saito, T. Tsukie, N. Hara, S. Ogishima, N. Kitamura, K. Akazawa, A. Kakita, H. Takahashi, S. Murayama, Y. Ihara, T. Ikeuchi, R. Kuwano

    TRANSLATIONAL PSYCHIATRY   4   e396   2014.6

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  • Entrapment of the inferior horns of the lateral ventricle with enlargement of the bilateral choroid plexus Reviewed

    Ryosuke Ogura, Junichi Yoshimura, Masakazu Sano, Shouichi Kawasaki, Kenichi Nishiyama, Kouichirou Okamoto, Hitoshi Takahashi, Yukihiko Fujii, Akiyoshi Kakita

    NEUROPATHOLOGY   34 ( 2 )   210 - 213   2014.4

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  • Coexistence of amyotrophic lateral sclerosis with neuro-Behcet's disease presenting as a longitudinally extensive spinal cord lesion: clinicopathologic features of an autopsied patient Reviewed

    Tomoe Sato, Haruka Ouchi, Junsuke Shimbo, Aki Sato, Motoyoshi Yamazaki, Hideki Hashidate, Shuichi Igarashi, Akiyoshi Kakita

    NEUROPATHOLOGY   34 ( 2 )   185 - 189   2014.4

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  • Superficial siderosis associated with aceruloplasminemia. Case report Reviewed

    Akira Matsushima, Toshikazu Yoshida, Kunihiro Yoshida, Shinji Ohara, Yasuko Toyoshima, Akiyoshi Kakita, Shu-ichi Ikeda

    JOURNAL OF THE NEUROLOGICAL SCIENCES   339 ( 1-2 )   231 - 234   2014.4

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  • Accumulation of the sigma-1 receptor is common to neuronal nuclear inclusions in various neurodegenerative diseases Reviewed

    Yasuo Miki, Fumiaki Mori, Tomoya Kon, Kunikazu Tanji, Yasuko Toyoshima, Mari Yoshida, Hidenao Sasaki, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROPATHOLOGY   34 ( 2 )   148 - 158   2014.4

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  • ALS-associated protein FIG4 is localized in Pick and Lewy bodies, and also neuronal nuclear inclusions, in polyglutamine and intranuclear inclusion body diseases Reviewed

    Tomoya Kon, Fumiaki Mori, Kunikazu Tanji, Yasuo Miki, Yasuko Toyoshima, Mari Yoshida, Hidenao Sasaki, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROPATHOLOGY   34 ( 1 )   19 - 26   2014.2

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  • Co-localization of Bunina bodies and TDP-43 inclusions in lower motor neurons in amyotrophic lateral sclerosis Reviewed

    Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROPATHOLOGY   34 ( 1 )   71 - 76   2014.2

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    DOI: 10.1111/neup.12044

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  • Hypertrophic pachymeningitis: significance of myeloperoxidase anti-neutrophil cytoplasmic antibody Reviewed

    Akiko Yokoseki, Etsuji Saji, Musashi Arakawa, Takayuki Kosaka, Mariko Hokari, Yasuko Toyoshima, Kouichirou Okamoto, Shigeki Takeda, Kazuhiro Sanpei, Hirotoshi Kikuchi, Shunsei Hirohata, Kouhei Akazawa, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa, Izumi Kawachi

    BRAIN   137 ( Pt 2 )   520 - 536   2014.2

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  • Neuronal differentiation associated with Gli3 expression predicts favorable outcome for patients with medulloblastoma Reviewed

    Hiroaki Miyahara, Manabu Natsumeda, Junichi Yoshimura, Ryosuke Ogura, Kenichi Okazaki, Yasuko Toyoshima, Yukihiko Fujii, Hitoshi Takahashi, Akiyoshi Kakita

    NEUROPATHOLOGY   34 ( 1 )   1 - 10   2014.2

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    DOI: 10.1111/neup.12052

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  • The Kick-In System: A Novel Rapid Knock-In Strategy Reviewed

    Yuko Tomonoh, Masanobu Deshimaru, Kimi Araki, Yasuhiro Miyazaki, Tomoko Arasaki, Yasuyoshi Tanaka, Haruna Kitamura, Fumiaki Mori, Koichi Wakabayashi, Sayaka Yamashita, Ryo Saito, Masayuki Itoh, Taku Uchida, Junko Yamada, Keisuke Migita, Shinya Ueno, Hiroki Kitaura, Akiyoshi Kakita, Christoph Lossin, Yukio Takano, Shinichi Hirose

    PLOS ONE   9 ( 2 )   e88549   2014.2

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  • An attempt of non-human primate modeling of schizophrenia with neonatal challenges of epidermal growth factor. Reviewed

    Sakai M, Kashiwahara M, Kakita A, Nawa H

    J Addict Res Ther   5   170   2014.2

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    DOI: 10.4172/2155-6105.1000170.

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  • Increased l1 retrotransposition in the neuronal genome in schizophrenia. Reviewed International journal

    Bundo Miki, Toyoshima Manabu, Okada Yohei, Akamatsu Wado, Ueda Junko, Nemoto-Miyauchi Taeko, Sunaga Fumiko, Toritsuka Michihiro, Ikawa Daisuke, Kakita Akiyoshi, Kato Motoichiro, Kasai Kiyoto, Kishimoto Toshifumi, Nawa Hiroyuki, Okano Hideyuki, Yoshikawa Takeo, Kato Tadafumi, Iwamoto Kazuya

    Neuron   81 ( 2 )   306 - 313   2014.1

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  • Progressive Neurodegeneration After Experimental Brain Trauma: Association With Chronic Microglial Activation Reviewed

    Shinsui Tatsumi, Maya Mimuro, Yasushi Iwasaki, Ryosuke Takahashi, Akiyoshi Kakita, Hitoshi Takahashi, Mari Yoshida

    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY   73 ( 1 )   30 - 38   2014.1

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  • Increased l1 retrotransposition in the neuronal genome in schizophrenia. Reviewed International journal

    Bundo M, Toyoshima M, Okada Y, Akamatsu W, Ueda J, Nemoto-Miyauchi T, Sunaga F, Toritsuka M, Ikawa D, Kakita A, Kato M, Kasai K, Kishimoto T, Nawa H, Okano H, Yoshikawa T, Kato T, Iwamoto K

    Neuron   81 ( 2 )   306 - 313   2014.1

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    Recent studies indicate that long interspersed nuclear element-1 (L1) are mobilized in the genome of human neural progenitor cells and enhanced in Rett syndrome and ataxia telangiectasia. However, whether aberrant L1 retrotransposition occurs in mental disorders is unknown. Here, we report high L1 copy number in schizophrenia. Increased L1 was demonstrated in neurons from prefrontal cortex of patients and in induced pluripotent stem (iPS) cell-derived neurons containing 22q11 deletions. Whole-genome sequencing revealed brain-specific L1 insertion in patients localized preferentially to synapse- and schizophrenia-related genes. To study the mechanism of L1 transposition, we examined perinatal environmental risk factors for schizophrenia in animal models and observed an increased L1 copy number after immune activation by poly-I:C or epidermal growth factor. These findings suggest that hyperactive retrotransposition of L1 in neurons triggered by environmental and/or genetic risk factors may contribute to the susceptibility and pathophysiology of schizophrenia.

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  • Haploinsufficiency of CSF-1R and clinicopathologic characterization in patients with HDLS Reviewed

    Takuya Konno, Masayoshi Tada, Mari Tada, Akihide Koyama, Hiroaki Nozaki, Yasuo Harigaya, Jin Nishimiya, Akiko Matsunaga, Nobuaki Yoshikura, Kenji Ishihara, Musashi Arakawa, Aiko Isami, Kenichi Okazaki, Hideaki Yokoo, Kyoko Itoh, Makoto Yoneda, Mitsuru Kawamura, Takashi Inuzuka, Hitoshi Takahashi, Masatoyo Nishizawa, Osamu Onodera, Akiyoshi Kakita, Takeshi Ikeuchi

    NEUROLOGY   82 ( 2 )   139 - 148   2014.1

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  • Argyrophilic grains are reliable disease-specific features of corticobasal degeneration Reviewed

    Shinsui Tatsumi, Maya Mimuro, Yasushi Iwasaki, Ryosuke Takahashi, Akiyoshi Kakita, Hitoshi Takahashi, Mari Yoshida

    Journal of Neuropathology and Experimental Neurology   73 ( 1 )   30 - 38   2014.1

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  • 著明な筋痙攣・線維束性収縮を伴い抗VGKC複合体抗体が高値であった筋萎縮性側索硬化症の1剖検例 Reviewed

    佐藤晶, 酒井直子, 新保淳輔, 橋立英樹, 五十嵐修一, 柿田明美, 山崎元義

    臨床神経   54 ( 1 )   32 - 37   2014.1

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  • FUS colocalizes with polyglutamine, but not with TDP-43 in neuronal intranuclear inclusions in spinocerebellar ataxia type 2 Reviewed

    F. Mori, Y. Toyoshima, K. Tanji, A. Kakita, H. Takahashi, K. Wakabayashi

    Neuropathology and Applied Neurobiology   40 ( 3 )   351 - 355   2014

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  • Histopathologic features of glia in human epileptogenic brain lesions Reviewed

    Akiyoshi Kakita

    Clinical Neurology   54 ( 12 )   1136 - 1138   2014

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    DOI: 10.5692/clinicalneurol.54.1136

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  • Hypertrophic pachymeningitis: Significance of myeloperoxidase anti-neutrophil cytoplasmic antibody Reviewed

    Akiko Yokoseki, Etsuji Saji, Musashi Arakawa, Takayuki Kosaka, Mariko Hokari, Yasuko Toyoshima, Kouichirou Okamoto, Shigeki Takeda, Kazuhiro Sanpei, Hirotoshi Kikuchi, Shunsei Hirohata, Kouhei Akazawa, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa, Izumi Kawachi

    Brain   137 ( 2 )   520 - 536   2014

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  • Lack of genetic association between TREM2 and late-onset Alzheimer's disease in a Japanese population. Reviewed International journal

    Akinori Miyashita, Yanan Wen, Nobutaka Kitamura, Etsuro Matsubara, Takeshi Kawarabayashi, Mikio Shoji, Naoki Tomita, Katsutoshi Furukawa, Hiroyuki Arai, Takashi Asada, Yasuo Harigaya, Masaki Ikeda, Masakuni Amari, Haruo Hanyu, Susumu Higuchi, Masatoyo Nishizawa, Masaichi Suga, Yasuhiro Kawase, Hiroyasu Akatsu, Masaki Imagawa, Tsuyoshi Hamaguchi, Masahito Yamada, Takashi Morihara, Masatoshi Takeda, Takeo Takao, Kenji Nakata, Ken Sasaki, Ken Watanabe, Kenji Nakashima, Katsuya Urakami, Terumi Ooya, Mitsuo Takahashi, Takefumi Yuzuriha, Kayoko Serikawa, Seishi Yoshimoto, Ryuji Nakagawa, Yuko Saito, Hiroyuki Hatsuta, Shigeo Murayama, Akiyoshi Kakita, Hitoshi Takahashi, Haruyasu Yamaguchi, Kohei Akazawa, Ichiro Kanazawa, Yasuo Ihara, Takeshi Ikeuchi, Ryozo Kuwano

    Journal of Alzheimer's disease : JAD   41 ( 4 )   1031 - 8   2014

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    Rare non-synonymous variants of TREM2 have recently been shown to be associated with Alzheimer's disease (AD) in Caucasians. We here conducted a replication study using a well-characterized Japanese sample set, comprising 2,190 late-onset AD (LOAD) cases and 2,498 controls. We genotyped 10 non-synonymous variants (Q33X, Y38C, R47H, T66M, N68K, D87N, T96K, R98W, H157Y, and L211P) of TREM2 reported by Guerreiro et al. (2013) by means of the TaqMan and dideoxy sequencing methods. Only three variants, R47H, H157Y, and L211P, were polymorphic (range of minor allele frequency [MAF], 0.0002-0.0059); however, no significant association with LOAD was observed in these variants. Considering low MAF of variants examined and our study sample size, further genetic analysis with a larger sample set is needed to firmly evaluate whether or not TREM2 is associated with LOAD in Japanese.

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  • Aberration of the spliceosome in amyotrophic lateral sclerosis Reviewed

    Tomohiko Ishihara, Akiyoshi Kakita, Hitoshi Takahashi, Osamu Onodera, Masatoyo Nishizawa

    Clinical Neurology   54 ( 12 )   1155 - 1157   2014

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    DOI: 10.5692/clinicalneurol.54.1155

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  • Analysis of microRNA from archived formalin-fixed paraffin-embedded specimens of amyotrophic lateral sclerosis Reviewed

    Koichi Wakabayashi, Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Jun Utsumi, Hidenao Sasaki

    ACTA NEUROPATHOLOGICA COMMUNICATIONS   2 ( 1 )   173   2014

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  • Accumulation of 2-hydroxyglutarate in gliomas correlates with survival: a study by 3.0-tesla magnetic resonance spectroscopy Reviewed

    Manabu Natsumeda, Hironaka Igarashi, Toshiharu Nomura, Ryosuke Ogura, Yoshihiro Tsukamoto, Tsutomu Kobayashi, Hiroshi Aoki, Kouichirou Okamoto, Akiyoshi Kakita, Hitoshi Takahashi, Tsutomu Nakada, Yukihiko Fujii

    ACTA NEUROPATHOLOGICA COMMUNICATIONS   2 ( 1 )   158   2014

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  • An autopsy case of amyotrophic lateral sclerosis with prominent muscle cramps, fasciculation, and high titer of anti-voltage gated potassium channel (VGKC) complex antibody Reviewed

    Aki Sato, Naoko Sakai, Junsuke Shinbo, Hideki Hashidate, Shuichi Igarashi, Akiyoshi Kakita, Motoyoshi Yamazaki

    Clinical Neurology   54 ( 1 )   32 - 37   2014

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    DOI: 10.5692/clinicalneurol.54.32

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  • Phosphorylation of serine 349 of p62 in Alzheimer's disease brain Reviewed

    Kunikazu Tanji, Yasuo Miki, Taku Ozaki, Atsushi Maruyama, Hidemi Yoshida, Junsei Mimura, Tomoh Matsumiya, Fumiaki Mori, Tadaatsu Imaizumi, Ken Itoh, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    ACTA NEUROPATHOLOGICA COMMUNICATIONS   2 ( 1 )   50   2014

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  • Valosin-containing protein immunoreactivity in tauopathies, synucleinopathies, polyglutamine diseases and intranuclear inclusion body disease Reviewed

    Fumiaki Mori, Kunikazu Tanji, Yasuko Toyoshima, Hidenao Sasaki, Mari Yoshida, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROPATHOLOGY   33 ( 6 )   637 - 644   2013.12

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  • Oligodendroglioma (WHO grade I) in a young epilepsy patient: A specific entity lying within the spectrum of dysembryoplastic neuroepithelial tumor? Reviewed

    Hitoshi Takahashi, Akiyoshi Kakita, Masaru Tomikawa, Kouichirou Okamoto, Shigeki Kameyama

    NEUROPATHOLOGY   33 ( 6 )   645 - 651   2013.12

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  • 本邦における中枢神経系炎症性脱髄疾患の認知機能障害の特徴

    佐治 越爾, 河内 泉, 荒川 武蔵, 穂苅 万李子, 横関 明子, 豊島 靖子, 赤澤 宏平, 柿田 明美, 高橋 均, 西澤 正豊

    臨床神経学   53 ( 12 )   1627 - 1627   2013.12

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  • 中枢神経系炎症性脱髄疾患の大脳皮質病変の検討

    荒川 武蔵, 河内 泉, 豊島 靖子, 佐治 越爾, 横関 明子, 穂苅 万李子, 柿田 明美, 高橋 均, 西澤 正豊

    臨床神経学   53 ( 12 )   1462 - 1462   2013.12

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  • 本邦の中枢神経系脱髄疾患の大脳皮質病変の検出に3D Double Inversion Recovery法は有用である

    佐治 越爾, 河内 泉, 荒川 武蔵, 横関 明子, 穂苅 万李子, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊

    神経免疫学   18 ( 1 )   128 - 128   2013.11

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  • ANCA関連肥厚性硬膜炎の臨床病理学的特徴

    横関 明子, 河内 泉, 佐治 越爾, 荒川 武蔵, 穂苅 万李子, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊

    神経免疫学   18 ( 1 )   117 - 117   2013.11

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  • Neuromyelitis opticaの中枢神経組織と末梢血における形質芽細胞動態の解析

    荒川 武蔵, 河内 泉, 佐治 越爾, 横関 明子, 穂苅 万李子, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊

    神経免疫学   18 ( 1 )   91 - 91   2013.11

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  • Malignant peripheral nerve sheath tumor of the trigeminal nerve: Clinicopathologic features in a young adult patient Reviewed

    Yoko Nakayama, Masatoshi Watanabe, Kenji Suzuki, Hiroyuki Usuda, Iwao Emura, Ryosuke Ogura, Atsushi Shiga, Yasuko Toyoshima, Hitoshi Takahashi, Tadashi Kawaguchi, Akiyoshi Kakita

    Neuropathology   33 ( 5 )   541 - 546   2013.10

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  • 晩期発症型アルツハイマー病とTREM2の関連解析 Reviewed

    宮下 哲典, 温 雅楠, 初田 裕幸, 村山 繁雄, 山口 晴保, 赤津 裕康, 柿田 明美, 高橋 均, 井原 康夫, 池内 健, 桑野 良三, JGSCAD(The Japanese Genetic Study Consortium for Alzheimer's Disease)

    Dementia Japan   27 ( 4 )   483 - 483   2013.10

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  • Decreased number of Gemini of coiled bodies and U12 snRNA level in amyotrophic lateral sclerosis Reviewed

    Tomohiko Ishihara, Yuko Ariizumi, Atsushi Shiga, Taisuke Kato, Chun-Feng Tan, Tatsuya Sato, Yukari Miki, Mariko Yokoo, Takeshi Fujino, Akihide Koyama, Akio Yokoseki, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi, Osamu Onodera

    HUMAN MOLECULAR GENETICS   22 ( 20 )   4136 - 4147   2013.10

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    DOI: 10.1093/hmg/ddt262

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  • Sporadic ALS with compound heterozygous mutations in the SQSTM1 gene Reviewed

    Hiroshi Shimizu, Yasuko Toyoshima, Atsushi Shiga, Akio Yokoseki, Keiko Arakawa, Yumi Sekine, Takayoshi Shimohata, Takeshi Ikeuchi, Masatoyo Nishizawa, Akiyoshi Kakita, Osamu Onodera, Hitoshi Takahashi

    Acta Neuropathologica   126 ( 3 )   453 - 459   2013.9

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    DOI: 10.1007/s00401-013-1150-5

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  • Surgical pathologic features of cerebral cortical lesions taken from 600 patients with intractable epilepsy Reviewed

    Akiyoshi Kakita

    BRAIN & DEVELOPMENT   35 ( 8 )   793 - 801   2013.9

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    DOI: 10.1016/j.braindev.2013.03.008

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  • 側頭葉てんかんを呈した類上皮腫の3症例

    平石 哲也, 福多 真史, 大石 誠, 高尾 哲郎, 柿田 明美, 藤井 幸彦

    てんかん研究   31 ( 2 )   407 - 407   2013.9

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  • Glioneuonal tumorの周囲脳組織のイメージング解析と病理組織学的所見の検討

    福多 真史, 北浦 弘樹, 大石 誠, 高尾 哲郎, 平石 哲也, 澁木 克栄, 柿田 明美, 藤井 幸彦

    てんかん研究   31 ( 2 )   405 - 405   2013.9

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  • Epstein-Barr virus-associated primary central nervous system cytotoxic T-cell lymphoma Reviewed

    Ryosuke Ogura, Hiroshi Aoki, Manabu Natsumeda, Hiroshi Shimizu, Tsutomu Kobayashi, Tomohisa Saito, Jun Takizawa, Kouichirou Okamoto, Go Hasegawa, Hajime Umezu, Kouichi Ohshima, Hitoshi Takahashi, Yukihiko Fujii, Akiyoshi Kakita

    NEUROPATHOLOGY   33 ( 4 )   436 - 441   2013.8

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    DOI: 10.1111/neup.12005

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  • Transportin 1 accumulates in FUS inclusions in adult-onset ALS without FUS mutation Reviewed

    R. Takeuchi, Y. Toyoshima, M. Tada, A. Shiga, H. Tanaka, M. Shimohata, K. Kimura, T. Morita, A. Kakita, M. Nishizawa, H. Takahashi

    Neuropathology and Applied Neurobiology   39 ( 5 )   580 - 584   2013.8

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    Hiroki Kitaura, Akiyoshi Kakita

    NEUROPATHOLOGY   33 ( 4 )   469 - 474   2013.8

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    DOI: 10.1111/neup.12017

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  • Progressive multifocal leukoencephalopathy developed 26 years after renal transplantation Reviewed

    Shigemi Nagayama, Yuichiro Gondo, Shin-ichi Araya, Naomi Minato, Michiyo Fujita-Nakata, Muichi Kaito, Megumi Nakanishi, Keiko Tanaka, Hideki Yamaya, Hitoshi Yokoyama, Kazuo Nakamichi, Masayuki Saijo, Kouichirou Okamoto, Yasuko Toyoshima, Akiyoshi Kakita, Makoto Matsui

    CLINICAL NEUROLOGY AND NEUROSURGERY   115 ( 8 )   1482 - 1484   2013.8

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    DOI: 10.1016/j.clineuro.2012.11.016

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  • Transient exposure of neonatal mice to neuregulin-1 results in hyperdopaminergic states in adulthood: implication in neurodevelopmental hypothesis for schizophrenia (vol 16, pg 307-320, 2011) Reviewed

    Kato T, Abe Y, Sotoyama H, Kakita A, Kominami R, Hirokawa S, Ozaki M, Takahashi H, Nawa H

    MOLECULAR PSYCHIATRY   18 ( 8 )   951   2013.8

  • Mutations of para-hydroxybenzoate-polyprenyltransferase gene (COQ2) are involved in familial and sporadic multiple system atrophy. Reviewed

    Mitsui J, Matsukawa T, Ishiura H, Fukuda Y, Ichikawa Y, Date H, Ahsan B, Nakahara Y, Momose Y, Takahashi Y, Iwata A, Goto J, Yamamoto Y, Komata M, Shirahige K, Hara K, Kakita A, Yamada M, Takahashi H, Onodera O, Nishizawa M, Takashima H, SatakeW, Toda T, Kuwano R, Watanabe H, Ito M, Sobue G, Soma H, Yabe I, Sasaki H, Aoki M, Ishikawa K, Mizusawa H, Kanai K, Hattori T, Kuwabara S, Arai K, Koyano S, Kuroiwa Y, Hasegawa K, Yuasa T, Yasui K, Nakashima K, Izumi Y, Kaji R, Kato T, Kusunoki S, Osaki Y, Horiuchi M, Kondo T, Murayama S, Dürr A, Brice A, Filla A, Klockgether T, Wüllner U, Nicolson G, Gilman S, Tanner M. C, Kukull A. W, Lee M.-Y. V, Masliah E, Low A. P, Sandroni P, Trojanowski Q. J, Ozelius L, Foroud T, Tsuji S

    The New England Journal of Medicine   369 ( 3 )   233 - 244   2013.7

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    The multiple-Ststem Atrophy Research Collaboration.

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  • Neurobehavioral deficits of epidermal growth factor-overexpressing transgenic mice: impact on dopamine metabolism. Reviewed

    Eda Takeyoshi, Mizuno Makoto, Araki Kazuaki, Iwakura Yuriko, Namba Hisaaki, Sotoyama Hidekazu, Kakita Akiyoshi, Takahashi Hitoshi, Satoh Hiroshi, Chan Siu-Yuen, Nawa Hiroyuki

    Neurosci Lett   547   21 - 25   2013.6

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    Epidermal growth factor (EGF) and its family member neuregulin-1 are implicated in the etiology of schizophrenia. Our recent pharmacological studies indicate that EGF injections to neonatal and adult rats both induce neurobehavioral deficits relevant to schizophrenia. We, however, did not evaluate the genetic impact of EGF transgene on neurobehavioral traits. Here we analyzed transgenic mice carrying the transgene of mouse EGF cDNA. As compared to control littermates, heterozygous EGF transgenic mice had an increase in EGF mRNA levels and showed significant decreases in prepulse inhibition and context-dependent fear learning, but there were no changes in locomotor behaviors and sound startle responses. In addition, these transgenic mice exhibited higher behavioral sensitivity to the repeated cocaine injections. There were neurochemical alterations in metabolic enzymes of dopamine (i.e., tyrosine hydroxylase, dopa decarboxylase, catechol-O-methyl transferase) and monoamine contents in various brain regions of the EGF transgenic mice, but there were no apparent neuropathological signs in the brain. The present findings rule out the indirect influence of anti-EGF antibody production

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  • MRIで髄膜造影を呈し脳生検で診断した脳アミロイドβ関連血管炎の1例 Reviewed

    小池佑佳, 大内東香, 佐藤朋江, 新保淳輔, 佐藤晶, 佐々木修, 渋谷宏行, 岡本浩一郎, 柿田明美, 五十嵐修一

    Brain and Nerve   65 ( 6 )   693 - 697   2013.6

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  • Amyloid beta-related angiitis: Brain lesions showing leptomeningeal gadolinium enhancement on MRI and characteristic surgical pathologic features Reviewed

    Yuka Koike, Haruka Ouchi, Tomoe Sato, Junsuke Shimbo, Aki Sato, Osamu Sasaki, Hiroyuki Shibuya, Kouichirou Okamoto, Akiyoshi Kakita, Shuichi Igarashi

    Brain and Nerve   65 ( 6 )   693 - 697   2013.6

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  • Neurobehavioral deficits of epidermal growth factor-overexpressing transgenic mice: Impact on dopamine metabolism Reviewed

    Takeyoshi Eda, Makoto Mizuno, Kazuaki Araki, Yuriko Iwakura, Hisaaki Namba, Hidekazu Sotoyama, Akiyoshi Kakita, Hitoshi Takahashi, Hiroshi Satoh, Siu-Yuen Chan, Hiroyuki Nawa

    NEUROSCIENCE LETTERS   547   21 - 25   2013.6

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  • Cerebral astroblastoma in an adult: An immunohistochemical, ultrastructural and genetic study Reviewed

    Yong-Juan Fu, Yoshinori Taniguchi, Shigekazu Takeuchi, Atsushi Shiga, Kouichirou Okamoto, Junko Hirato, Sumihito Nobusawa, Yoichi Nakazato, Akiyoshi Kakita, Hitoshi Takahashi

    Neuropathology   33 ( 3 )   312 - 319   2013.6

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    DOI: 10.1111/j.1440-1789.2012.01351.x

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  • てんかん外科病理学の実際 Reviewed

    柿田 明美

    新潟医学会誌   127 ( 5 )   221 - 237   2013.5

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  • Suppressed expression of autophagosomal protein LC3 in cortical tubers of tuberous sclerosis complex Reviewed

    Hiroaki Miyahara, Manabu Natsumeda, Atsushi Shiga, Hiroshi Aoki, Yasuko Toyoshima, Yingjun Zheng, Ryoko Takeuchi, Hiroatsu Murakami, Hiroshi Masuda, Shigeki Kameyama, Tatsuro Izumi, Yukihiko Fujii, Hitoshi Takahashi, Akiyoshi Kakita

    Brain Pathology   23 ( 3 )   254 - 262   2013.5

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    DOI: 10.1111/j.1750-3639.2012.00634.x

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  • 脱髄・髄鞘障害性疾患 Reviewed

    柿田 明美

    第9回神経病理コアカリキュラム教育セミナー   86 - 95   2013.4

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  • Progression of paralysis is the most useful factor for differentiating malignant from benign intramedullary tumors Reviewed

    T. Ito, K. Sawakami, S. Ishikawa, T. Hirano, N. Endo, A. Kakita, H. Takahashi

    SPINAL CORD   51 ( 4 )   319 - 321   2013.4

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  • Plasma matrix metalloproteinase-3 correlates with the clinical severity in men with multiple system atrophy. Reviewed

    Sasaki H, Matsushima M, Hama Y, Sakushima K, Nakamura M, Yabe I, Oba K, Tanji K, Mori F, Wakabayashi K, Kakita A, Takahashi H, Utsumi J

    Neurology and Clinical Neuroscience   1 ( 2 )   69 - 77   2013.3

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  • Selenomethionine Protects against Neuronal Degeneration by Methylmercury in the Developing Rat Cerebrum Reviewed

    Mineshi Sakamoto, Akira Yasutake, Akiyoshi Kakita, Masae Ryufuku, Hing Man Chan, Megumi Yamamoto, Sanae Oumi, Sayaka Kobayashi, Chiho Watanabe

    ENVIRONMENTAL SCIENCE & TECHNOLOGY   47 ( 6 )   2862 - 2868   2013.3

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  • Significance of horizontal propagation of synchronized activities in human epileptic neocortex investigated by optical imaging and immunohistological study Reviewed

    Tetsuya Hiraishi, Hiroki Kitaura, Makoto Oishi, Masafumi Fukuda, Shigeki Kameyama, Hitoshi Takahashi, Akiyoshi Kakita, Yukihiko Fujii

    Epilepsy Research   104 ( 1-2 )   59 - 67   2013.3

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    DOI: 10.1016/j.eplepsyres.2012.09.014

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  • Hereditary Diffuse Leukoencephalopathy with Spheroids (HDLS): Clinical Characteristics and Molecular Analyses of CSF-1R Reviewed

    Konno Takuya, Tada Masayoshi, Koyama Akihide, Tada Mari, Sugai Akihiro, Nozaki Hiroaki, Matsunaga Akiko, Harigaya Yasuo, Nishimiya Jin, Ishihara Kenji, Yoneda Makoto, Kakita Akiyoshi, Takahashi Hitoshi, Kawamura Mitsuru, Onodera Osamu, Nishizawa Masatoyo, Ikeuchi Takeshi

    NEUROLOGY   80   2013.2

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  • DPP6 as a candidate gene for neuroleptic-induced tardive dyskinesia Reviewed

    S. Tanaka, A. Syu, H. Ishiguro, T. Inada, Y. Horiuchi, M. Ishikawa, M. Koga, E. Noguchi, N. Ozaki, T. Someya, A. Kakita, H. Takahashi, H. Nawa, T. Arinami

    Pharmacogenomics Journal   13 ( 1 )   27 - 34   2013.2

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    DOI: 10.1038/tpj.2011.36

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  • DPP6 as a candidate gene for neuroleptic-induced tardive dyskinesia Reviewed

    S. Tanaka, A. Syu, H. Ishiguro, T. Inada, Y. Horiuchi, M. Ishikawa, M. Koga, E. Noguchi, N. Ozaki, T. Someya, A. Kakita, H. Takahashi, H. Nawa, T. Arinami

    PHARMACOGENOMICS JOURNAL   13 ( 1 )   27 - 34   2013.2

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  • Brain expression level and activity of HDAC6 protein in neurodegenerative dementia. Reviewed International journal

    Saori Odagiri, Kunikazu Tanji, Fumiaki Mori, Yasuo Miki, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    Biochemical and biophysical research communications   430 ( 1 )   394 - 9   2013.1

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    Histone deacetylase 6 (HDAC6) is a multifunctional cytoplasmic protein that plays an especially critical role in the formation of aggresomes, where aggregates of excess protein are deposited. Previous immunohistochemical studies have shown that HDAC6 accumulates in Lewy bodies in Parkinson's disease and dementia with Lewy bodies (DLB) as well as in glial cytoplasmic inclusions in multiple system atrophy (MSA). However, it is uncertain whether the level and activity of HDAC6 are altered in the brains of patients with neurodegenerative dementia. In the present study, we demonstrated that the level of HDAC6 was not altered in the temporal cortex of patients with Alzheimer's disease and DLB in comparison with controls. In contrast, the level of HDAC6 was significantly increased in the temporal cortex of patients with frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP) and in the cerebellar white matter of patients with MSA. However, the level of acetylated α-tubulin, one of the substrates of HDAC6, was not altered in FTLD-TDP and MSA relative to controls. These findings suggest that the induced level of HDAC6 in the brain is insufficient for manifestation of its activity in FTLD-TDP and MSA.

    DOI: 10.1016/j.bbrc.2012.11.034

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  • Epilepsy Japan Speaks Reviewed

    KAKITA Akiyoshi

    International Epilepsy News   183   10 - 11   2013.1

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  • Alteration of autophagosomal proteins in the brain of multiple system atrophy Reviewed

    Kunikazu Tanji, Saori Odagiri, Atsushi Maruyama, Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    Neurobiology of Disease   49 ( 1 )   190 - 198   2013.1

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    DOI: 10.1016/j.nbd.2012.08.017

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  • Cognitive impairment and cortical degeneration in neuromyelitis optica Reviewed

    Etsuji Saji, Musashi Arakawa, Kaori Yanagawa, Yasuko Toyoshima, Akiko Yokoseki, Kouichirou Okamoto, Mika Otsuki, Kohei Akazawa, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa, Izumi Kawachi

    Annals of Neurology   73 ( 1 )   65 - 76   2013.1

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    DOI: 10.1002/ana.23721

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  • Cognitive Impairment and Cortical Degeneration in Neuromyelitis Optica Reviewed

    Etsuji Saji, Musashi Arakawa, Kaori Yanagawa, Yasuko Toyoshima, Akiko Yokoseki, Kouichirou Okamoto, Mika Otsuki, Kohei Akazawa, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa, Izumi Kawachi

    ANNALS OF NEUROLOGY   73 ( 1 )   65 - 76   2013.1

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  • Keap1 Is Localized in Neuronal and Glial Cytoplasmic Inclusions in Various Neurodegenerative Diseases Reviewed

    Kunikazu Tanji, Atsushi Maruyama, Saori Odagiri, Fumiaki Mori, Ken Itoh, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY   72 ( 1 )   18 - 28   2013.1

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    DOI: 10.1097/NEN.0b013e31827b5713

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  • Phenotypic Spectrum of COL4A1 Mutations: Porencephaly to Schizencephaly Reviewed

    Yuriko Yoneda, Kazuhiro Haginoya, Mitsuhiro Kato, Hitoshi Osaka, Kenji Yokochi, Hiroshi Arai, Akiyoshi Kakita, Takamichi Yamamoto, Yoshiro Otsuki, Shin-ichi Shimizu, Takahito Wada, Norihisa Koyama, Yoichi Mino, Noriko Kondo, Satoru Takahashi, Shinichi Hirabayashi, Jun-ichi Takanashi, Akihisa Okumura, Toshiyuki Kumagai, Satori Hirai, Makoto Nabetani, Shinji Saitoh, Ayako Hattori, Mami Yamasaki, Akira Kumakura, Yoshinobu Sugo, Kiyomi Nishiyama, Satoko Miyatake, Yoshinori Tsurusaki, Hiroshi Doi, Noriko Miyake, Naomichi Matsumoto, Hirotomo Saitsu

    ANNALS OF NEUROLOGY   73 ( 1 )   48 - 57   2013.1

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  • Electrocorticographic-histopathologic correlations implying epileptogenicity of dysembryoplastic neuroepithelial tumor Reviewed

    Kota Kagawa, Koji Iida, Akiyoshi Kakita, Masaya Katagiri, Takeshi Nishimoto, Akira Hashizume, Yoshihiro Kiura, Ryosuke Hanaya, Kazuhiko Sugiyama, Koji Arihiro, Kazunori Arita, Kaoru Kurisu

    Neurologia Medico-Chirurgica   53 ( 10 )   676 - 687   2013

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    DOI: 10.2176/nmc.oa2012-0420

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  • SORL1 is Genetically Associated with Neuropathologically Characterized Late-Onset Alzheimer's Disease Reviewed

    Yanan Wen, Akinori Miyashita, Nobutaka Kitamura, Tamao Tsukie, Yuko Saito, Hiroyuki Hatsuta, Shigeo Murayama, Akiyoshi Kakita, Hitoshi Takahashi, Hiroyasu Akatsu, Takayuki Yamamoto, Kenji Kosaka, Haruyasu Yamaguchi, Kohei Akazawa, Yasuo Ihara, Ryozo Kuwano

    JOURNAL OF ALZHEIMERS DISEASE   35 ( 2 )   387 - 394   2013

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    DOI: 10.3233/JAD-122395

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  • Phagocytized corpora amylacea as a histological hallmark of astrocytic injury in neuromyelitis optica Reviewed

    Aya Suzuki, Hideaki Yokoo, Akiyoshi Kakita, Hitoshi Takahashi, Yasuo Harigaya, Hayato Ikota, Yoichi Nakazato

    NEUROPATHOLOGY   32 ( 6 )   587 - 594   2012.12

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  • 中枢神経系炎症性脱髄疾患におけるCCR6陽性T細胞の解析

    佐治 越爾, 河内 泉, 荒川 武蔵, 柳川 香織, 横関 明子, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊

    臨床神経学   52 ( 12 )   1399 - 1399   2012.12

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  • Involvement of the ?-Secretase-Mediated EphA4 Signaling Pathway in Synaptic Pathogenesis of Alzheimer's Disease Reviewed

    Chiyuki Matsui, Eiji Inoue, Akiyoshi Kakita, Kohei Arita, Maki Deguchi-Tawarada, Aki Togawa, Akio Yamada, Yoshimi Takai, Hitoshi Takahashi

    BRAIN PATHOLOGY   22 ( 6 )   776 - 787   2012.11

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    DOI: 10.1111/j.1750-3639.2012.00587.x

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  • Coexistence of Huntington's disease and amyotrophic lateral sclerosis: a clinicopathologic study Reviewed

    Mari Tada, Elizabeth A. Coon, Alexander P. Osmand, Patricia A. Kirby, Wayne Martin, Marguerite Wieler, Atsushi Shiga, Hiroe Shirasaki, Masayoshi Tada, Takao Makifuchi, Mitsunori Yamada, Akiyoshi Kakita, Masatoyo Nishizawa, Hitoshi Takahashi, Henry L. Paulson

    ACTA NEUROPATHOLOGICA   124 ( 5 )   749 - 760   2012.11

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  • p62/sequestosome 1 binds to TDP-43 in brains with frontotemporal lobar degeneration with TDP-43 inclusions Reviewed

    Kunikazu Tanji, Hai-Xin Zhang, Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    JOURNAL OF NEUROSCIENCE RESEARCH   90 ( 10 )   2034 - 2042   2012.10

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  • Endosomal sorting related protein CHMP2B is localized in Lewy bodies and glial cytoplasmic inclusions in alpha-synucleinopathy Reviewed

    Satoshi Tanikawa, Fumiaki Mori, Kunikazu Tanji, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROSCIENCE LETTERS   527 ( 1 )   16 - 21   2012.10

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  • Analysis of Chromosome 19q13.42 Amplification in Embryonal Brain Tumors with Ependymoblastic Multilayered Rosettes Reviewed

    Sumihito Nobusawa, Hideaki Yokoo, Junko Hirato, Akiyoshi Kakita, Hitoshi Takahashi, Takashi Sugino, Kazuhiro Tasaki, Hideaki Itoh, Tsutomu Hatori, Yoshie Shimoyama, Atsuko Nakazawa, Shigeru Nishizawa, Hiroshi Kishimoto, Keiko Matsuoka, Masahiro Nakayama, Naoki Okura, Yoichi Nakazato

    BRAIN PATHOLOGY   22 ( 5 )   689 - 697   2012.9

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  • ブレインバンク:ローカルな活動からグローバルな役割を.―新潟大学脳研究所の取り組み― Reviewed

    柿田 明美

    新潟県医師会報   ( 750 )   2 - 7   2012.9

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  • Novel pathological abnormalities of deep brain structures including dysplastic neurons in anterior striatum associated with focal cortical dysplasia in epilepsy Clinical article Reviewed

    Takanobu Kaido, Taisuke Otsuki, Akiyoshi Kakita, Kenji Sugai, Yoshiaki Saito, Takafumi Sakakibara, Akio Takahashi, Yuu Kaneko, Yuko Saito, Hitoshi Takahashi, Ryoko Honda, Eiji Nakagawa, Masayuki Sasaki, Masayuki Itoh

    JOURNAL OF NEUROSURGERY-PEDIATRICS   10 ( 3 )   217 - 225   2012.9

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  • てんかんにて発症した海綿状血管腫の周囲脳組織のイメージング解析と病理組織学的所見の検討

    福多 真史, 北浦 弘樹, 大石 誠, 平石 哲也, 澁木 克栄, 柿田 明美, 藤井 幸彦

    てんかん研究   30 ( 2 )   398 - 398   2012.9

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  • NMO Neuromyelitis opticaにおける神経変性機構の検討

    荒川 武蔵, 河内 泉, 豊島 靖子, 佐治 越爾, 柳川 香織, 横関 明子, 柿田 明美, 高橋 均, 西澤 正豊

    日本神経免疫学会学術集会抄録集   24回   58 - 58   2012.9

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  • NMO/筋炎 Neuromyelitis opticaの末梢血CD4陽性T細胞における免疫動態解析

    佐治 越爾, 河内 泉, 荒川 武蔵, 柳川 香織, 横関 明子, 穂苅 万李子, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊

    日本神経免疫学会学術集会抄録集   24回   74 - 74   2012.9

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  • 統合失調症様類似の精神症状を伴ったneuromyelitis opticaの解析

    横関 明子, 河内 泉, 柳川 香織, 佐治 越爾, 荒川 武蔵, 穂苅 万季子, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊

    日本神経免疫学会学術集会抄録集   24回   103 - 103   2012.9

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  • Primary lateral sclerosis: Upper-motor-predominant amyotrophic lateral sclerosis with frontotemporal lobar degeneration - immunohistochemical and biochemical analyses of TDP-43 Reviewed

    Takayuki Kosaka, Yong-Juan Fu, Atsushi Shiga, Haruka Ishidaira, Chun-Feng Tan, Takashi Tani, Ryoko Koike, Osamu Onodera, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    NEUROPATHOLOGY   32 ( 4 )   373 - 384   2012.8

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  • Autophagy-related proteins (p62, NBR1 and LC3) in intranuclear inclusions in neurodegenerative diseases Reviewed

    Fumiaki Mori, Kunikazu Tanji, Saori Odagiri, Yasuko Toyoshima, Mari Yoshida, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROSCIENCE LETTERS   522 ( 2 )   134 - 138   2012.8

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  • Autophagic adapter protein NBR1 is localized in Lewy bodies and glial cytoplasmic inclusions and is involved in aggregate formation in alpha-synucleinopathy Reviewed

    Saori Odagiri, Kunikazu Tanji, Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    ACTA NEUROPATHOLOGICA   124 ( 2 )   173 - 186   2012.8

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  • Alteration of POLDIP3 Splicing Associated with Loss of Function of TDP-43 in Tissues Affected with ALS Reviewed

    Atsushi Shiga, Tomohiko Ishihara, Akinori Miyashita, Misaki Kuwabara, Taisuke Kato, Norihiro Watanabe, Akie Yamahira, Chigusa Kondo, Akio Yokoseki, Masuhiro Takahashi, Ryozo Kuwano, Akiyoshi Kakita, Masatoyo Nishizawa, Hitoshi Takahashi, Osamu Onodera

    PLOS ONE   7 ( 8 )   e43120   2012.8

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  • Characteristics of Aquaporin Expression Surrounding Senile Plaques and Cerebral Amyloid Angiopathy in Alzheimer Disease Reviewed

    Akihiko Hoshi, Teiji Yamamoto, Keiko Shimizu, Yoshikazu Ugawa, Masatoyo Nishizawa, Hitoshi Takahashi, Akiyoshi Kakita

    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY   71 ( 8 )   750 - 759   2012.8

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  • Periventricular nodular heterotopia functionally couples with the overlying hippocampus Reviewed

    Hiroki Kitaura, Makoto Oishi, Nobuyuki Takei, Yong-Juan Fu, Tetsuya Hiraishi, Masafumi Fukuda, Hitoshi Takahashi, Katsuei Shibuki, Yukihiko Fujii, Akiyoshi Kakita

    EPILEPSIA   53 ( 7 )   e127 - e131   2012.7

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  • Periventricular nodular heterotopia functionally couples with the overlying hippocampus

    Hiroki Kitaura, Makoto Oishi, Nobuyuki Takei, Yong-Juan Fu, Tetsuya Hiraishi, Masafumi Fukuda, Hitoshi Takahashi, Katsuei Shibuki, Yukihiko Fujii, Akiyoshi Kakita

    Epilepsia   53 ( 7 )   e127 - e131   2012.7

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  • Dynein and dynactin components modulate neurodegeneration induced by excitotoxicity Reviewed

    Takeshi Fujiwara, Koji Morimoto, Akiyoshi Kakita, Hitoshi Takahashi

    JOURNAL OF NEUROCHEMISTRY   122 ( 1 )   162 - 174   2012.7

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  • Ubiquilin immunoreactivity in cytoplasmic and nuclear inclusions in synucleinopathies, polyglutamine diseases and intranuclear inclusion body disease Reviewed

    Fumiaki Mori, Kunikazu Tanji, Saori Odagiri, Yasuko Toyoshima, Mari Yoshida, Teruaki Ikeda, Hidenao Sasaki, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    ACTA NEUROPATHOLOGICA   124 ( 1 )   149 - 151   2012.7

  • Immunohistochemical analysis of Marinesco bodies, using antibodies against proteins implicated in the ubiquitin-proteasome system, autophagy and aggresome formation Reviewed

    Saori Odagiri, Kunikazu Tanji, Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Tetsu Kamitani, Koichi Wakabayashi

    NEUROPATHOLOGY   32 ( 3 )   261 - 266   2012.6

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  • Optineurin immunoreactivity in neuronal nuclear inclusions of polyglutamine diseases (Huntington's, DRPLA, SCA2, SCA3) and intranuclear inclusion body disease Reviewed

    Fumiaki Mori, Kunikazu Tanji, Yasuko Toyoshima, Mari Yoshida, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    ACTA NEUROPATHOLOGICA   123 ( 5 )   747 - 749   2012.5

  • Lymphoplasmacyte-rich meningioma: A convexity mass with regional enhancement in the adjacent brain parenchyma Reviewed

    Yoko Nakayama, Masatoshi Watanabe, Kenji Suzuki, Hiroyuki Usuda, Iwao Emura, Yasuko Toyoshima, Hitoshi Takahashi, Tadashi Kawaguchi, Akiyoshi Kakita

    NEUROPATHOLOGY   32 ( 2 )   174 - 179   2012.4

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  • Epidermoid cyst involving the medial temporal lobe: Surgical pathologic features of the epileptogenic lesion Reviewed

    Tetsuya Hiraishi, Makoto Oishi, Hiroki Kitaura, Masae Ryufuku, Yong-Juan Fu, Masafumi Fukuda, Hitoshi Takahashi, Yukihiko Fujii, Akiyoshi Kakita

    NEUROPATHOLOGY   32 ( 2 )   196 - 201   2012.4

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  • Profound downregulation of the RNA editing enzyme ADAR2 in ALS spinal motor neurons Reviewed

    Takuto Hideyama, Takenari Yamashita, Hitoshi Aizawa, Shoji Tsuji, Akiyoshi Kakita, Hitoshi Takahashi, Shin Kwak

    NEUROBIOLOGY OF DISEASE   45 ( 3 )   1121 - 1128   2012.3

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  • Co-occurrence of argyrophilic grain disease in sporadic amyotrophic lateral sclerosis Reviewed

    K. Soma, Y. -J. Fu, K. Wakabayashi, O. Onodera, A. Kakita, H. Takahashi

    NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY   38 ( 1 )   54 - 60   2012.2

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  • Vertebral basilar system dolichoectasia with marked infiltration of IgG4-containing plasma cells: A manifestation of IgG4-related disease? Reviewed

    Yasuko Toyoshima, Iwao Emura, Yoshitake Umeda, Nobuya Fujita, Akiyoshi Kakita, Hitoshi Takahashi

    NEUROPATHOLOGY   32 ( 1 )   100 - 104   2012.2

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  • Association of SNPs linked to increased expression of SLC1A1 with schizophrenia. Reviewed International journal

    Yasue Horiuchi, Syuhei Iida, Minori Koga, Hiroki Ishiguro, Yoshimi Iijima, Toshiya Inada, Yuichiro Watanabe, Toshiyuki Someya, Hiroshi Ujike, Nakao Iwata, Norio Ozaki, Hiroshi Kunugi, Mamoru Tochigi, Masanari Itokawa, Makoto Arai, Kazuhiro Niizato, Shuji Iritani, Akiyoshi Kakita, Hitoshi Takahashi, Hiroyuki Nawa, Tadao Arinami

    American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics   159B ( 1 )   30 - 7   2012.1

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  • Association of SNPs linked to increased expression of SLC1A1 with schizophrenia. Reviewed

    Horiuchi Y, Iida S, Koga M, Ishiguro H, Iijima Y, Inada T, Watanabe Y, Someya T, Ujike H, Iwata N, Ozaki N, Kunugi H, Tochigi M, Itokawa M, Arai M, Niizato K, Iritani S, Kakita A, Takahashi H, Nawa H, Arinami T

    American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics   159B ( 1 )   30 - 37   2012.1

  • 脳神経疾患の診断に必須な組織染色 Reviewed

    柿田 明美

    新潟県臨床検査技師会誌   52 ( 1 )   2 - 5   2012.1

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  • Difference in MSA Phenotype Distribution Between Populations: Genetics or Environment? Reviewed

    Tetsutaro Ozawa, Tamas Revesz, Dominic Paviour, Andrew J. Lees, Niall Quinn, Mari Tada, Akiyoshi Kakita, Osamu Onodera, Koichi Wakabayashi, Hitoshi Takahashi, Masatoyo Nishizawa, Janice L. Holton

    JOURNAL OF PARKINSONS DISEASE   2 ( 1 )   7 - 18   2012

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  • Unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve in Parkinson&apos;s disease Reviewed

    S. Orimo, T. Uchihara, T. Kanazawa, Y. Itoh, K. Wakabayashi, A. Kakita, H. Takahashi

    NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY   37 ( 7 )   791 - 802   2011.12

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  • Immunohistochemical expression of fibroblast growth factor-2 in developing human cerebrum and epilepsy-associated malformations of cortical development Reviewed

    Manami Ueda, Chitose Sugiura, Kousaku Ohno, Akiyoshi Kakita, Akira Hori, Eisaku Ohama, Harry V. Vinters, Hajime Miyata

    NEUROPATHOLOGY   31 ( 6 )   589 - 598   2011.12

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  • Accumulation of histone deacetylase 6, an aggresome-related protein, is specific to Lewy bodies and glial cytoplasmic inclusions Reviewed

    Yasuo Miki, Fumiaki Mori, Kunikazu Tanji, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROPATHOLOGY   31 ( 6 )   561 - 568   2011.12

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  • 髄膜形態からみたneuromyelitis opticaの病態形成メカニズムの解析

    柳川 香織, 河内 泉, 豊島 靖子, 横関 明子, 佐治 越爾, 柿田 明美, 高橋 均, 西澤 正豊

    臨床神経学   51 ( 12 )   1235 - 1235   2011.12

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  • スペクトラルドメイン光干渉断層計を使った中枢神経系脱髄疾患の病態メカニズムの解析

    佐治 越爾, 河内 泉, 柳川 香織, 横関 明子, 高木 峰夫, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊

    臨床神経学   51 ( 12 )   1221 - 1221   2011.12

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  • Routine aspiration method during filter-protected carotid stenting: histological evaluation of captured debris and predictors for debris amount Reviewed

    Takatoshi Sorimachi, Akiyoshi Kakita, Kenichi Morita, Kazuhiko Nishino, Osamu Sasaki, Tetsuo Koike, Takashi Kumagai, Yasushi Ito, Yukihiko Fujii

    ACTA NEUROCHIRURGICA   153 ( 11 )   2159 - 2167   2011.11

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  • Hypertrophy of hippocampal end folium neurons in patients with mesial temporal lobe epilepsy Reviewed

    Masae Ryufuku, Yasuko Toyoshima, Hiroki Kitaura, Yingjun Zheng, Yong-Juan Fu, Hiroaki Miyahara, Hiroatsu Murakami, Hiroshi Masuda, Shigeki Kameyama, Hitoshi Takahashi, Akiyoshi Kakita

    NEUROPATHOLOGY   31 ( 5 )   476 - 485   2011.10

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  • Synphilin-1-Binding Protein NUB1 is Colocalized With Nonfibrillar, Proteinase K-Resistant alpha-Synuclein in Presynapses in Lewy Body Disease Reviewed

    Kunikazu Tanji, Fumiaki Mori, Katsumi Kito, Akiyoshi Kakita, Junsei Mimura, Ken Itoh, Hitoshi Takahashi, Tetsu Kamitani, Koichi Wakabayashi

    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY   70 ( 10 )   879 - 889   2011.10

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  • Induction of autophagy in temozolomide treated malignant gliomas Reviewed

    Manabu Natsumeda, Hiroshi Aoki, Hiroaki Miyahara, Naoki Yajima, Takeo Uzuka, Yasuko Toyoshima, Akiyoshi Kakita, Hitoshi Takahashi, Yukihiko Fujii

    NEUROPATHOLOGY   31 ( 5 )   486 - 493   2011.10

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  • フラビン蛋白蛍光イメージング解析により脳室周囲異所性灰白質と側頭葉内側構造の生理学的関連を捉えた側頭葉てんかん手術例

    大石 誠, 北浦 弘樹, 福多 真史, 平石 哲也, 藤井 幸彦, 柿田 明美

    臨床神経生理学   39 ( 5 )   420 - 420   2011.10

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  • Spatiotemporal dynamics of epileptiform propagations: Imaging of human brain slices

    Hiroki Kitaura, Tetsuya Hiraishi, Hiroatsu Murakami, Hiroshi Masuda, Masafumi Fukuda, Makoto Oishi, Masae Ryufuku, Yong-Juan Fu, Hitoshi Takahashi, Shigeki Kameyama, Yukihiko Fujii, Katsuei Shibuki, Akiyoshi Kakita

    NeuroImage   58 ( 1 )   50 - 59   2011.9

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  • Spatiotemporal dynamics of epileptiform propagations: Imaging of human brain slices Reviewed

    Hiroki Kitaura, Tetsuya Hiraishi, Hiroatsu Murakami, Hiroshi Masuda, Masafumi Fukuda, Makoto Oishi, Masae Ryufuku, Yong-Juan Fu, Hitoshi Takahashi, Shigeki Kameyama, Yukihiko Fujii, Katsuei Shibuki, Akiyoshi Kakita

    NEUROIMAGE   58 ( 1 )   50 - 59   2011.9

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  • Spinocerebellar ataxia type 2 (SCA2) is associated with TDP-43 pathology Reviewed

    Yasuko Toyoshima, Hajime Tanaka, Mitsuteru Shimohata, Kakuhei Kimura, Takashi Morita, Akiyoshi Kakita, Hitoshi Takahashi

    ACTA NEUROPATHOLOGICA   122 ( 3 )   375 - 378   2011.9

  • Alteration of autophagosomal proteins (LC3, GABARAP and GATE-16) in Lewy body disease Reviewed

    Kunikazu Tanji, Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROBIOLOGY OF DISEASE   43 ( 3 )   690 - 697   2011.9

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    DOI: 10.1016/j.nbd.2011.05.022

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  • 自然免疫システムからみたneuromyelitis optica脊髄病変の解析

    柳川 香織, 河内 泉, 豊島 靖子, 荒川 武蔵, 横関 明子, 佐治 越爾, 柿田 明美, 高橋 均, 西澤 正豊

    日本神経免疫学会学術集会抄録集   23回   112 - 112   2011.9

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  • Enhancement of native and phosphorylated TDP-43 immunoreactivity by proteinase K treatment following autoclave heating Reviewed

    Fumiaki Mori, Kunikazu Tanji, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROPATHOLOGY   31 ( 4 )   401 - 404   2011.8

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    DOI: 10.1111/j.1440-1789.2010.01184.x

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  • Prenatal Stress Inhibits Neuronal Maturation through Downregulation of Mineralocorticoid Receptors Reviewed

    Makoto Tamura, Mari Sajo, Akiyoshi Kakita, Norio Matsuki, Ryuta Koyama

    JOURNAL OF NEUROSCIENCE   31 ( 32 )   11505 - 11514   2011.8

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    DOI: 10.1523/JNEUROSCI.3447-10.2011

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  • Indication of intraoperative immunohistochemistry for accurate pathological diagnosis of brain tumors Reviewed

    Takeo Uzuka, Hiroshi Aoki, Manabu Natsumeda, Akiyoshi Kakita, Hitoshi Takahashi, Yukihiko Fujii

    BRAIN TUMOR PATHOLOGY   28 ( 3 )   239 - 246   2011.7

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  • Inhibition of VEGF signaling pathway attenuates hemorrhage after tPA treatment Reviewed

    Masato Kanazawa, Hironaka Igarashi, Kunio Kawamura, Tetsuya Takahashi, Akiyoshi Kakita, Hitoshi Takahashi, Tsutomu Nakada, Masatoyo Nishizawa, Takayoshi Shimohata

    JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM   31 ( 6 )   1461 - 1474   2011.6

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    DOI: 10.1038/jcbfm.2011.9

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  • Anaplastic astrocytoma with angiocentric ependymal differentiation Reviewed

    Hiroaki Miyahara, Yasuko Toyoshima, Manabu Natsumeda, Takeo Uzuka, Hiroshi Aoki, Yoko Nakayama, Kouichiou Okamoto, Yukihiko Fujii, Akiyoshi Kakita, Hitoshi Takahashi

    NEUROPATHOLOGY   31 ( 3 )   292 - 298   2011.6

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    DOI: 10.1111/j.1440-1789.2010.01161.x

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  • 脱髄・髄鞘障害性疾患 Reviewed

    柿田 明美

    第7回 神経病理コアカリキュラム教育セミナー ハンドアウト   77 - 85   2011.6

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  • Microglial Cystatin F Expression Is a Sensitive Indicator for Ongoing Demyelination With Concurrent Remyelination Reviewed

    Jianmei Ma, Kenji F. Tanaka, Takahiro Shimizu, Claude C. A. Bernard, Akiyoshi Kakita, Hitoshi Takahashi, Steven E. Pfeiffer, Kazuhiro Ikenaka

    JOURNAL OF NEUROSCIENCE RESEARCH   89 ( 5 )   639 - 649   2011.5

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  • Biochemical and histopathological alterations in TAR DNA-binding protein-43 after acute ischemic stroke in rats Reviewed

    Masato Kanazawa, Akiyoshi Kakita, Hironaka Igarashi, Tetsuya Takahashi, Kunio Kawamura, Hitoshi Takahashi, Tsutomu Nakada, Masatoyo Nishizawa, Takayoshi Shimohata

    JOURNAL OF NEUROCHEMISTRY   116 ( 6 )   957 - 965   2011.3

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    DOI: 10.1111/j.1471-4159.2010.06860.x

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  • Inhibition of VEGF Signaling Pathway Attenuates Hemorrhagic Transformation after tPA Treatment Reviewed

    Takayoshi Shimohata, Niigata Japan, Masato Kanazawa, Hironaka Igarashi, Tetsuya Takahashi, Kunio Kawamura, Akiyoshi Kakita, Hitoshi Takahashi, Tsutomu Nakada, Masatoyo Nishizawa

    NEUROLOGY   76 ( 9 )   A447 - A448   2011.3

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  • Transient exposure of neonatal mice to neuregulin-1 results in hyperdopaminergic states in adulthood: implication in neurodevelopmental hypothesis for schizophrenia Reviewed

    T. Kato, Y. Abe, H. Sotoyama, A. Kakita, R. Kominami, S. Hirokawa, M. Ozaki, H. Takahashi, H. Nawa

    MOLECULAR PSYCHIATRY   16 ( 3 )   307 - 320   2011.3

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  • Transient exposure of neonatal mice to neuregulin-1 results in hyperdopaminergic states in adulthood: Implication in neurodevelopmental hypothesis for schizophrenia Reviewed

    T. Kato, Y. Abe, H. Sotoyama, A. Kakita, R. Kominami, S. Hirokawa, M. Ozaki, H. Takahashi, H. Nawa

    Molecular Psychiatry   16 ( 3 )   307 - 320   2011.3

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  • Survival motor neuron (SMN) protein in the spinal anterior horn cells of patients with sporadic amyotrophic lateral sclerosis Reviewed

    Yingshan Piao, Tomoyo Hashimoto, Sachiko Takahama, Akiyoshi Kakita, Takashi Komori, Takashi Morita, Hitoshi Takahashi, Toshio Mizutani, Kiyomitsu Oyanagi

    BRAIN RESEARCH   1372   152 - 159   2011.2

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    DOI: 10.1016/j.brainres.2010.11.070

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  • Balloon cells in the dentate gyrus in hippocampal sclerosis associated with non-herpetic acute limbic encephalitis Reviewed

    Hiroaki Miyahara, Masae Ryufuku, Yong-Juan Fu, Hiroki Kitaura, Hiroatsu Murakami, Hiroshi Masuda, Shigeki Kameyama, Hitoshi Takahashi, Akiyoshi Kakita

    SEIZURE-EUROPEAN JOURNAL OF EPILEPSY   20 ( 1 )   87 - 89   2011.1

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  • てんかん原性病巣における細胞内情報伝達経路関連蛋白の発現解析 Reviewed

    柿田明美, 鄭 英君, 龍福雅恵, 北浦弘樹, 村上博淳, 増田 浩, 亀山茂樹, 高橋 均, 武井延之

    てんかん治療研究振興財団研究年報 2011   22   31 - 38   2011

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  • 急性脳虚血によるTDP-43の生化学的・組織学的変化の検討 Reviewed

    下畑亨良, 金澤雅人, 柿田明美, 五十嵐博中, 高橋哲哉, 川村邦雄, 高橋 均, 中田 力, 西澤正豊

    脳循環代謝   22 ( 2 )   40 - 45   2011

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  • Widespread ischemic brain lesions caused by vasculopathy associated with neurofibromatosis type 1 Reviewed

    Kenichi Okazaki, Akiyoshi Kakita, Hajime Tanaka, Kakuhei Kimura, Makoto Minagawa, Takashi Morita, Hitoshi Takahashi

    NEUROPATHOLOGY   30 ( 6 )   627 - 633   2010.12

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    DOI: 10.1111/j.1440-1789.2009.01097.x

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  • Neuromyelitis optica spectrum disorderの精神神経症状と高次脳機能障害

    佐治 越爾, 河内 泉, 柳川 香織, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊

    臨床神経学   50 ( 12 )   1211 - 1211   2010.12

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  • The phenotype spectrum of Japanese multiple system atrophy Reviewed

    T. Ozawa, M. Tada, A. Kakita, O. Onodera, M. Tada, T. Ishihara, T. Morita, T. Shimohata, K. Wakabayashi, H. Takahashi, M. Nishizawa

    JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY   81 ( 11 )   1253 - 1255   2010.11

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    DOI: 10.1136/jnnp.2009.182576

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  • TDP-43プロテイノパチーとしてのFTLD/ALS Reviewed

    石原智彦, 有泉優子, 志賀 篤, 横関明男, 佐藤達哉, 豊島靖子, 柿田明美, 高橋 均, 西澤正豊, 小野寺理

    臨床神経   50 ( 11 )   1022 - 1024   2010.11

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    DOI: 10.5692/clinicalneurol.50.1022

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  • TDP-43/ALSの臨床と病理 Reviewed

    小野寺理, 横関明男, 譚 春鳳, 石原智彦, 西平 靖, 豊島靖子, 柿田明美, 西澤正豊, 高橋 均

    臨床神経   50 ( 11 )   940 - 942   2010.11

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    DOI: 10.5692/clinicalneurol.50.940

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  • [FTLD/ALS as TDP-43 proteinopathies]. Reviewed

    Ishihara T, Ariizumi Y, Shiga A, Yokoseki A, Sato T, Toyoshima Y, Kakita A, Takahashi H, Nishizawa M, Onodera O

    Rinsho shinkeigaku = Clinical neurology   50 ( 11 )   1022 - 1024   2010.11

  • てんかん焦点の外科病理2 Reviewed

    柿田 明美

    Epilepsy   4 ( 2 )   80 - 83   2010.11

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  • [Human brain resource--experience at the Brain Research Institute,University of Niigata]. Reviewed

    Kakita A, Takahashi H

    Brain and nerve = Shinkei kenkyu no shinpo   62 ( 10 )   1019 - 1024   2010.10

  • [Human Brain Resource  Experience at the Brain Research Insitute, University of Niigata] Reviewed

    Kakita A, Takahashi H   62 ( 10 )   1019 - 1024   2010.10

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  • Foix-Alajouanine症候群の病理 Reviewed

    松尾宏俊, 柿田明美, 高橋 均

    神経内科   73 ( 3 )   246 - 250   2010.9

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  • 新皮質てんかん病巣における興奮伝播様式の解析 ヒト脳スライス標本を用いた光学的イメージング

    北浦 弘樹, 平石 哲也, 村上 博淳, 増田 浩, 福多 真史, 大石 誠, 龍福 雅恵, 付 永娟, 高橋 均, 亀山 茂樹, 藤井 幸彦, 澁木 克栄, 柿田 明美

    てんかん研究   28 ( 2 )   232 - 233   2010.9

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  • Proteinase K-resistant alpha-synuclein is deposited in presynapses in human Lewy body disease and A53T alpha-synuclein transgenic mice Reviewed

    Kunikazu Tanji, Fumiaki Mori, Junsei Mimura, Ken Itoh, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    ACTA NEUROPATHOLOGICA   120 ( 2 )   145 - 154   2010.8

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  • Renal sclerosing peritubular nodules in a patient with neurofibromatosis type 2: A case report with immunohistochemical and electron microscopic studies. Reviewed

    Morita T, Kimura K, Kakita A

    Human pathology   41 ( 7 )   1051 - 2; author reply 1052   2010.7

  • Sporadic four-repeat tauopathy with frontotemporal lobar degeneration, Parkinsonism, and motor neuron disease: a distinct clinicopathological and biochemical disease entity Reviewed

    Yong-Juan Fu, Yasushi Nishihira, Shigetoshi Kuroda, Yasuko Toyoshima, Tomohiko Ishihara, Makoto Shinozaki, Akinori Miyashita, Yue-Shan Piao, Chun-Feng Tan, Takashi Tani, Ryoko Koike, Keisuke Iwanaga, Mitsuhiro Tsujihata, Osamu Onodera, Ryozo Kuwano, Masatoyo Nishizawa, Akiyoshi Kakita, Takeshi Ikeuchi, Hitoshi Takahashi

    ACTA NEUROPATHOLOGICA   120 ( 1 )   21 - 32   2010.7

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  • Neurocutaneous melanosis: surgical pathological features of an apparently hamartomatous lesion in the amygdala Case report Reviewed

    Yong-Juan Fu, Nobuhito Morota, Atsuko Nakagawa, Hitoshi Takahashi, Akiyoshi Kakita

    JOURNAL OF NEUROSURGERY-PEDIATRICS   6 ( 1 )   82 - 86   2010.7

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    DOI: 10.3171/2010.3.PEDS1025

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  • Supportive evidence for reduced expression of GNB1L in schizophrenia. Reviewed

    Ishiguro Hiroki, Koga Minori, Horiuchi Yasue, Noguchi Emiko, Morikawa Miyuki, Suzuki Yoshimi, Arai Makoto, Niizato Kazuhiro, Iritani Shyuji, Itokawa Masanari, Inada Toshiya, Iwata Nakao, Ozaki Norio, Ujike Hiroshi, Kunugi Hiroshi, Sasaki Tsukasa, Takahashi Makoto, Watanabe Yuichiro, Someya Toshiyuki, Kakita Akiyoshi, Takahashi Hitoshi, Nawa Hiroyuki, Arinami Tadao

    Schizophr Bull   36 ( 4 )   756 - 765   2010.7

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  • Supportive evidence for reduced expression of GNB1L in schizophrenia Reviewed

    Hiroki Ishiguro, Minori Koga, Yasue Horiuchi, Emiko Noguchi, Miyuki Morikawa, Yoshimi Suzuki, Makoto Arai, Kazuhiro Niizato, Shyuji Iritani, Masanari Itokawa, Toshiya Inada, Nakao Iwata, Norio Ozaki, Hiroshi Ujike, Hiroshi Kunugi, Tsukasa Sasaki, Makoto Takahashi, Yuichiro Watanabe, Toshiyuki Someya, Akiyoshi Kakita, Hitoshi Takahashi, Hiroyuki Nawa, Tadao Arinami

    Schizophrenia Bulletin   36 ( 4 )   756 - 765   2010.7

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  • Relationship between Bunina bodies and TDP-43 inclusions in spinal anterior horn in amyotrophic lateral sclerosis Reviewed

    F. Mori, K. Tanji, Y. Miki, A. Kakita, H. Takahashi, K. Wakabayashi

    NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY   36 ( 4 )   345 - 352   2010.6

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    DOI: 10.1111/j.1365-2990.2010.01081.x

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  • Brain cannabinoid CB2 receptor in schizophrenia. Reviewed

    Ishiguro Hiroki, Horiuchi Yasue, Ishikawa Maya, Koga Minori, Imai Keiko, Suzuki Yoshimi, Morikawa Miyuki, Inada Toshiya, Watanabe Yuichiro, Takahashi Makoto, Someya Toshiyuki, Ujike Hiroshi, Iwata Nakao, Ozaki Norio, Onaivi Emmanuel S, Kunugi Hiroshi, Sasaki Tsukasa, Itokawa Masanari, Arai Makoto, Niizato Kazuhiro, Iritani Shyuji, Naka Izumi, Ohashi Jun, Kakita Akiyoshi, Takahashi Hitoshi, Nawa Hiroyuki, Arinami Tadao

    Biol Psychiatry   67 ( 10 )   974 - 982   2010.5

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    DOI: 10.1016/j.biopsych.2009.09.024

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  • Brain Cannabinoid CB2 Receptor in Schizophrenia Reviewed

    Hiroki Ishiguro, Yasue Horiuchi, Maya Ishikawa, Minori Koga, Keiko Imai, Yoshimi Suzuki, Miyuki Morikawa, Toshiya Inada, Yuichiro Watanabe, Makoto Takahashi, Toshiyuki Someya, Hiroshi Ujike, Nakao Iwata, Norio Ozaki, Emmanuel S. Onaivi, Hiroshi Kunugi, Tsukasa Sasaki, Masanari Itokawa, Makoto Arai, Kazuhiro Niizato, Shyuji Iritani, Izumi Naka, Jun Ohashi, Akiyoshi Kakita, Hitoshi Takahashi, Hiroyuki Nawa, Tadao Arinami

    Biological Psychiatry   67 ( 10 )   974 - 982   2010.5

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  • てんかん焦点の外科病理 1 Reviewed

    柿田 明美

    Epilepsy   4 ( 1 )   4 - 6   2010.5

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  • Anterior striatum with dysmorphic neurons associated with the epileptogenesis of focal cortical dysplasia Reviewed

    Takanobu Kaido, Taisuke Otsuki, Yuu Kaneko, Akio Takahashi, Akiyoshi Kakita, Hitoshi Takahashi, Yoshiaki Saito, Eiji Nakagawa, Kenji Sugai, Masayuki Sasaki

    SEIZURE-EUROPEAN JOURNAL OF EPILEPSY   19 ( 4 )   256 - 259   2010.5

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    DOI: 10.1016/j.seizure.2010.02.003

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  • TRIM9, a novel brain-specific E3 ubiquitin ligase, is repressed in the brain of Parkinson&apos;s disease and dementia with Lewy bodies Reviewed

    Kunikazu Tanji, Tetsu Kamitani, Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROBIOLOGY OF DISEASE   38 ( 2 )   210 - 218   2010.5

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    DOI: 10.1016/j.nbd.2010.01.007

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  • 大脳皮質・白質を侵すdiffuse astrocytomaを背景に、angiocentric glioma様組織像を示した1生検例

    宮原 弘明, 豊島 靖子, 宇塚 岳夫, 青木 洋, 中山 遙子, 柿田 明美, 高橋 均

    Brain Tumor Pathology   27 ( Suppl. )   126 - 126   2010.5

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  • Association of the HSPG2 gene with neuroleptic-induced tardive dyskinesia. Reviewed

    Syu Aoi, Ishiguro Hiroki, Inada Toshiya, Horiuchi Yasue, Tanaka Syunsuke, Ishikawa Maya, Arai Makoto, Itokawa Masanari, Niizato Kazuhiro, Iritani Shuji, Ozaki Norio, Takahashi Makoto, Kakita Akiyoshi, Takahashi Hitoshi, Nawa Hiroyuki, Keino-Masu Kazuko, Arikawa-Hirasawa Eri, Arinami Tadao

    Neuropsychopharmacology   35 ( 5 )   1155 - 1164   2010.4

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    DOI: 10.1038/npp.2009.220

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  • Association of the HSPG2 Gene with Neuroleptic-Induced Tardive Dyskinesia Reviewed

    Aoi Syu, Hiroki Ishiguro, Toshiya Inada, Yasue Horiuchi, Syunsuke Tanaka, Maya Ishikawa, Makoto Arai, Masanari Itokawa, Kazuhiro Niizato, Shuji Iritani, Norio Ozaki, Makoto Takahashi, Akiyoshi Kakita, Hitoshi Takahashi, Hiroyuki Nawa, Kazuko Keino-Masu, Eri Arikawa-Hirasawa, Tadao Arinami

    NEUROPSYCHOPHARMACOLOGY   35 ( 5 )   1155 - 1164   2010.4

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  • Increased expression and activation of cytosolic phospholipase A(2) in the spinal cord of patients with sporadic amyotrophic lateral sclerosis Reviewed

    Noriyuki Shibata, Akiyoshi Kakita, Hitoshi Takahashi, Yuetsu Ihara, Keigo Nobukuni, Harutoshi Fujimura, Saburo Sakoda, Makio Kobayashi

    ACTA NEUROPATHOLOGICA   119 ( 3 )   345 - 354   2010.3

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  • MS/NMO リンパ球浸潤形態からみたneuromyelitis opticaの脊髄病変

    河内 泉, 柳川 香織, 豊島 靖子, 佐治 越爾, 柿田 明美, 高橋 均, 西澤 正豊

    日本神経免疫学会学術集会抄録集   22回   39 - 39   2010.3

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  • Molecular characterization and gene disruption of a novel zinc-finger protein, HIT-4, expressed in rodent brain Reviewed

    Yasutaka Tanabe, Akiko Hirano, Takuji Iwasato, Shigeyoshi Itohara, Kazuaki Araki, Tsuyoshi Yamaguchi, Tomio Ichikawa, Toshiro Kumanishi, Yoshifusa Aizawa, Hitoshi Takahashi, Akiyoshi Kakita, Hiroyuki Nawa

    Journal of Neurochemistry   112 ( 4 )   1035 - 1044   2010.2

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  • Molecular characterization and gene disruption of a novel zinc-finger protein, HIT-4, expressed in rodent brain Reviewed

    Yasutaka Tanabe, Akiko Hirano, Takuji Iwasato, Shigeyoshi Itohara, Kazuaki Araki, Tsuyoshi Yamaguchi, Tomio Ichikawa, Toshiro Kumanishi, Yoshifusa Aizawa, Hitoshi Takahashi, Akiyoshi Kakita, Hiroyuki Nawa

    JOURNAL OF NEUROCHEMISTRY   112 ( 4 )   1035 - 1044   2010.2

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  • Ictal bradycardia in an infant following surgical treatment for hemimegalencephaly Reviewed

    Hiroaki Miyahara, Kouji Sonoda, Naho Okazaki, Kazuhito Sekiguchi, Tatsuya Kawano, Kensuke Akiyoshi, Tomoki Maeda, Tatsuro Izumi

    PEDIATRICS INTERNATIONAL   52 ( 1 )   156 - 157   2010.2

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    DOI: 10.1111/j.1442-200X.2009.02982.x

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  • Increased Levels of Soluble LR11 in Cerebrospinal Fluid of Patients with Alzheimer Disease Reviewed

    Takeshi Ikeuchi, Satoshi Hirayama, Takashi Miida, Isamu Fukamachi, Takayoshi Tokutake, Hiroyuki Ebinuma, Kohei Takubo, Hiroyuki Kaneko, Kensaku Kasuga, Akiyoshi Kakita, Hitoshi Takahashi, Hideaki Bujo, Yasushi Saito, Masatoyo Nishizawa

    DEMENTIA AND GERIATRIC COGNITIVE DISORDERS   30 ( 1 )   28 - 32   2010

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    DOI: 10.1159/000315539

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  • The clinical and pathological spectrum of TDP-43 associated ALS Reviewed

    Osamu Onodera, AMo Yokoseki, Chun-Feng Tan, Tomohiko Ishihara, Yasushi Nishiira, Yasuko Toyoshima, AMyoshi Kakita, Masatoyo Nishizawa, Hitoshi Takahashi

    Clinical Neurology   50 ( 11 )   940 - 942   2010

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    DOI: 10.5692/clinicalneurol.50.940

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  • Persistent cleavage and nuclear translocation of apoptosis-inducing factor in motor neurons in the spinal cord of sporadic amyotrophic lateral sclerosis patients Reviewed

    Noriyuki Shibata, Akiyoshi Kakita, Hitoshi Takahashi, Yuetsu Ihara, Keigo Nobukuni, Harutoshi Fujimura, Saburo Sakoda, Shoichi Sasaki, Tomoko Yamamoto, Makio Kobayashi

    ACTA NEUROPATHOLOGICA   118 ( 6 )   755 - 762   2009.12

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    DOI: 10.1007/s00401-009-0580-6

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  • Isolation and Characterization of Patient-derived, Toxic, High Mass Amyloid beta-Protein (A beta) Assembly from Alzheimer Disease Brains Reviewed

    Akihiko Noguchi, Satoko Matsumura, Mari Dezawa, Mari Tada, Masako Yanazawa, Akane Ito, Manami Akioka, Satoru Kikuchi, Michio Sato, Shouji Ideno, Munehiro Noda, Atsushi Fukunari, Shin-ichi Muramatsu, Yutaka Itokazu, Kazuki Sato, Hitoshi Takahashi, David B. Teplow, Yo-ichi Nabeshima, Akiyoshi Kakita, Kazutomo Imahori, Minako Hoshi

    JOURNAL OF BIOLOGICAL CHEMISTRY   284 ( 47 )   32895 - 32905   2009.11

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    DOI: 10.1074/jbc.M109.000208

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  • Neuropathological similarities and differences between frontotemporal lobar degeneration with ubiquitin inclusions and amyotrophic lateral sclerosis with dementia Reviewed

    Chun-Feng Tan, Yasuko Toyoshima, Akiyoshi Kakita, Hitoshi Takahashi

    Brain and Nerve   61 ( 11 )   1319 - 1327   2009.11

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  • Pathologic and immunologic profiles of a limited form of neuromyelitis optica with myelitis Reviewed

    K. Yanagawa, I. Kawachi, Y. Toyoshima, A. Yokoseki, M. Arakawa, A. Hasegawa, T. Ito, N. Kojima, R. Koike, K. Tanaka, T. Kosaka, C. -F. Tan, A. Kakita, K. Okamoto, M. Tsujita, K. Sakimura, H. Takahashi, M. Nishizawa

    NEUROLOGY   73 ( 20 )   1628 - 1637   2009.11

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    DOI: 10.1212/WNL.0b013e3181c1deb9

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  • Selective occurrence of TDP-43-immunoreactive inclusions in the lower motor neurons in Machado-Joseph disease Reviewed

    Chun-Feng Tan, Mitsunori Yamada, Yasuko Toyoshima, Akio Yokoseki, Yukari Miki, Yasuhiro Hoshi, Hiroyuki Kaneko, Takeshi Ikeuchi, Osamu Onodera, Akiyoshi Kakita, Hitoshi Takahashi

    ACTA NEUROPATHOLOGICA   118 ( 4 )   553 - 560   2009.10

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    DOI: 10.1007/s00401-009-0552-x

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  • Cerebellar Involvement in Progressive Supranuclear Palsy: A Clinicopathological Study Reviewed

    Masato Kanazawa, Takayoshi Shimohata, Yasuko Toyoshima, Mari Tada, Akiyoshi Kakita, Takashi Morita, Tetsutaro Ozawa, Hitoshi Takahashi, Masatoyo Nishizawa

    MOVEMENT DISORDERS   24 ( 9 )   1312 - 1318   2009.7

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  • Depletion of medullary serotonergic neurons in patients with multiple system atrophy who succumbed to sudden death Reviewed

    Mari Tada, Akiyoshi Kakita, Yasuko Toyoshima, Osamu Onodera, Tetsutaro Ozawa, Takashi Morita, Masatoyo Nishizawa, Hitoshi Takahashi

    BRAIN   132 ( Pt 7 )   1810 - 1819   2009.7

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  • Involvement of SMARCA2/BRM in the SWI/SNF chromatin-remodeling complex in schizophrenia Reviewed

    Minori Koga, Hiroki Ishiguro, Saori Yazaki, Yasue Horiuchi, Makoto Arai, Kazuhiro Niizato, Shuji Iritani, Masanari Itokawa, Toshiya Inada, Nakao Iwata, Norio Ozaki, Hiroshi Ujike, Hiroshi Kunugi, Tsukasa Sasaki, Makoto Takahashi, Yuichiro Watanabe, Toshiyuki Someya, Akiyoshi Kakita, Hitoshi Takahashi, Hiroyuki Nawa, Christian Muchardt, Moshe Yaniv, Tadao Arinami

    HUMAN MOLECULAR GENETICS   18 ( 13 )   2483 - 2494   2009.7

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  • Expression of ErbB4 in substantia nigra dopamine neurons of monkeys and humans Reviewed

    Yingjun Zheng, Akiya Watakabe, Masahiko Takada, Akiyoshi Kakita, Hisaaki Namba, Hitoshi Takahashi, Tetsuo Yamamori, Hiroyuki Nawa

    PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY   33 ( 4 )   701 - 706   2009.6

  • Activity-dependent glial swelling is impaired in aquaporin-4 knockout mice Reviewed

    Hiroki Kitaura, Mika Tsujita, Vincent J. Huber, Akiyoshi Kakita, Katsuei Shibuki, Kenji Sakimura, Ingrid L. Kwee, Tsutomu Nakada

    NEUROSCIENCE RESEARCH   64 ( 2 )   208 - 212   2009.6

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  • Activity-dependent glial swelling is impaired in aquaporin-4 knockout mice.

    Kitaura Hiroki, Tsujita Mika, Huber Vincent J, Kakita Akiyoshi, Shibuki Katsuei, Sakimura Kenji, Kwee Ingrid L, Nakada Tsutomu

    Neurosci Res   64 ( 2 )   208 - 212   2009.6

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    We investigated the role of aquaporin-4 (AQP4), a water channel expressed in glial cells, in neural activity mediated morphological changes observed in brain slice preparation. Changes in flavoprotein fluorescence (FF) and infrared light scattering (LS) signals were measured before and after repetitive stimulation of layer VI in rostral somatosensory cortical slices taken from AQP4 knockout (KO) and wild-type (WT) mice. Changes in FF, which reflect neural aerobic activities, were comparable for the two groups in all cortical layers. However, changes in LS signals, which are indicative of cell swelling, were significantly decreased in layer I of AQP4 KO mice compared to that of WT mice. We conclude that AQP4 likely plays a significant role in neural activity-dependent glial swelling.

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  • Genetic association study on in and around the APOE in late-onset Alzheimer disease in Japanese Reviewed

    Norihiro Takei, Akinori Miyashita, Tarriao Tsukie, Hiroyuki Arai, Takashi Asada, Masaki Imagawa, Mikio Shoji, Susumu Higuchi, Katsuya Urakami, Hideo Kimura, Akiyoshi Kakita, Hitoshi Takahashi, Shoji Tsuji, Ichiro Kanazawa, Yasuo Ihara, Shoji Odani, Ryozo Kuwano

    GENOMICS   93 ( 5 )   441 - 448   2009.5

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  • TDP-43 May Contribute To The Protective Effects Of Hypothermia Against Rat Focal Cerebral Ischemia Reviewed

    Masato Kanazawa, Akiyoshi Kakita, Hironaka Igarashi, Tetsuya Takahashi, Hitoshi Takahashi, Masatoyo Nishizawa, Tsutomu Nakada, Takayoshi Shimohata

    STROKE   40 ( 4 )   E223 - E223   2009.4

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  • Caspase 3-Dependent Proteolytic Cleavage of TDP-43 in a Model of Transient Middle Cerebral Artery Occlusion Reviewed

    Masato Kanazawa, Akiyoshi Kakita, Hironaka Igarashi, Tetsuya Takahashi, Hitoshi Takahashi, Masatoyo Nishizawa, Tsutomu Nakada, Takayoshi Shimohata

    NEUROLOGY   72 ( 11 )   A401 - A401   2009.3

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  • Sporadic amyotrophic lateral sclerosis of long duration is associated with relatively mild TDP-43 pathology Reviewed

    Yasushi Nishihira, Chun-Feng Tan, Yasuhiro Hoshi, Keisuke Iwanaga, Megumi Yamada, Izumi Kawachi, Mitsuhiro Tsujihata, Isao Hozumi, Takashi Morita, Osamu Onodera, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    ACTA NEUROPATHOLOGICA   117 ( 1 )   45 - 53   2009.1

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    DOI: 10.1007/s00401-008-0443-6

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  • Sporadic amyotrophic lateral sclerosis of long duration is associated with relatively mild TDP-43 pathology. Reviewed

    Nishihira Yasushi, Tan Chun-Feng, Hoshi Yasuhiro, Iwanaga Keisuke, Yamada Megumi, Kawachi Izumi, Tsujihata Mitsuhiro, Hozumi Isao, Morita Takashi, Onodera Osamu, Nishizawa Masatoyo, Kakita Akiyoshi, Takahashi Hitoshi

    Acta Neuropathol   117 ( 1 )   45 - 53   2009.1

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    Recently, sporadic amyotrophic lateral sclerosis (SALS), a fatal neurological disease, has been shown to be a multisystem proteinopathy of TDP-43 in which both neurons and glial cells in the central nervous system are widely affected. In general, the natural history of SALS is short (&lt;5 years). However, it is also known that a few patients may survive for 10 years or more, even without artificial respiratory support (ARS). In the present study using TDP-43 immunohistochemistry, we examined various regions of the nervous system in six patients with SALS of long duration (10-20 years) without ARS, in whom lower motor-predominant disease with Bunina bodies and ubiquitinated inclusions (UIs) in the affected lower motor neurons was confirmed. One case also showed UIs in the hippocampal dentate granule cells (UDG). In all cases, except one with UDG, the occurrence of TDP-43-immunoreactive (ir) neuronal cytoplasmic inclusions (NCIs) was confined to a few regions in the spinal cord and brainstem, including the anterior horns. In one case with UDG, TDP-43-ir NCIs were also detected in the substantia nigra, and some regions of the cerebrum, including the hippocampal dentate gyrus (granule c

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  • Diagnosis and treatment for focal cortical dysplasia Reviewed

    Hiroshi Masuda, Hiroatsu Murakami, Shigeki Kameyama, Akiyoshi Kakita

    Japanese Journal of Neurosurgery   18 ( 8 )   577 - 585   2009

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  • Involvement of SMARCA2/BRM in the SWI/SNF chromatin-remodeling complex in schizophrenia Reviewed

    Minori Koga, Hiroki Ishiguro, Saori Yazaki, Yasue Horiuchi, Makoto Arai, Kazuhiro Niizato, Shuji Iritani, Masanari Itokawa, Toshiya Inada, Nakao Iwata, Norio Ozaki, Hiroshi Ujike, Hiroshi Kunugi, Tsukasa Sasaki, Makoto Takahashi, Yuichiro Watanabe, Toshiyuki Someya, Akiyoshi Kakita, Hitoshi Takahashi, Hiroyuki Nawa, Christian Muchardt, Moshe Yaniv, Tadao Arinami

    Human Molecular Genetics   18 ( 13 )   2483 - 2494   2009

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  • Activation of Signal Transducer and Activator of Transcription-3 in the Spinal Cord of Sporadic Amyotrophic Lateral Sclerosis Patients Reviewed

    Noriyuki Shibata, Akiyoshi Kakita, Hitoshi Takahashi, Yuetsu Ihara, Keigo Nobukuni, Harutoshi Fujimura, Saburo Sakoda, Shoichi Sasaki, Makoto Iwata, Shunichi Morikawa, Asao Hirano, Makio Kobayashi

    NEURODEGENERATIVE DISEASES   6 ( 3 )   118 - 126   2009

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  • 視神経脊髄炎(NMO)におけるアストロサイト障害の関連

    三須 建郎, 藤原 一男, 柿田 明美, 高野 里菜, 高橋 利幸, 高橋 均, 糸山 泰人

    臨床神経学   48 ( 12 )   1217 - 1217   2008.12

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  • Cardiac sympathetic denervation in Parkinson's disease linked to SNCA duplication Reviewed

    Satoshi Orimo, Toshiki Uchihara, Ayako Nakamura, Fumiaki Mori, Takeshi Ikeuchi, Osamu Onodera, Masatoyo Nishizawa, Atsushi Ishikawa, Akiyoshi Kakita, Koichi Wakabayashi, Hitoshi Takahashi

    ACTA NEUROPATHOLOGICA   116 ( 5 )   575 - 577   2008.11

  • Marinesco-Sjogren syndrome with atrophy of the brain stem tegmentum and dysplastic cytoarchitecture in the cerebral cortex Reviewed

    Kenji Sakai, Mari Tada, Yosuke Yonemochi, Takashi Nakajima, Osamu Onodera, Hitoshi Takahashi, Akiyoshi Kakita

    NEUROPATHOLOGY   28 ( 5 )   541 - 546   2008.10

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    DOI: 10.1111/j.1440-1789.2008.00884.x

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  • Sporadic amyotrophic lateral sclerosis: two pathological patterns shown by analysis of distribution of TDP-43-immunoreactive neuronal and glial cytoplasmic inclusions Reviewed

    Yasushi Nishihira, Chun-Feng Tan, Osamu Onodera, Yasuko Toyoshima, Mitsunori Yamada, Takashi Morita, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    ACTA NEUROPATHOLOGICA   116 ( 2 )   169 - 182   2008.8

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  • 死後脳を用いた晩期発症型アルツハイマー病の網羅的遺伝子発現解析

    宮下 哲典, 斉藤 佑子, 柿田 明美, 荻島 創一, 田中 博, 村山 繁雄, 高橋 均, 井原 康夫, 桑野 良三

    Dementia Japan   22 ( 2 )   176 - 176   2008.8

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  • Glial clusters and perineuronal glial satellitosis in the basal ganglia of neurofibromatosis type 1 Reviewed

    Osamu Yokota, Kuniaki Tsuchiya, Masaharu Hayashi, Akiyoshi Kakita, Kiyoshi Ohwada, Hideki Ishizu, Hitoshi Takahashi, Haruhiko Akiyama

    ACTA NEUROPATHOLOGICA   116 ( 1 )   57 - 66   2008.7

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  • Venous congestive myelopathy: Three autopsy cases showing a variety of clinicopathologic features Reviewed

    Koushun Matsuo, Akiyoshi Kakita, Nobutaka Ishizu, Kohtaro Endo, Yumiko Watanabe, Takashi Morita, Hitoshi Takahashi

    NEUROPATHOLOGY   28 ( 3 )   303 - 308   2008.6

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    DOI: 10.1111/j.1440-1789.2007.00880.x

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  • Effects of perinatal coexposure to methylmercury and polychlorinated biphenyls on neurobehavioral development in mice Reviewed

    Norio Sugawara, Takashi Ohba, Kunihiko Nakai, Akiyoshi Kakita, Tomoyuki Nakamura, Keita Suzuki, Satomi Kameo, Miyuki Shimada, Naoyuki Kurokawa, Chieko Satoh, Hiroshi Satoh

    ARCHIVES OF TOXICOLOGY   82 ( 6 )   387 - 397   2008.6

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    DOI: 10.1007/s00204-007-0254-x

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  • Patients homozygous and heterozygous for SNCA duplication in a family with parkinsonism and dementia Reviewed

    Takeshi Ikeuchi, Akiyoshi Kakita, Atsushi Shiga, Kensaku Kasuga, Hiryoyuki Kaneko, Chun-Feng Tan, Jiro Idezuka, Koichi Wakabayashi, Osamu Onodera, Takeshi Iwatsubo, Masatoyo Nishizawa, Hitoshi Takahashi, Atsushi Ishikawa

    ARCHIVES OF NEUROLOGY   65 ( 4 )   514 - 519   2008.4

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  • alpha-Synuclein pathology in the neostriatum in Parkinson's disease Reviewed

    Fumiaki Mori, Kunikazu Tanji, Haixin Zhang, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    ACTA NEUROPATHOLOGICA   115 ( 4 )   453 - 459   2008.4

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    DOI: 10.1007/s00401-007-0316-4

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  • TDP-43 mutation in familial amyotrophic lateral sclerosis Reviewed

    Akio Yokoseki, Atsushi Shiga, Chun-Feng Tan, Asako Tagawa, Hiroyuki Kaneko, Akihide Koyama, Hiroto Eguchi, Akira Tsujino, Takeshi Ikeuchi, Akiyoshi Kakita, Koichi Okamoto, Masatoyo Nishizava, Hitoshi Takahashi, Osamu Onodera

    ANNALS OF NEUROLOGY   63 ( 4 )   538 - 542   2008.4

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  • 抗アクアポリン4抗体関連神経疾患の病態機序 Neuromyelitis opticaの病巣におけるアストロサイト障害の検討

    三須 建郎, 藤原 一男, 高野 里菜, 高橋 利幸, 柿田 明美, 今野 秀彦, 高橋 均, 糸山 泰人

    神経免疫学   16 ( 1 )   51 - 51   2008.4

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  • The wide spectrum of clinicopathological manifestations in pathologically proven progressive supranuclear palsy: A study of Japanese patients Reviewed

    Masato Kanazawa, Takayoshi Shimohata, Yasuko Toyoshima, Mari Tada, Akiyoshi Kakita, Tetsutaro Ozawa, Takashi Morita, Hitoshi Takahashi, Masatoya Nishizawa

    NEUROLOGY   70 ( 11 )   A385 - A385   2008.3

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  • Axonal alpha-synuclein aggregates herald centripetal degeneration of cardiac sympathetic nerve in Parkinsons disease Reviewed

    Satoshi Orimo, Toshiki Uchihara, Ayako Nakamura, Fumiaki Mori, Akiyoshi Kakita, Koichi Wakabayashi, Hitoshi Takahashi

    BRAIN   131 ( Pt 3 )   642 - 650   2008.3

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    DOI: 10.1093/brain/awm302

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  • Spinal cord tau pathology in cervical spondylotic myelopathy Reviewed

    Hiroshi Shimizu, Akiyoshi Kakita, Hitoshi Takahashi

    ACTA NEUROPATHOLOGICA   115 ( 2 )   185 - 192   2008.2

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    DOI: 10.1007/s00401-007-0321-7

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  • TDP-43-immunoreactive neuronal and glial inclusions in the neostriatum in amyotrophic lateral sclerosis with and without dementia Reviewed

    Haixin Zhang, Chun-Feng Tan, Fumiaki Mori, Kunikazu Tanji, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    ACTA NEUROPATHOLOGICA   115 ( 1 )   115 - 122   2008.1

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    DOI: 10.1007/s00401-007-0285-7

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  • TDP-43 mutation in familial amyotrophic lateral sclerosis Reviewed

    Akio Yokoseki, Atsushi Shiga, Chun Feng Tan, Asako Tagawa, Hiroyuki Kaneko, Akihide Koyama, Hiroto Eguchi, Akira Tsujino, Takeshi Ikeuchi, Akiyoshi Kakita, Koichi Okamoto, Masatoyo Nishizawa, Hitoshi Takahashi, Osamu Onodera

    NEUROSCIENCE RESEARCH   61   S267 - S267   2008

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  • Genetic association of CTNNA3 with late-onset Alzheimer's disease in females. Reviewed International journal

    Akinori Miyashita, Hiroyuki Arai, Takashi Asada, Masaki Imagawa, Etsuro Matsubara, Mikio Shoji, Susumu Higuchi, Katsuya Urakami, Akiyoshi Kakita, Hitoshi Takahashi, Shinichi Toyabe, Kohei Akazawa, Ichiro Kanazawa, Yasuo Ihara, Ryozo Kuwano

    Human molecular genetics   16 ( 23 )   2854 - 69   2007.12

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    Alzheimer's disease (AD), the most common form of dementia in the elderly, was found to exhibit a trend toward a higher risk in females than in males through epidemiological studies. Therefore, we hypothesized that gender-related genetic risks could exist. To reveal the ones for late-onset AD (LOAD), we extended our previous genetic work on chromosome 10q (genomic region, 60-107 Mb), and single nucleotide polymorphism (SNP)-based genetic association analyses were performed on the same chromosomal region, where the existence of genetic risk factors for plasma Abeta42 elevation in LOAD was implied on a linkage analysis. Two-step screening of 1140 SNPs was carried out using a total of 1408 subjects with the APOE-epsilon3*3 genotype: we first genotyped an exploratory sample set (LOAD, 363; control, 337), and then genotyped some associated SNPs in a validation sample set (LOAD, 336; control, 372). Seven SNPs, spanning about 38 kb, in intron 9 of CTNNA3 were found to show multiple-hit association with LOAD in females, and exhibited more significant association on Mantel-Haenszel test (allelic P-values(MH-F) = 0.000005945-0.0007658). Multiple logistic regression analysis of a total of 2762 subjects (LOAD, 1313; controls, 1449) demonstrated that one of the seven SNPs directly interacted with the female gender, but not with the male gender. Furthermore, we found that this SNP exhibited no interaction with the APOE-epsilon4 allele. Our data suggest that CTNNA3 may affect LOAD through a female-specific mechanism independent of the APOE-epsilon4 allele.

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  • 5 海面状血管腫と脳動静脈奇形 Reviewed

    亀山茂樹, 柿田明美

    脳神経外科   35 ( 12 )   1199 - 1206   2007.12

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  • [Magnetic resonance imaging and pathology in epilepsy (5). Cavernous angioma and arteriovenous malformation]. Reviewed

    Kameyama S, Kakita A

    No shinkei geka. Neurological surgery   35 ( 12 )   1199 - 1206   2007.12

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  • The cellular and behavioral consequences of interleukin-1 alpha penetration through the blood-brain barrier of neonatal rats: A critical period for efficacy Reviewed

    M. Tohmi, N. Tsuda, Y. Zheng, M. Mizuno, H. Sotoyama, M. Shibuya, M. Kawamura, A. Kakita, H. Takahashi, H. Nawa

    NEUROSCIENCE   150 ( 1 )   234 - 250   2007.11

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  • Enhanced accumulation of phosphorylated alpha-synuclein and elevated beta-amyloid 42/40 ratio caused by expression of the presenilin-1 Delta T440 mutant associated with familial Lewy body disease and variant Alzheimer's disease Reviewed

    Hiroyuki Kaneko, Akiyoshi Kakita, Kensaku Kasuga, Hiroaki Nozaki, Atsushi Ishikawa, Akinori Miyashita, Ryozo Kuwano, Genta Ito, Takeshi Iwatsubo, Hitoshi Takahashi, Masatoyo Nishizawa, Osamu Onodera, Sangram S. Sisodia, Takeshi Ikeuchi

    JOURNAL OF NEUROSCIENCE   27 ( 48 )   13092 - 13097   2007.11

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    DOI: 10.1523/JNEUROSCI.4244-07.2007

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  • てんかん外科病理学の実際 Reviewed

    柿田 明美

    病理と臨床   25 ( 10 )   990 - 996   2007.10

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  • 4 結節性硬化症 Reviewed

    亀山茂樹, 柿田明美

    脳神経外科   35 ( 10 )   1027 - 1035   2007.10

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  • Immunohistochemical localization of NUB1, a synphilin-1-binding protein, in neurodegenerative disorders Reviewed

    Kunikazu Tanji, Fumiaki Mori, Akiyoshi Kakita, Haixin Zhang, Katsumi Kito, Tetsu Kamitani, Hitoshi Takahashi, Koichi Wakabayashi

    ACTA NEUROPATHOLOGICA   114 ( 4 )   365 - 371   2007.10

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    DOI: 10.1007/s00401-007-0238-1

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  • Magnetic resonance Imaging and pathology in epilepsy (4) tuberous sclerosis Reviewed

    Shigeki Kaneyama, Akiyoshi Kakita

    NEUROLOGICAL SURGERY   35 ( 10 )   1027 - 1035   2007.10

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  • Decreased cardiac uptake of MIBG is a potential biomarker for the presence of Lewy bodies Reviewed

    Satoshi Orimo, Takeshi Amino, Toshiki Uchihara, Fumiaki Mori, Akiyoshi Kakita, Koichi Wakabayashi, Hitoshi Takahashi

    JOURNAL OF NEUROLOGY   254 ( Suppl 4 )   21 - 28   2007.8

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  • 3 Dysembryonic neuroepithelial tumorと腫瘍性病変 Reviewed

    亀山茂樹, 柿田明美

    脳神経外科   35 ( 8 )   833 - 841   2007.8

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  • [Magnetic resonance imaging and pathology in epilepsy (3). Dysembryoplastic neuroepithelial tumor and neoplastic lesions]. Reviewed

    Kameyama S, Kakita A

    No shinkei geka. Neurological surgery   35 ( 8 )   833 - 841   2007.8

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  • 硬膜に発生母地を認めなかった大脳円蓋部solitary fibrous tumorの1例 Reviewed

    佐野正和, 斉藤明彦, 西平 靖, 大石 誠, 柿田明美, 高橋 均, 藤井幸彦

    脳神経外科   35 ( 7 )   697 - 702   2007.7

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  • 2 内側側頭葉てんかんと海馬硬化 Reviewed

    亀山茂樹, 柿田明美

    脳神経外科   35 ( 7 )   719 - 729   2007.7

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  • Sacral parasite with histopathological features of an unequally conjoined twin Reviewed

    Yutaka Hirayama, Masayuki Kubota, Akiyoshi Kakita, Takashi Kawasaki, Go Hasegawa, Shinji Tanaka, Masahiro Ohtaki, Satoru Yamazaki, Naoki Okuyama, Minoru Yagi, Makoto Naito

    PEDIATRIC SURGERY INTERNATIONAL   23 ( 7 )   715 - 720   2007.7

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  • Magnetic resonance imaging and pathology in Epilepsy (2) mesial temporal lobe epilepsy and hippocampal sclerosis Reviewed

    Shigeki Kameyama, Akiyoshi Kakita

    NEUROLOGICAL SURGERY   35 ( 7 )   719 - 729   2007.7

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  • [A case of solitary fibrous tumor in the cerebral convexity indicating its non-dural origin]. Reviewed

    Sano M, Saito A, Nishihira Y, Oishi M, Kakita A, Takahashi H, Fujii Y

    No shinkei geka. Neurological surgery   35 ( 7 )   697 - 702   2007.7

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  • 1 限局性皮質形成異常 Reviewed

    亀山茂樹, 柿田明美

    脳神経外科   35 ( 6 )   623 - 630   2007.6

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  • Focal cortical dysplasia Reviewed

    Shigeki Kameyama, Akiyoshi Kakita

    NEUROLOGICAL SURGERY   35 ( 6 )   615 - 622   2007.6

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  • [Magnetic resonance imaging and pathology in epilepsy (1) focal cortical dysplasia]. Reviewed

    Kameyama S, Kakita A

    No shinkei geka. Neurological surgery   35 ( 6 )   615 - 622   2007.6

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  • Loss of aquaporin 4 in lesions of neuromyelitis optica: distinction from multiple sclerosis Reviewed

    T. Misu, K. Fujihara, A. Kakita, H. Konno, M. Nakamura, S. Watanabe, T. Takahashi, I. Nakashima, H. Takahashi, Y. Itoyama

    BRAIN   130 ( Pt 5 )   1224 - 1234   2007.5

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  • TDP-43 immunoreactivity in neuronal inclusions in familial amyotrophic lateral sclerosis with or without SOD1 gene mutation Reviewed

    Chun-Feng Tan, Hiroto Eguchi, Asako Tagawa, Osamu Onodera, Takuya Iwasaki, Akira Tsujino, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    ACTA NEUROPATHOLOGICA   113 ( 5 )   535 - 542   2007.5

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  • Multiplex families with multiple system atrophy Reviewed

    Kenju Hara, Yoshio Momose, Susumu Tokiguchi, Mitsuteru Shimohata, Kenshi Terajima, Osamu Onodera, Akiyoshi Kakita, Mitsunori Yamada, Hitoshi Takahashi, Motoyuki Hirasawa, Yoshikuni Mizuno, Katsuhisa Ogata, Jun Goto, Ichiro Kanazawa, Masatoyo Nishizawa, Shoji Tsuji

    ARCHIVES OF NEUROLOGY   64 ( 4 )   545 - 551   2007.4

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    DOI: 10.1001/archneur.64.4.545

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  • Frontal anaplastic oligodendroglioma showing multi-organ metastases after a long clinical course - Case report Reviewed

    Takeo Uzuka, Akiyoshi Kakita, Chikanori Inenaga, Hideaki Takahashi, Ryuichi Tanaka, Hitoshi Takahashi

    NEUROLOGIA MEDICO-CHIRURGICA   47 ( 4 )   174 - 177   2007.4

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  • Distinct clinical phenotypes of pathologically proven progressive supranuclear palsy: Richardson's syndrome, PSP-Parkinsonism and PSP-cerebral cortical dysfunction Reviewed

    Masato Kanazawa, Takayoshi Shimohata, Akiyoshi Kakita, Mari Tada, Yasuko Toyoshima, Takashi Morita, Hitoshi Takahashi, Masatoyo Nishizawa

    NEUROLOGY   68 ( 12 )   A49 - A49   2007.3

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  • Early development of autonomic dysfunction may predict poor prognosis in patients with multiple system atrophy Reviewed

    Mari Tada, Osamu Onodera, Masayoshi Tada, Tetsutaro Ozawa, Yue-Shan Piao, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa

    ARCHIVES OF NEUROLOGY   64 ( 2 )   256 - 260   2007.2

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    DOI: 10.1001/archneur.64.2.256

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  • Protein-bound crotonaldehyde accumulates in the spinal cord of superoxide dismutase-1 mutation-associated familial amyotrophic lateral sclerosis and its transgenic mouse model Reviewed

    Noriyuki Shibata, Motoko Kawaguchi, Koji Uchida, Akiyoshi Kakita, Hitoshi Takahashi, Ryoichi Nakano, Harutoshi Fujimura, Saburo Sakoda, Yuetsu Ihara, Keigo Nobukuni, Yasushi Takehisa, Shigetoshi Kuroda, Yasumasa Kokubo, Shigeki Kuzuhara, Taku Honma, Yoko Mochizuki, Tomohiko Mizutani, Satoshi Yamada, Sono Toi, Shoichi Sasaki, Makoto Iwata, Asao Hirano, Tomoko Yamamoto, Yoichiro Kato, Tatsuo Sawada, Makio Kobayashi

    NEUROPATHOLOGY   27 ( 1 )   49 - 61   2007.2

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    DOI: 10.1111/j.1440-1789.2006.00746.x

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  • Cardiac sympathetic denervation in the preclinical stage of Parkinson’s disease Reviewed

    Orimo S, Takahashi A, Uchihara T, Mori F, Kakita A, Wakabayashi K, Takahashi H

    Brain Pathology   17 ( 1 )   24 - 30   2007.1

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  • [Pathological and biochemical studies of 30 Niigata autopsy cases related to Minamata disease]. Reviewed

    Eto K, Takahashi H, Kakita A, Tokunaga H, Yasutake A, Nakano A, Sawada M, Kinjo Y

    Nihon eiseigaku zasshi. Japanese journal of hygiene   62 ( 1 )   70 - 88   2007.1

  • Degeneration of cardiac sympathetic nerve begins in the early disease process of Parkinson's disease Reviewed

    Satoshi Orimo, Atsushi Takahashi, Toshiki Uchihara, Fumiaki Mori, Akiyoshi Kakita, Koichi Wakabayashi, Hitoshi Takahashi

    BRAIN PATHOLOGY   17 ( 1 )   24 - 30   2007.1

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    DOI: 10.1111/j.1750-3639.2006.00032.x

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  • Degeneration of cardiac sympathetic nerve can occur in multiple system atrophy Reviewed

    Satoshi Orimo, Toshiro Kanazawa, Ayako Nakamura, Toshiki Uchihara, Fumiaki Mori, Akiyoshi Kakita, Koichi Wakabayashi, Hitoshi Takahashi

    ACTA NEUROPATHOLOGICA   113 ( 1 )   81 - 86   2007.1

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    DOI: 10.1007/s00401-006-0160-y

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  • Tryptophan metabolism and epileptogenicity in malformations of cortical development (MCDs) – tissue microarray immunohistochemical study on kynurenine pathway. Reviewed

    Miyata H, Vinters HV, Kakita A, Ohama E

    Ann. Rep. Jpn. Epi. Res. Found.   18   37 - 42   2007

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  • Sustained brain-derived neurotrophic factor up-regulation and sensorimotor gating abnormality induced by postnatal exposure to phencyclidine: comparison with adult treatment Reviewed

    Makoto Takahashi, Akiyoshi Kakita, Takashi Futamura, Yuichiro Watanabe, Makoto Mizuno, Kenji Sakimura, Eero Castren, Toshitaka Nabeshima, Toshiyuki Someya, Hiroyuki Nawa

    JOURNAL OF NEUROCHEMISTRY   99 ( 3 )   770 - 780   2006.11

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    DOI: 10.1111/j.1471-4159.2006.04106.x

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  • A possible variant of neuro-Behcet disease presenting chronic progressive ataxia without mucocutaneo-ocular symptoms Reviewed

    Masaki Hirose, Takeshi Ikeuchi, Shintaro Hayashi, Kenshi Terajima, Kotaro Endo, Tsunemi Hayashi, Akiyoshi Kakita, Teruo Kimura, Hitoshi Takahashi, Masatoyo Nishizawa

    RHEUMATOLOGY INTERNATIONAL   27 ( 1 )   61 - 65   2006.11

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    DOI: 10.1007/s00296-006-0171-y

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  • 中枢神経系の発生とその異常 Reviewed

    柿田 明美

    第36回小児神経学セミナー講義用テキスト   23 - 27   2006.10

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  • Nitric oxide in cerebrospinal fluid and local inducible nitric oxide synthase after cauda equina compression in rats Reviewed

    Xianjun Wang, Shinji Kimura, Akiyoshi Kakita, Noboru Hosaka, Hiroshi Denda, Takui Ito, Toru Hirano, Naoto Endo

    NEUROREPORT   17 ( 14 )   1473 - 1478   2006.10

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    DOI: 10.1097/01.wnr.0000234746.35195.b0

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  • Corticobasal degeneration with focal, massive tau accumulation in the subcortical white matter astrocytes Reviewed

    Kenji Sakai, Yue-Shan Piao, Koki Kikugawa, Shinji Ohara, Masato Hasegawa, Hiroki Takano, Masayuki Fukase, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    ACTA NEUROPATHOLOGICA   112 ( 3 )   341 - 348   2006.9

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    DOI: 10.1007/s00401-006-0093-5

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  • Peroxisomal disorders Reviewed

    KAKITA Akiyoshi

    24 ( 8 )   854 - 855   2006.8

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  • Relationship among alpha-synuclein accumulation, dopamine synthesis, and neurodegeneration in Parkinson disease substantia nigra Reviewed

    Fumiaki Mori, Makoto Nishie, Akiyoshi Kakita, Makoto Yoshimoto, Hitosh Takahashi, Koichi Wakabayashi

    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY   65 ( 8 )   808 - 815   2006.8

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    DOI: 10.1097/01.jnen.0000230520.47768.1a

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  • Lysosomal disorders---(2) 糖蛋白代謝異常症・ムコ多糖症,他 Reviewed

    柿田 明美

    Clinical Neuroscience   24 ( 7 )   736 - 737   2006.7

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  • Pathological heterogeneity of the precentral gyrus in Pick's disease: A study of 16 autopsy cases Reviewed

    K Tsuchiya, YS Piao, T Oda, A Mochizuki, K Arima, K Hasegawa, C Haga, A Kakita, K Hori, Tominaga, I, S Yagishita, H Akiyama, H Takahashi

    ACTA NEUROPATHOLOGICA   112 ( 1 )   29 - 42   2006.7

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    DOI: 10.1007/s00401-005-0028-6

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  • Dynamin-binding protein gene on chromosome 10q is associated with late-onset Alzheimer's disease Reviewed

    R Kuwano, A Miyashita, H Arai, T Asada, M Imagawa, M Shoji, S Higuchi, K Urakami, A Kakita, H Takahashi, T Tsukie, S Toyabe, K Akazawa, Kanazawa, I, Y Ihara

    HUMAN MOLECULAR GENETICS   15 ( 13 )   2170 - 2182   2006.7

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    DOI: 10.1093/hmg/ddl142

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  • Lysosomal disorders---(1) 脂質蓄積症 Reviewed

    柿田 明美

    Clinical Neuroscience   24 ( 6 )   624 - 625   2006.6

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  • Transcranial imaging of audiogenic epileptic foci in the cortex of DBA/2J mice Reviewed

    T Takao, H Murakami, M Fukuda, T Kawaguchi, A Kakita, H Takahashi, M Kudoh, R Tanaka, K Shibuki

    NEUROREPORT   17 ( 3 )   267 - 271   2006.2

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    DOI: 10.1097/01.wnr.0000201505.61373.42

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  • 統合失調症の母体ウイルス感染仮説の実験的検証とサイトカインの関連性探求 Reviewed

    青木弘行, 水野 誠, 柿田明美, 那波宏之

    精神薬療研究年報   38   204 - 209   2006

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  • 統合失調症の発達障害仮説とドパミン神経栄養因子 Reviewed

    那波宏之, 柿田明美

    細胞   37 ( 14 )   565 - 568   2005.12

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  • Sporadic four-repeat tauopathy with frontotemporal degeneration, parkinsonism and motor neuron disease Reviewed

    YS Piao, CF Tan, K Iwanaga, A Kakita, H Takano, M Nishizawa, T Lashley, T Revesz, A Lees, R Silva, M Tsujihata, H Takahashi

    ACTA NEUROPATHOLOGICA   110 ( 6 )   600 - 609   2005.12

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    DOI: 10.1007/s00401-005-1086-5

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  • ヒト脳の形成障害:とくにMigratin Disordersの病理 Reviewed

    柿田 明美

    脳21   8 ( 3 )   268 - 273   2005.7

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  • Sporadic fatal insomnia with spongiform degeneration in the thalamus and widespread PrPSc deposits in the brain. Reviewed

    Piao YS, Kakita A, Watanabe H, Kitamoto T, Takahashi H

    Neuropathology : official journal of the Japanese Society of Neuropathology   25 ( 2 )   144 - 149   2005.6

  • Lysosomal and peroxisomal disorders Reviewed

    柿田 明美

    教育コース「神経病理学の基礎」ハンドアウトテクスト   26 - 37   2005.5

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    第46回日本神経病理学会総会学術研究会

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  • Influences of dopaminergic lesion on epidermal growth factor-ErbB signals in Parkinson's disease and its model: neurotrophic implication in nigrostriatal neurons Reviewed

    Y Iwakura, YS Piao, M Mizuno, N Takei, A Kakita, H Takahashi, H Nawa

    JOURNAL OF NEUROCHEMISTRY   93 ( 4 )   974 - 983   2005.5

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    DOI: 10.1111/j.1471-4159.2005.03073.x

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  • Effect over time of endotoxin adsorption therapy in sepsis Reviewed

    T Ueno, M Sugino, H Nemoto, H Shoji, A Kakita, M Watanabe

    THERAPEUTIC APHERESIS AND DIALYSIS   9 ( 2 )   128 - 136   2005.4

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  • Cerebral lipoma and the underlying cortex of the temporal lobe: pathological features associated with the malformation Reviewed

    A Kakita, C Inenaga, S Kameyama, H Masuda, T Ueno, J Honma, M Shimohata, H Takahashi

    ACTA NEUROPATHOLOGICA   109 ( 3 )   339 - 345   2005.4

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    DOI: 10.1007/s00401-004-0955-7

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  • Pathologic features of dysplasia and accompanying alterations observed in surgical specimens from patients with intractable epilepsy Reviewed

    A Kakita, S Kameyama, S Hayashi, H Masuda, H Takahashi

    JOURNAL OF CHILD NEUROLOGY   20 ( 4 )   341 - 350   2005.4

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    DOI: 10.1177/08830738050200041301

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  • Frontotemporal dementia with co-occurrence of astrocytic plaques and tufted astrocytes, and severe degeneration of the cerebral white matter: a variant of corticobasal degeneration? Reviewed

    CF Tan, YS Piao, A Kakita, M Yamada, H Takano, M Tanaka, A Mano, K Makino, M Nishizawa, K Wakabayashi, H Takahashi

    ACTA NEUROPATHOLOGICA   109 ( 3 )   329 - 338   2005.4

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    DOI: 10.1007/s00401-004-0933-0

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  • ErbB1 receptor ligands attenuate the expression of synaptic scaffolding proteins, GRIP1 and SAP97, in developing neocortex Reviewed

    D Yokomaku, H Jourdi, A Kakita, T Nagano, H Takahashi, N Takei, H Nawa

    NEUROSCIENCE   136 ( 4 )   1037 - 1047   2005

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    DOI: 10.1016/j.neuroscience.2005.08.014

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  • An autopsy case of systemic vasculitis associated with hepatitis C virus-related mixedcryoglobulinemia presenting severe peripheral neuropathy Reviewed

    Mari Tada, Satoshi Naruse, Aki Arai, Aki Sato, Keiko Tanaka, Yue-Shan Piao, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa, Shoji Tsuji

    Clinical Neurology   44 ( 10 )   686 - 690   2004.10

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  • beta-Synuclein gene alterations in dementia with Lewy bodies Reviewed

    H Ohtake, P Limprasert, Y Fan, O Onodera, A Kakita, H Takahashi, LT Bonner, DW Tsuang, IVJ Murray, VMY Lee, JQ Trojanowski, A Ishikawa, J Idezuka, M Murata, T Toda, TD Bird, JB Leverenz, S Tsuji, AR La Spada

    NEUROLOGY   63 ( 5 )   805 - 811   2004.9

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  • Dose-dependent effects of methylmercury administered during neonatal brain spurt in rats Reviewed

    M Sakamoto, A Kakita, RB de Oliveira, HS Pan, H Takahashi

    DEVELOPMENTAL BRAIN RESEARCH   152 ( 2 )   171 - 176   2004.9

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    DOI: 10.1016/j.devbrainres.2004.06.016

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  • Perinatal inflammatory cytokine challenge results in distinct neurobehavioral alterations in rats: implication in psychiatric disorders of developmental origin Reviewed

    M Tohmi, N Tsuda, Y Watanabe, A Kakita, H Nawa

    NEUROSCIENCE RESEARCH   50 ( 1 )   67 - 75   2004.9

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    DOI: 10.1016/j.neures.2004.05.010

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  • Autopsy findings of a craniopharyngioma with a natural course over 60 years Reviewed

    C Inenaga, A Kakita, Y Iwasaki, K Yamatani, H Takahashi, EO Backlund

    SURGICAL NEUROLOGY   61 ( 6 )   536 - 540   2004.6

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    DOI: 10.1016/j.surneu.2003.08.014

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  • Possible involvement of p38 MAP kinase in prostaglandin E1-induced ALP activity in osteoblast-like cells Reviewed

    A Kakita, A Suzuki, Y Ono, Y Miura, M Itoh, Y Oiso

    PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS   70 ( 5 )   469 - 474   2004.5

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    DOI: 10.1016/j.plefa.2003.09.003

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  • Effects of methylmercury on developing brain. Neuropathological aspects Reviewed

    Kakita A, Sakamoto M, Ikuta F, Takahashi H

    Proceedings of NIMD Forum 2003   64 - 89   2004.3

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  • Neonatal impact of leukemia inhibitory factor on neurobehavioral development in rats Reviewed

    Y Watanabe, S Hashimoto, A Kakita, H Takahashi, J Ko, M Mizuno, T Someya, PH Patterson, H Nawa

    NEUROSCIENCE RESEARCH   48 ( 3 )   345 - 353   2004.3

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    DOI: 10.1016/j.neures.2003.12.001

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  • Changes in methylmercury accumulation in the brain of rat offspring throughout gestation and during suckling Reviewed

    Sheng Pan Huan, Mineshi Sakamoto, R. B. Oliveira, Jie Liu Xiao, Akiyoshi Kakita, Makoto Futatsuka

    Toxicological and Environmental Chemistry   86 ( 1-4 )   161 - 168   2004.1

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    DOI: 10.1080/02772240400007005

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  • Prefrontal abnormality of Schizophrenia revealed by DNA microarray. Reviewed

    Sugai, T, Kawamura, M, Iritani, S, Araki, K, Makifuchi, T, Imai, C, Nakamura, R, Kakita, A, Takahashi, H, Nawa, H

    Ann. NY. Acad. Sci.   2004

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  • Prefrontal abnormality of schizophrenia revealed by DNA microarray - Impact on glial and neurotrophic gene expression Reviewed

    T Sugai, M Kawamura, S Iritani, K Araki, T Makifuchi, C Imai, R Nakamura, A Kakita, H Takahashi, H Nawa

    CURRENT STATUS OF DRUG DEPENDENCE / ABUSE STUDIES: CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE AND NEUROTOXICITY   1025   84 - 91   2004

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    DOI: 10.1196/annals.1316.011

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  • Study on development of psychotropics by use of genomic information for the prevention of suicides. Research on the molecular mechanism of repair by neurotropic factor in functional disorder of neural circuit that associates with suicidal ideation and the

    染矢俊幸, 渡部雄一郎, 外山英和, 柿田明美, 那波宏之

    ゲノム情報の利用による自殺防止を目指した向精神薬開発に関する研究 平成13-15年度 総合研究報告書   22 - 26   2004

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    J-GLOBAL

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  • Extracerebral ectopic mass with huge cysts in the anterior cranial cavity. Reviewed

    Toyoshima Y, Kakita A, Yamada M, Sato G, Mori H, Okamoto K, Tanaka R, Takahashi H

    Neuropathology : official journal of the Japanese Society of Neuropathology   23 ( 4 )   301 - 306   2003.12

  • Disruption of postnatal progenitor migration and consequent abnormal pattern of glial distribution in the cerebrum following administration of methylmercury Reviewed

    A Kakita, C Inenaga, M Sakamoto, H Takahashi

    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY   62 ( 8 )   835 - 847   2003.8

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  • A decrease in interleukin-1 receptor antagonist expression in the prefrontal cortex of schizophrenic patients Reviewed

    K Toyooka, Y Watanabe, S Iritani, E Shimizu, M Iyo, R Nakamura, K Asama, T Makifuchi, A Kakita, H Takahashi, T Someya, H Nawa

    NEUROSCIENCE RESEARCH   46 ( 3 )   299 - 307   2003.7

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    DOI: 10.1016/S0168-0102(03)00093-2

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  • Primary lateral sclerosis: A rare upper-motor-predominant form of amyotrophic lateral sclerosis often accompanied by frontotemporal lobar degeneration with ubiquitinated neuronal inclusions? Report of an autopsy case and a review of the literature Reviewed

    CF Tan, A Kakita, YS Piao, K Kikugawa, K Endo, M Tanaka, K Okamoto, H Takahashi

    ACTA NEUROPATHOLOGICA   105 ( 6 )   615 - 620   2003.6

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    DOI: 10.1007/s00401-003-0687-0

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  • グリア芽細胞の移動障害 : メチル水銀投与モデルを用いた解析

    柿田 明美, 稲永 親憲, 坂本 峰至, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   23   2003.5

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  • Stimulatory effect of prostaglandin F-2 alpha on Na-dependent phosphate transport in osteoblast-like cells

    Sato, I, A Suzuki, A Kakita, Y Ono, Y Miura, M Itoh, Y Oiso

    PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS   68 ( 5 )   311 - 315   2003.5

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  • alpha-synuclein pathology affecting Bergmann glia of the cerebellum in patients with alpha-synucleinopathies Reviewed

    YS Piao, F Mori, S Hayashi, K Tanji, M Yoshimoto, A Kakita, K Wakabayashi, H Takahashi

    ACTA NEUROPATHOLOGICA   105 ( 4 )   403 - 409   2003.4

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    DOI: 10.1007/s00401-002-0655-0

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  • Some glial progenitors in the neonatal subventricular zone migrate through the corpus callosum to the contralateral cerebral hemisphere Reviewed

    A Kakita, M Zerlin, H Takahashi, JE Goldman

    JOURNAL OF COMPARATIVE NEUROLOGY   458 ( 4 )   381 - 388   2003.4

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  • Lung carcinoma metastasis presenting as a pineal region tumor. Reviewed

    Kakita A, Kobayashi K, Aoki N, Eguchi I, Morita T, Takahashi H

    Neuropathology : official journal of the Japanese Society of Neuropathology   23 ( 1 )   57 - 60   2003.3

  • てんかんの病理.外科手術標本に見られる大脳皮質形成異常所見 Reviewed

    柿田明美, 高橋 均

    神経内科   58 ( 2 )   151 - 161   2003.2

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  • Neuropathology with clinical correlations of sporadic amyotrophic lateral sclerosis: 102 autopsy cases examined between 1962 and 2000. Reviewed

    Piao YS, Wakabayashi K, Kakita A, Yamada M, Hayashi S, Morita T, Ikuta F, Oyanagi K, Takahashi H

    Brain pathology (Zurich, Switzerland)   13 ( 1 )   10 - 22   2003.1

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  • Regeneration of Schwann cells during extrinsic hepatic reinnervation following liver transplantation in rats Reviewed

    Izumi Sakamoto, T. Takahashi, T. Ueno, A. Kakita, I. Hayashi, S. Yamashina

    Transplantation Proceedings   35 ( 1 )   573 - 574   2003

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    DOI: 10.1016/S0041-1345(02)03809-5

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  • Neonatal perturbation of neurotrophic signaling results in abnormal sensorimotor gating and social interaction in adults: implication for epidermal growth factor in cognitive development Reviewed

    T Futamura, A Kakita, M Tohmi, H Sotoyama, H Takahashi, H Nawa

    MOLECULAR PSYCHIATRY   8 ( 1 )   19 - 29   2003

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    DOI: 10.1038/sj.mp.4001138

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  • A primary CNS lymphoma in spontaneous remission for 3.5 years after initial detection of the lesions by MRI Reviewed

    Takashi Kon, Akiyoshi Kakita, Akira Koide, Hiroshi Mori, Ryuichi Tanaka, Hitoshi Takahashi

    Brain Tumor Pathology   20 ( 1 )   27 - 31   2003

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  • Neonatal perturbation of neurotrophic signaling results in abnormal sensorimotor gating and social interaction in adults: implication for epidermal growth factor in cognitive development (vol 8, pg 19, 2003) Reviewed

    T Futamura, A Kakita, M Tohmi, H Sotoyama, H Takahashi, H Nawa

    MOLECULAR PSYCHIATRY   8 ( 5 )   565 - 565   2003

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  • Bilateral periventricular nodular heterotopia due to filamin 1 gene mutation: widespread glomeruloid microvascular anomaly and dysplastic cytoarchitecture in the cerebral cortex Reviewed

    A Kakita, S Hayashi, F Moro, R Guerrini, T Ozawa, K Ono, S Kameyama, CA Walsh, H Takahashi

    ACTA NEUROPATHOLOGICA   104 ( 6 )   649 - 657   2002.12

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    DOI: 10.1007/s00401-002-0594-9

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  • Selective reduction of a PDZ protein, SAP-97, in the prefrontal cortex of patients with chronic schizophrenia Reviewed

    K Toyooka, S Iritani, T Makifuchi, O Shirakawa, N Kitamura, K Maeda, R Nakamura, K Niizato, M Watanabe, A Kakita, H Takahashi, T Someya, H Nawa

    JOURNAL OF NEUROCHEMISTRY   83 ( 4 )   797 - 806   2002.11

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    DOI: 10.1046/j.1471-4159.2002.01181.x

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  • Neuronal migration disturbance and consequent cytoarchitecture in the cerebral cortex following transplacental administration of methylmercury Reviewed

    A Kakita, C Inenaga, M Sakamoto, H Takahashi

    ACTA NEUROPATHOLOGICA   104 ( 4 )   409 - 417   2002.10

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    DOI: 10.1007/s00401-002-0571-3

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  • Evaluation of changes in methylmercury accumulation in the developing rat brain and its effects: a study with consecutive and moderate dose exposure throughout gestation and lactation periods Reviewed

    M Sakamoto, A Kakita, K Wakabayashi, H Takahashi, A Nakano, H Akagi

    BRAIN RESEARCH   949 ( 1-2 )   51 - 59   2002.9

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  • Fusiform gyrus epilepsy: the use of ictal magnetoencephalography - Case report Reviewed

    M Oishi, S Kameyama, N Morota, M Tomikawa, M Wachi, A Kakita, H Takahashi, R Tanaka

    JOURNAL OF NEUROSURGERY   97 ( 1 )   200 - 204   2002.7

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    DOI: 10.3171/jns.2002.97.1.0200

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  • Cerebellar cortical tau pathology in progressive supranuclear palsy and corticobasal degeneration Reviewed

    YS Piao, S Hayashi, K Wakabayashi, A Kakita, Aida, I, M Yamada, H Takahashi

    ACTA NEUROPATHOLOGICA   103 ( 5 )   469 - 474   2002.5

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    DOI: 10.1007/s00401-001-0488-2

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  • メチル水銀投与により惹起された発生期大脳の未分化細胞移動障害

    柿田 明美, 稲永 親憲, 坂本 峰至, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   22   2002.5

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  • 発生期脳における未分化細胞の移動経路と動態 Reviewed

    柿田 明美

    新潟医学会雑誌   116 ( 3 )   1 - 7   2002

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  • 進行性核上性麻痺:パーキンソン症状と中等度の痴呆を呈した一剖検例 Reviewed

    会田 泉, 稲永親憲, 柿田明美, 石川 厚

    神経内科   56 ( 3 )   209 - 211   2002

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  • Bilateral periventricular nodular heterotopia with an exon 11 (Val528Met) filamin 1 gene mutation. Reviewed

    Kakita A, Hayashi S, Moro F, Guerrini R, Ozawa T, Ono K, Kameyama S, Walsh CA, Takahashi H

    Ann. Rep. Jpn. Epi. Res. Found.   14   67 - 75   2002

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  • Urinary trypsin inhibitor exerts protective effects on the hepatic microvasculature in hypotensive brain-dead rats Reviewed

    T Takahashi, K Itahashi, Y Ito, T Ueno, A Kakita

    PROCEEDINGS OF THE 37TH CONGRESS OF THE EUROPEAN SOCIETY FOR SURGICAL RESEARCH   257 - 260   2002

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  • Abnormal expression of epidermal growth factor and its receptor in the forebrain and serum of schizophrenic patients Reviewed

    T Futamura, K Toyooka, S Iritani, K Niizato, R Nakamura, K Tsuchiya, T Someya, A Kakita, H Takahashi, H Nawa

    MOLECULAR PSYCHIATRY   7 ( 7 )   673 - 682   2002

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  • 発生期脳における未分化細胞の移動経路 ─ ストリートとアベニュー ─ Reviewed

    柿田明美, 高橋 均

    新潟大学学報   ( 665 )   2001.11

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  • Slowly progressive dementia and multiple cerebral cortical infarctions following mitral valve replacement Reviewed

    A Ishikawa, A Kakita, J Goto, H Tanaka, H Takahashi

    CLINICAL NEUROPATHOLOGY   20 ( 6 )   239 - 242   2001.11

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  • Experimentally induced leptomeningeal glioneuronal heterotopia and underlying cortical dysplasia of the lateral limbic area in rats treated transplacentally with methylmercury Reviewed

    A Kakita, K Wakabayashi, YS Piao, H Takahashi

    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY   60 ( 8 )   768 - 777   2001.8

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  • Aprosencephaly: histopathological features of the rudimentary forebrain and retina Reviewed

    A Kakita, S Hayashi, M Arakawa, H Takahashi

    ACTA NEUROPATHOLOGICA   102 ( 1 )   110 - 116   2001.7

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  • A quantitative study on the expression of synapsin II and N-ethylmaleimide-sensitive fusion protein in schizophrenic patients Reviewed

    C Imai, T Sugai, S Iritani, K Niizato, R Nakamura, T Makifuchi, A Kakita, H Takahashi, H Nawa

    NEUROSCIENCE LETTERS   305 ( 3 )   185 - 188   2001.6

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    DOI: 10.1016/S0304-3940(01)01844-4

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  • Expression of calbindin D-28k and parvalbumin in cerebral cortical dysgenesis induced by administration of ethylnitrosourea to rats at the stage of neurogenesis Reviewed

    K Oyanagi, A Kakita, K Kawasaki, S Hayashi, M Yamada

    ACTA NEUROPATHOLOGICA   101 ( 4 )   375 - 382   2001.4

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  • Migration pathways and behavior of glial progenitors in the postnatal forebrain. Reviewed

    Kakita A

    Human cell   14 ( 1 )   59 - 75   2001.3

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  • Ubiquitinated neuronal inclusions in the neostriatum in patients with amyotrophic lateral sclerosis with and without dementia - A study of 60 patients 31 to 87 years of age Reviewed

    K Wakabayashi, YS Piao, S Hayashi, A Kakita, M Yamada, H Takahashi

    CLINICAL NEUROPATHOLOGY   20 ( 2 )   47 - 52   2001.3

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  • Calpain-mediated degradation of p35 to p25 in postmortem human and rat brains Reviewed

    S Taniguchi, Y Fujita, S Hayashi, A Kakita, H Takahashi, S Murayama, TC Saido, S Hisanaga, T Iwatsubo, M Hasegawa

    FEBS LETTERS   489 ( 1 )   46 - 50   2001.1

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    DOI: 10.1016/S0014-5793(00)02431-5

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  • Surgical strategy and outcomes for epileptic patients with focal cortical dysplasia or dysembryoplastic neuroepithelial tumor Reviewed

    S Kameyama, M Fukuda, M Tomikawa, N Morota, M Oishi, M Wachi, O Kanazawa, M Sasagawa, A Kakita, H Takahashi

    EPILEPSIA   42   37 - 41   2001

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  • Symptomatic child case of subependymoma in the fourth ventricle without hydrocephalus Reviewed

    Gomes Ivan Fontenele, Kouichirou Okamoto, Jusuke Ito, Akiyoshi Kakita, Hiroshi Mori, Yasuko Toyoshima, Kunio Sakai, Kazuhiro Ishikawa

    Radiation Medicine - Medical Imaging and Radiation Oncology   19 ( 1 )   37 - 42   2001

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  • Erratum: Intrauterine methylmercury intoxication. Consequence of the inherent brain lesions and cognitive dysfunction in maturity (Brain Research (2000) 877 (322-330) PII: S0006899300027177)) Reviewed

    Akiyoshi Kakita, Koichi Wakabayashi, Mu Su, Yuichiro Yoneoka, Mineshi Sakamoto, Fusahiro Ikuta, Hitoshi Takahashi

    Brain Research   887 ( 2 )   488   2000.12

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  • Erratum to: "Intrauterine methylmercury intoxication. Consequence of the inherent brain lesions and cognitive dysfunction in maturity". Reviewed

    Kakita A, Wakabayashi K, Su M, Yoneoka Y, Sakamoto M, Ikuta F, Takahashi H

    Brain research   887 ( 2 )   488   2000.12

  • Intrauterine methylmercury intoxication - Consequence of the inherent brain lesions and cognitive dysfunction in maturity Reviewed

    A Kakita, K Wakabayashi, M Su, Y Yoneoka, M Sakamoto, F Ikuta, H Takahashi

    BRAIN RESEARCH   877 ( 2 )   322 - 330   2000.9

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    DOI: 10.1016/S0006-8993(00)02717-7

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  • Parkinsonism in HIV encephalopathy. Reviewed

    Tanaka M, Endo K, Suzuki T, Kakita A, Takahashi H, Sata T

    Movement disorders : official journal of the Movement Disorder Society   15 ( 5 )   1032 - 1033   2000.9

  • Distinct pattern of neuronal degeneration in the fetal rat brain induced by consecutive transplacental administration of methylmercury Reviewed

    A Kakita, K Wakabayashi, M Su, M Sakamoto, F Ikuta, H Takahashi

    BRAIN RESEARCH   859 ( 2 )   233 - 239   2000.3

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    DOI: 10.1016/S0006-8993(00)01964-8

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  • Determinants of tapping speed in normal control subjects and subjects with Parkinson's disease: Differing effects of brief and continued practice Reviewed

    Masami Tanaka, Kotaro Endo, Takashi Suzuki, Akiyoshi Kakita, Hitoshi Takahashi, Tetsutaro Sata

    Movement Disorders   15 ( 5 )   843 - 849   2000

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    DOI: 10.1002/1531-8257(200009)15:5<843::AID-MDS1013>3.0.CO;2-2

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  • Patterns and dynamics of SVZ cell migration in the postnatal forebrain: Monitoring living progenitors in slice preparations Reviewed

    A Kakita, JE Goldman

    NEURON   23 ( 3 )   461 - 472   1999.7

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    DOI: 10.1016/S0896-6273(00)80800-4

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  • Patients with temporal lobe epilepsy show an increase in brain-derived neurotrophic factor protein and its correlation with neuropeptide Y Reviewed

    M Takahashi, S Hayashi, A Kakita, K Wakabayashi, M Fukuda, S Kameyama, R Tanaka, H Takahashi, H Nawa

    BRAIN RESEARCH   818 ( 2 )   579 - 582   1999.2

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  • てんかん原性病巣としてのCortical Dysplasiaにおける結節性硬化症原因遺伝子蛋白Tuberinの発現 Reviewed

    高橋 均, 柿田明美, 水口 雅, 高嶋幸男, 亀山茂樹, 福多真史, 田中隆一

    てんかん治療研究振興財団研究年報   11   53 - 57   1999

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  • Reply to Altschuler, letter to the editors of Altschuler E.L. Reviewed

    Kakita A, Takahashi H

    Acta Neuropathologica   97 ( 1 )   103 - 104   1999

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  • Hereditary dentatorubral-pallidoluysian atrophy: detection of widespread ubiquitinated neuronal and glial intranuclear inclusions in the brain Reviewed

    Y Hayashi, A Kakita, M Yamada, R Koide, S Igarashi, H Takano, T Ikeuchi, K Wakabayashi, S Egawa, S Tsuji, H Takahashi

    ACTA NEUROPATHOLOGICA   96 ( 6 )   547 - 552   1998.12

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  • Accumulation of alpha-synuclein/NACP is a cytopathological feature common to Lewy body disease and multiple system atrophy Reviewed

    K Wakabayashi, S Hayashi, A Kakita, M Yamada, Y Toyoshima, M Yoshimoto, H Takahashi

    ACTA NEUROPATHOLOGICA   96 ( 5 )   445 - 452   1998.11

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  • Process of repair in the neuroepithelium of developing rat brain during neurogenesis: chronological and quantitative observation of DNA-replicating cells Reviewed

    K Oyanagi, A Kakita, M Yamada, K Kawasaki, S Hayashi, F Ikura

    DEVELOPMENTAL BRAIN RESEARCH   108 ( 1-2 )   229 - 238   1998.6

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  • Apolipoprotein E epsilon 4 allele and progression of cortical Lewy body pathology in Parkinson's disease Reviewed

    K Wakabayashi, A Kakita, S Hayashi, K Okuizumi, O Onodera, H Tanaka, A Ishikawa, S Tsuji, H Takahashi

    ACTA NEUROPATHOLOGICA   95 ( 5 )   450 - 454   1998.5

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  • Hereditary dentatorubral-pallidoluysian atrophy: ubiquitinated filamentous inclusions in the cerebellar dentate nucleus neurons Reviewed

    Y Hayashi, A Kakita, M Yamada, S Egawa, S Oyanagi, H Naito, S Tsuji, H Takahashi

    ACTA NEUROPATHOLOGICA   95 ( 5 )   479 - 482   1998.5

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  • Selective involvement of large motor neurons in the spinal cord of rats treated with methylmercury Reviewed

    M Su, K Wakabayashi, A Kakita, F Ikuta, H Takahashi

    JOURNAL OF THE NEUROLOGICAL SCIENCES   156 ( 1 )   12 - 17   1998.3

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    DOI: 10.1016/S0022-510X(98)00030-6

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  • Widespread neuronal degeneration in rats following oral administration of methylmercury during the postnatal developing phase: A model of fetal-type Minamata disease Reviewed

    M Sakamoto, K Wakabayashi, A Kakita, H Takahashi, T Adachi, A Nakano

    BRAIN RESEARCH   784 ( 1-2 )   351 - 354   1998.2

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    DOI: 10.1016/S0006-8993(97)01400-5

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  • Pick's disease: selective occurrence of apolipoprotein E-immunoreactive Pick bodies in the limbic system Reviewed

    S Hayashi, K Wakabayashi, K Iwanaga, A Kakita, K Seki, M Tanaka, K Okuizumi, O Onodera, H Tanaka, S Tsuji, H Takahashi

    ACTA NEUROPATHOLOGICA   95 ( 1 )   1 - 4   1998.1

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  • Prevertebral abscesses with a protracted insidious clinical course and subsequent lethal, acute pyogenic meningitis and septic shock Reviewed

    Tetsutaro Ozawa, Osamu Onodera, Akiyoshi Kakita, Kenju Aoki, Keiko Tanaka, Yoshiaki Soma, Hitoshi Takahashi, Shoji Tsuji

    Brain and Nerve   50 ( 1 )   75 - 79   1998.1

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  • 不顕性に経過したprevertebral abscessー急性化膿性髄膜炎と敗血症性ショックをきたしたI剖検例 Reviewed

    小澤鉄太郎, 小野寺理, 柿田明美, 青木賢樹, 田中恵子, 相馬芳明, 高橋 均, 辻省次

    脳神経   50   75 - 79   1998

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  • Cyclopia: histogenesis of the single optic nerve Reviewed

    A Kakita, K Wakabayashi, N Sekizuka, H Takahashi

    ACTA NEUROPATHOLOGICA   94 ( 5 )   509 - 513   1997.11

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  • Degeneration of spinal dorsal root ganglia in adult rats treated with methylmercury: Chronological observations on the cell bodies, centrally directed axons and presynaptic terminals Reviewed

    M Su, A Kakita, K Wakabayashi, M Yamada, H Takahashi, F Ikuta

    NEUROPATHOLOGY   17 ( 3 )   201 - 207   1997.9

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    DOI: 10.1111/j.1440-1789.1997.tb00039.x

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  • Adrenoleukodystrophy with involvement of the cerebral cortex Reviewed

    A Kakita, A Ishikawa, R Koike, S Tsuji, H Takahashi

    NEUROPATHOLOGY   17 ( 2 )   106 - 111   1997.6

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    DOI: 10.1111/j.1440-1789.1997.tb00022.x

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  • Eosinophilic intranuclear inclusions in the hippocampal pyramidal neurons of a patient with amyotrophic lateral sclerosis Reviewed

    A Kakita, K Oyanagi, H Nagai, H Takahashi

    ACTA NEUROPATHOLOGICA   93 ( 5 )   532 - 536   1997.5

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  • Expression of the LIS-1 gene product in brain anomalies with a migration disorder Reviewed

    H Isumi, S Takashima, A Kakita, M Yamada, K Ikeda, M Mizuguchi

    PEDIATRIC NEUROLOGY   16 ( 1 )   42 - 44   1997.1

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  • Degeneration of the synaptic boutons of parallel fibers in rats treated with methylmercury: Chronological observations Reviewed

    M Su, A Kakita, M Yamada, H Takahashi, F Ikuta

    NEUROPATHOLOGY   16 ( 3 )   172 - 177   1996.9

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  • Variability of brain lesions in rats administered methylmercury at various postnatal development phases Reviewed

    K Wakabayashi, A Kakita, M Sakamoto, M Su, K Iwanaga, F Ikuta

    BRAIN RESEARCH   705 ( 1-2 )   267 - 272   1995.12

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    DOI: 10.1016/0006-8993(95)01208-7

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  • LISSENCEPHALY GENE-PRODUCT - LOCALIZATION IN THE CENTRAL-NERVOUS-SYSTEM AND LOSS OF IMMUNOREACTIVITY IN MILLER-DIEKER SYNDROME Reviewed

    M MIZUGUCHI, S TAKASHIMA, A KAKITA, M YAMADA, K IKEDA

    AMERICAN JOURNAL OF PATHOLOGY   147 ( 4 )   1142 - 1151   1995.10

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  • Pleomorphic xanthoastrocytoma: New ultrastructural observations Reviewed

    Hitoshi Takahashi, Akiyoshi Kakita, Yoshiho Honda, Shigeki Kameyama, Ryuichi Tanaka, Fusahiro Ikuta

    Neuropathology   15 ( 3-4 )   133 - 137   1995

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    DOI: 10.1111/j.1440-1789.1995.tb00256.x

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  • Clear cell variants of intracranial tumors: meningioma and ependymoma. Reviewed

    Kakita A, Takahashi H, Fusejima T, Konno K, Nakazawa T, Aoki K, Tanaka R, Ikuta F

    Noshuyo byori = Brain tumor pathology   12 ( 2 )   111 - 116   1995

  • LEWY BODIES IN THE CEREBELLAR DENTATE NUCLEUS OF A PATIENT WITH PARKINSONS-DISEASE Reviewed

    A KAKITA, H TAKAHASHI, Y HOMMA, F IKUTA

    PATHOLOGY INTERNATIONAL   44 ( 12 )   878 - 880   1994.12

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  • Immunohistochemical study of lacrimal gland epithelial tumors using Alpha-1 proteinase inhibitor. Reviewed

    Ishimoto K, Tosaka Y, Sawaguchi S, Kakita A

    Folia Ophthalmologica Japonica   45   35 - 38   1994

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  • SPECIFIC EXPRESSION OF INOSITOL 1,4,5-TRISPHOSPHATE 3-KINASE IN DENDRITIC SPINES Reviewed

    M YAMADA, A KAKITA, M MIZUGUCHI, SG RHEE, SU KIM, F IKUTA

    BRAIN RESEARCH   606 ( 2 )   335 - 340   1993.3

  • DEVELOPMENTAL PROFILE OF INOSITOL 1,4,5-TRISPHOSPHATE 3-KINASE IN RAT CEREBELLAR CORTEX - LIGHT AND ELECTRON-MICROSCOPIC IMMUNOHISTOCHEMICAL STUDIES Reviewed

    M YAMADA, A KAKITA, M MIZUGUCHI, SG RHEE, SU KIM, F IKUTA

    DEVELOPMENTAL BRAIN RESEARCH   71 ( 1 )   137 - 145   1993.1

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  • Malignant syndrome induced by L-threo-3,4-dihydroxyphenylserine in a patient with Parkinson's disease. Reviewed

    Ishikawa A, Tanaka H, Miyatani N, Kakita A, Wakabayashi K

    Neurological Medicine   39   510 - 515   1993

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  • Expression of tenascin in neuroepithelial cells in developing rat telencephalic pallium. Reviewed

    KAKITA Akiyoshi

    Niigata Medical Journal   107 ( 10 )   911 - 917   1993

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:Niigata University  

    CiNii Article

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    Other Link: http://search.jamas.or.jp/link/ui/1994209318

  • Xeroderma pigmentosum with neurological abnorlmalities. Reviewed

    Takahashi H, Kakita A, Ikuta F

    Molecular Medicine   30   1174 - 1181   1993

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  • PRIMARY LEPTOMENINGEAL GLIOMA - ULTRASTRUCTURAL AND LAMININ IMMUNOHISTOCHEMICAL STUDIES Reviewed

    A KAKITA, K WAKABAYASHI, H TAKAHASHI, E OHAMA, F IKUTA, S TOKIGUCHI

    ACTA NEUROPATHOLOGICA   83 ( 5 )   538 - 542   1992.4

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  • ULTRASTRUCTURAL-LOCALIZATION OF INOSITOL 1,4,5-TRISPHOSPHATE 3-KINASE IN RAT CEREBELLAR CORTEX Reviewed

    M YAMADA, A KAKITA, M MIZUGUCHI, SG RHEE, SU KIM, F IKUTA

    BRAIN RESEARCH   578 ( 1-2 )   41 - 48   1992.4

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  • SYRINGOMYELIA - A NEUROPATHOLOGICAL STUDY OF 18 AUTOPSY CASES Reviewed

    K HINOKUMA, E OHAMA, K OYANAGI, A KAKITA, K KAWAI, F IKUTA

    ACTA PATHOLOGICA JAPONICA   42 ( 1 )   25 - 34   1992.1

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  • Immunohistochemical atudy of synaptic vesicle-specific protein in Creutzfeldt-Jacob disease brain. Reviewed

    Wakabayashi K, Kakita A, Takahashi H, Obata K, Ikuta F

    Neurological Sciences   36   503 - 510   1992

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    DOI: 10.11477/mf.1431900247

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  • Syringomyelia: A Neuropathological Study of 18 Autopsy Cases Reviewed

    Kaoru Hinokuma, Eisaku Ohama, Kiyomitsu Oyanagi, Akiyoshi Kakita, Kensuke Kawai, Fusahiro Ikuta

    Pathology International   42 ( 1 )   25 - 34   1992

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    DOI: 10.1111/j.1440-1827.1992.tb01107.x

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Books

  • 非定型パーキンソニズムー基礎と臨床ー

    他田真理, 柿田明美( Role: Contributor ,  Ⅱ.各論 1.多系統萎縮症 C.病理)

    文光堂  2019.5  ( ISBN:9784830615474

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    Total pages:242   Responsible for pages:pp.94-99   Language:Japanese Book type:Scholarly book

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  • ペランパネルによるてんかんの治療ストラテジー

    北浦弘樹, 柿田明美( Role: Contributor ,  AMPA型グルタミン酸受容体の構造とシナプス伝達機構)

    先端医学社  2019.1  ( ISBN:9784865503777

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    Total pages:89   Responsible for pages:pp.17-21   Language:Japanese Book type:Scholarly book

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  • カラーアトラス 病理組織の見方と鑑別診断.第6版

    豊島靖子, 柿田明美( Role: Contributor ,  神経 (2) 変性・炎症)

    医歯薬出版  2018.9  ( ISBN:9784263731857

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    Total pages:699   Responsible for pages:pp.473-505   Language:Japanese Book type:Scholarly book

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  • てんかん学用語事典

    柿田 明美( Role: Contributor ,  Focal cortical dysplasia (FCD))

    診断と治療社  2017.12  ( ISBN:9784787823410

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    Total pages:165   Responsible for pages:pp.59-60   Language:Japanese Book type:Dictionary, encyclopedia

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  • 脳腫瘍臨床病理カラーアトラス 第4版

    柿田 明美( Role: Contributor ,  Melanocytic lesions)

    医学書院  2017.10  ( ISBN:9784260030472

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    Total pages:232   Responsible for pages:pp.147-149   Language:Japanese Book type:Scholarly book

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  • 運動失調のみかた、考えかた –小脳と脊髄小脳変性症−

    清水宏, 柿田明美( Role: Contributor ,  脊髄小脳変性症の神経病理)

    中外医学社  2017.9  ( ISBN:9784498228900

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    Total pages:358   Responsible for pages:pp.300-307   Language:Japanese Book type:Scholarly book

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  • 稀少てんかんの診療指標

    柿田 明美( Role: Contributor ,  稀少てんかんの病理)

    診断と治療社  2017.4  ( ISBN:9784787823090

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    Total pages:276   Responsible for pages:pp.28-31   Language:Japanese Book type:Scholarly book

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  • 神経内科 Clinical questions and pearls:認知症

    清水 宏, 柿田明美( Role: Contributor ,  プリオン病とは何ですか?)

    中外医学社  2016.12  ( ISBN:9784498129863

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    Total pages:436   Responsible for pages:pp.374-378   Language:Japanese Book type:Textbook, survey, introduction

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  • てんかん白書

    丸栄一, 岡田元宏, 兼子直, 柿田明美, 高橋幸利( Role: Contributor ,  基礎研究とトランスレーショナル研究)

    南江堂  2016.10  ( ISBN:9784524259632

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    Total pages:206   Responsible for pages:pp.157-162   Language:Japanese Book type:Scholarly book

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  • 臨床てんかん学

    柿田 明美( Role: Contributor ,  海馬硬化(第3章 てんかんの病理学))

    医学書院  2015.11  ( ISBN:9784260021197

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    Total pages:688   Responsible for pages:pp.23-28   Language:Japanese Book type:Textbook, survey, introduction

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  • Posterior Fossa Tumors in Children

    Morota N, Kumabe T, Kakita A( Role: Contributor ,  Posterior fossa choroid plexus tumor. [Chapter 48])

    Springer International Publishing  2015.4  ( ISBN:9783319112732

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    Total pages:948   Responsible for pages:pp.723-743   Language:English Book type:Scholarly book

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  • てんかん専門医ガイドブック ―てんかんにかかわる医師のための基礎知識―

    柿田 明美( Role: Contributor ,  てんかん原性の病理)

    診断と治療社  2014.3  ( ISBN:9784787820341

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    Total pages:320   Responsible for pages:pp.27-30   Language:Japanese Book type:Textbook, survey, introduction

    第2章 てんかんの病因・病態生理

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  • 稀少難治てんかん診療マニュアル ①

    柿田 明美( Role: Contributor ,  限局性皮質異形成 Ⅰ.疾患の特徴と診断のポイント)

    診断と治療社  2013.4  ( ISBN:9784787819864

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    Total pages:186   Responsible for pages:pp.65-67   Language:Japanese Book type:Textbook, survey, introduction

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  • 稀少難治てんかん診療マニュアル ②

    柿田 明美( Role: Contributor ,  病理診断マニュアル Ⅱ.診断マニュアル)

    診断と治療社  2013.4 

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    Total pages:186   Responsible for pages:pp.114-116   Language:Japanese Book type:Textbook, survey, introduction

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  • 小児神経学の進歩.第41集

    遠山 潤, 柿田明美( Role: Contributor ,  動脈管開存の既往があり,難治性てんかんを示した女性例.Clinical Pathological Conference.)

    診断と治療社  2012.5  ( ISBN:9784787818850

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    Total pages:144   Responsible for pages:pp.78-101   Language:Japanese Book type:Scholarly book

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  • てんかんテキスト New Version

    柿田 明美( Role: Contributor ,  てんかんの病理)

    中山書店  2012.5  ( ISBN:9784521734408

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    Total pages:384   Responsible for pages:pp.25-32   Language:Japanese Book type:Textbook, survey, introduction

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  • Environmental Chemistry and Toxicology of Mercury

    Sakamoto M, Murata K, Kakita A, Sasaki M( Role: Contributor ,  Chapter 15. A review of mercury toxicity with special reference to methylmercury)

    John Wiley & Sons, Inc.  2012.1  ( ISBN:9780470578728

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    Total pages:574   Responsible for pages:pp.501-516   Language:English Book type:Scholarly book

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  • 脳腫瘍臨床病理カラーアトラス 第3版

    柿田 明美( Role: Contributor ,  Melanocytic tumors)

    医学書院  2009.5  ( ISBN:9784260007924

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    Total pages:216   Responsible for pages:pp.134-136   Language:Japanese Book type:Scholarly book

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  • 小児神経学の進歩 第36集

    柿田 明美( Role: Contributor ,  中枢神経系の発生とその異常)

    診断と治療社  2007.6  ( ISBN:9784787815613

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    Total pages:153   Responsible for pages:pp.37-46   Language:Japanese Book type:Scholarly book

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  • 難治性てんかんの外科治療—プラクティカル・ガイドブック

    柿田 明美( Role: Contributor ,  てんかん焦点の病理)

    診断と治療社  2007.1  ( ISBN:9784787815583

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    Total pages:257   Responsible for pages:pp.9-13   Language:Japanese Book type:Scholarly book

    第1章てんかんとは何か

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  • ブックレット新潟大学27.脳の神秘と疑問.─ヒトの脳は何を考える?

    柿田 明美( Role: Contributor ,  ヒトの脳の構造と細胞(第1章))

    新潟日報事業社  2004.4 

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    Total pages:72   Responsible for pages:pp.4-20   Language:Japanese Book type:General book, introductory book for general audience

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  • Pathology and Genetics: Developmental Neuropathology

    KAKITA Akiyoshi, Takahashi H( Role: Contributor ,  Hydrocephalus (Chapter 16))

    Neuropath Press  2004 

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    Responsible for pages:pp. 126-130   Language:English Book type:Textbook, survey, introduction

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  • Understanding of Minamata Disease. Methylmercury Poisoning in Minamata and Niigata, Japan.

    Kakita A, Wakabayashi K, Su M, Sakamoto M, Ikuta F, Takahashi H( Role: Contributor ,  Intrauterine methylmercury intoxication: pattern of neuronal degeneration in the fetal brain and consequence on higher brain function in maturity.)

    The Japan Public Health Association  2001 

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    Responsible for pages:pp.85-93   Language:English Book type:Scholarly book

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MISC

  • Search for APOE rare missense variants in a Japanese population

    宮下哲典, 大日方藍, 他田真理, 阿部学, 柿田明美, 池内健

    Bio Clinica   39 ( 4 )   2024

  • 非腫瘍性疾患における脳生検の適応決定に有用な画像所見

    木崎利哉, 金澤雅人, 石黒敬信, 棗田学, 岡本浩一郎, 大石誠, 柿田明美, 藤井幸彦, 小野寺理

    日本神経学会学術大会プログラム・抄録集   65th   2024

  • 【ALS-どこまでわかり,どこまで治るか】総論 グアム島と西ニューギニアのALSとPDCとは何であり,医学はそれらから何を学んだのか

    小柳 清光, 橋本 智代, 和田 学, 山崎 峰雄, 中原 亜紗, 柿田 明美

    Clinical Neuroscience   41 ( 3 )   325 - 329   2023.3

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  • 脳生検症例における診断と予後についての後方視的検討

    木崎利哉, 石黒敬信, 棗田学, 大石誠, 柿田明美, 藤井幸彦, 小野寺理, 金澤雅人

    日本神経学会学術大会プログラム・抄録集   64th   2023

  • Evaluation of the influence of confounding factors in comprehensive gene expression analysis of human postmortem brain

    旗野将貴, 宮原一総, 日野瑞城, 日野瑞城, 長岡敦子, 長岡敦子, 兪志前, 林秀樹, 柿田明美, 富田博秋, 三浦至, 國井泰人, 國井泰人

    日本生物学的精神医学会(Web)   45th   2023

  • Expression changes in molecules related to DNA double-strand break repair in a high stress response group of schizophrenia.

    宍戸理紗, 日野瑞城, 日野瑞城, 長岡敦子, 長岡敦子, 林秀樹, 柿田明美, 三浦至, 富田博秋, 國井泰人, 國井泰人

    日本生物学的精神医学会(Web)   45th   2023

  • Gene expression analysis of ZDHHC family of protein S-palmitoylating enzymes in postmortem brains of patients with schizophrenia

    細貝優人, 日野瑞城, 日野瑞城, 宍戸理紗, 長岡敦子, 長岡敦子, 林秀樹, 柿田明美, 富田博秋, 三浦至, 國井泰人, 國井泰人

    日本生物学的精神医学会(Web)   45th   2023

  • CPC: A case of subacute progressive focal neurological symptoms with renal infarction.

    長谷川絵理子, 岩渕洋平, 下島恭弘, 田澤浩一, 和田庸子, 金澤雅人, 小林大介, 柿田明美, 瀧澤淳, 鋪野紀好, 松本正孝, 須永眞司

    日本内科学会雑誌   111 ( 9 )   2022

  • Identification of DEGs in schizophrenia postmortem brains classified by stress-related molecules.

    宍戸理紗, 國井泰人, 國井泰人, 日野瑞城, 日野瑞城, 長岡敦子, 長岡敦子, 泉竜太, 柿田明美, 矢部博興

    日本生物学的精神医学会(Web)   44th   2022

  • 統合失調症患者とそのモデル動物の聴覚野におけるEGR1/zif268の発現変化

    岩倉百合子, 岩倉百合子, 川原玲香, 喜田聡, 喜田聡, 外山英和, GABDULKHAEV Ramil, 高橋均, 國井泰人, 國井泰人, 日野瑞城, 日野瑞城, 長岡敦子, 泉竜太, 宍戸理紗, 染矢俊幸, 矢部博興, 柿田明美, 那波宏之, 那波宏之

    日本神経化学会大会抄録集(Web)   65th   2022

  • OPRM1 rs1799971 polymorphism has an ethnicity-dependent impact on risk for schizophrenia by disturbing the opioids system: A Meta-analysis and Postmortem Brain Study

    宮原一総, 日野瑞城, 日野瑞城, 宍戸理紗, 泉竜太, 長岡敦子, 柿田明美, 矢部博興, 富田博秋, 富田博秋, 國井泰人, 國井泰人

    日本生物学的精神医学会(Web)   44th   2022

  • 加齢と関連したDNA脱メチル化がTDP-43量の自己調節機構を障害する

    小池佑佳, 須貝章弘, 原範和, 伊藤絢子, 横関明男, 石原智彦, 山岸拓磨, 坪口晋太朗, 他田真理, 池内健, 柿田明美, 小野寺理

    Dementia Japan   35 ( 4 )   2021

  • Clinicopathologic study of two patients with amyotrophic lateral sclerosis harboring TBK1 mutations

    TADA Mari, HATANO Yuya, TAKESHIMA Akari, SAITO Rie, SAJI Etsuji, TOKUTAKE Takayoshi, ISHIHARA Tomohiko, TOYOSHIMA Yasuko, ONODERA Osamu, KAKITA Akiyoshi

    日本神経学会学術大会プログラム・抄録集   62nd   2021

  • 神経変性疾患領域の基盤的調査研究 孤発性ALSにおける認知症発症リスクとしてのAPOE2

    小野寺理, 畠野雄也, 石原智彦, 他田真理, 柿田明美

    神経変性疾患領域の基盤的調査研究 令和2年度 総括・分担研究報告書(Web)   2021

  • Quantitative protein expression study in the postmortem brains of patients with schizophrenia-ALDH4A1 expression and its association with genetic polymorphism

    長岡敦子, 國井泰人, 國井泰人, 日野瑞城, 泉竜太, 宍戸理紗, 齊ノ内信, 柿田明美, 矢部博興

    日本生物学的精神医学会誌(Web)   32 ( 4 )   2021

  • 統合失調症の死後脳におけるサイトカインIL-1のタンパク質発現解析

    泉竜太, 國井泰人, 國井泰人, 長岡敦子, 長岡敦子, 日野瑞城, 齊ノ内信, 柿田明美, 矢部博興

    統合失調症研究   10 ( 1 )   2020

  • ヒト死後脳におけるAPP・APOEの遺伝子発現解析

    LIU Lixin, 宮下哲典, 村上涼太, ZHU Bin, 原範和, 菊地正隆, 月江珠緒, 樋口陽, 春日健作, 中谷明弘, 赤津裕康, 柿田明美, 村山繁雄, 池内健

    Dementia Japan   33 ( 4 )   519   2019.10

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    J-GLOBAL

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  • 視神経脊髄炎の病変局所における炎症極性の解析

    柳村 文寛, 佐治 越爾, 若杉 尚宏, 穂苅 万李子, 柳川 香織, 豊島 靖子, 高橋 均, 柿田 明美, 小野寺 理, 河内 泉

    神経免疫学   24 ( 1 )   131 - 131   2019.9

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  • 統合失調症患者における脳内コンドロイチン硫酸鎖の変化

    湯川 尊行, 岩倉 百合子, 武井 延之, 斎藤 摩美, 渡部 雄一郎, 豊岡 和彦, 五十嵐 道弘, 新里 和弘, 大島 健一, 國井 泰人, 矢部 博興, 松本 純弥, 和田 明, 日野 瑞城, 入谷 修司, 丹羽 真一, 竹内 亮子, 高橋 均, 柿田 明美, 染矢 俊幸, 那波 宏之

    精神神経学雑誌   ( 2019特別号 )   S410 - S410   2019.6

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  • 診断 悪性神経膠腫における術後静脈血栓塞栓症危険因子の検討 ポドプラニンとIDH変異の関係

    棗田 学, 渡邉 潤, 岡田 正康, 金丸 優, 塚本 佳広, 大石 誠, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   36 ( Suppl. )   070 - 070   2019.5

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  • Temozolomide and Notch inhibitor MRK-003 induce cell protective autophagy in malignant gliomas Reviewed

    Natsumeda Manabu, Aoki Hiroshi, Miyahara Hiroaki, Kakita Akiyoshi, Takahashi Hitoshi, Eberhart Charles G, Fujii Yukihiko

    BRAIN PATHOLOGY   29   142   2019.2

  • 7-tesla MR susceptibility-weighted imaging can dipict astrocytic and oligodendroglial pathology Reviewed

    Natsumeda Manabu, Matsuzawa Hitoshi, Tsukamoto Yoshihiro, Motohashi Kunio, Kanemaru Yu, Okamoto Kouichirou, Kakita Akiyoshi, Igarashi Hironaka, Nakata Tsutomu, Fujii Yukihiko

    BRAIN PATHOLOGY   29   68 - 69   2019.2

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  • Radiological, immunological, and pathological analysis of ependymal cells in neuromyelitis spectrum disorders

    Fumihiro Yanagimura, Etsuji Saji, Takahiro Wakasugi, Yasuko Toyoshima, Akiyoshi Kakita, Hitoshi Takahashi, Osamu Onodera, Izumi Kawachi

    BRAIN PATHOLOGY   29   134 - 134   2019.2

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  • Neuropathologic characteristics of patients with progressive suprenuclear palsy who died within four years after the disease onset

    Lu Zhang, Yasuko Toyoshima, Akari Takeshima, Hiroshi Shimizu, Itsuro Tomita, Osamu Onodera, Hitoshi Takahashi, Akiyoshi Kakita

    BRAIN PATHOLOGY   29   77 - 77   2019.2

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  • タンパク質定量解析における異なる二施設間で保管された死後脳試料の質の検討

    長岡敦子, 石橋美輝, 旗野将貴, 國井泰人, 國井泰人, 日野瑞城, 泉竜太, 竹島明, 那波宏之, 柿田明美, 矢部博興

    日本生物学的精神医学会(Web)   41st   2019

  • COX10変異とPMP22欠失を伴った白質脳症の一家系 臨床病理学的解析

    黒羽 泰子, 石黒 敬信, 長谷川 有香, 谷 卓, 高橋 哲哉, 松原 奈絵, 他田 真理, 河内 泉, 柿田 明美, 小野寺 理, 池内 健, 小池 亮子

    臨床神経学   58 ( Suppl. )   S327 - S327   2018.12

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  • COX10変異とPMP22欠失を伴った白質脳症の一家系 分子遺伝学的解析

    石黒 敬信, 黒羽 泰子, 原 範和, 目崎 直実, 三浦 健, 春日 健作, 長谷川 有香, 谷 卓, 高橋 哲哉, 松原 奈絵, 他田 真理, 河内 泉, 柿田 明美, 小野寺 理, 小池 亮子, 池内 健

    臨床神経学   58 ( Suppl. )   S327 - S327   2018.12

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  • HIGH DETECTION RATE OF MYD88MUTATIONS IN CEREBROSPINAL FLUID FROM PATIENTS WITH CENTRAL NERVOUS SYSTEM LYMPHOMAS Reviewed

    Watanabe Jun, Natsumeda Manabu, Okada Masayasu, Kobayashi Taiki, Kanemaru Yu, Oishi Makoto, Kakita Akiyoshi, Fujii Yukihiko

    NEURO-ONCOLOGY   20   169   2018.11

  • APOE遺伝型はAPPの遺伝子発現量に影響を及ぼすか? ヒト死後脳における検証

    村上 涼太, 朱 斌, 原 範和, 菊地 正隆, 月江 珠緒, 春日 健作, 宮下 哲典, 中谷 明弘, 赤津 裕康, 柿田 明美, 村山 繁雄, 池内 健

    Dementia Japan   32 ( 3 )   429 - 429   2018.9

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  • X-linked myotubular myopathyに合併した肝紫斑病による肝出血の1例

    会沢 慧亮, 舟山 一寿, 清水 宏, 田中 英智, 高橋 直也, 原田 夏実, 樋口 涼子, 青山 崇, 渡邉 拓, 柿田 明美, 高塚 尚和

    法医病理   24 ( 1 )   6 - 6   2018.6

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  • IDH変異型グリオーマの診断と術中治療―コラボレーションを通して実現を目指す―

    棗田学, 阿部英明, 岡田正康, 五十嵐博中, 中田力, 小山哲秀, 小野寺理, 柿田明美, 大石誠, 藤井幸彦

    日本蛋白質科学会年会プログラム・要旨集   18th   25   2018.5

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  • 長期間精神症状が先行した、PSEN1遺伝子変異を有する早期発症型家族性アルツハイマー病の1剖検例

    竹島 明, 他田 真理, 鈴木 正博, 春日 健作, 池内 健, 小野寺 理, 高橋 均, 柿田 明美, 伊古田 勇人

    信州医学雑誌   66 ( 1 )   110 - 111   2018.2

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  • 髄膜播種をきたしたEpithelioid glioblastomaの1例

    金丸 優, 棗田 学, 齋藤 理恵, 野澤 孝徳, 阿部 英明, 岡本 浩一郎, 大石 誠, 藤井 幸彦, 柿田 明美, 信澤 純人

    信州医学雑誌   66 ( 1 )   104 - 105   2018.2

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  • 長期間精神症状が先行した、PSEN1遺伝子変異を有する早期発症型家族性アルツハイマー病の1剖検例

    竹島 明, 他田 真理, 鈴木 正博, 春日 健作, 池内 健, 小野寺 理, 高橋 均, 柿田 明美, 伊古田 勇人

    信州医学雑誌   66 ( 1 )   110 - 111   2018.2

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  • 常染色体劣性遺伝性が疑われる若年発症 緩徐進行性小脳失調症の1剖検例

    齋藤 理恵, 他田 真理, 若林 允甫, 小野寺 理, 高橋 均, 池内 健, 柿田 明美, 横尾 英明

    信州医学雑誌   66 ( 1 )   111 - 112   2018.2

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  • 小胞体シャペロンをコードするCNPY3の劣性変異は早期発症てんかん性脳症を引き起こす

    才津浩智, 武藤弘樹, 加藤光広, 秋田天平, 柴田琢磨, 若本裕之, 池田浩子, 北浦弘樹, 青戸一司, 中島光子, 大場ちひろ, 宮武聡子, 三宅紀子, 柿田明美, 三宅健介, 福田敦夫, 松本直通

    日本先天異常学会学術集会プログラム・抄録集   58th   2018

  • 認知症臨床ゲノム情報データベース構築に関する開発研究

    池内健, 新飯田俊平, 佐々木貴史, 宮下哲典, 尾崎浩一, 広瀬信義, 中谷明弘, 柿田明美, 鈴木一詩, 齋藤祐子, 村山繁雄, 橋詰良夫, 寺田整司, 吉田真理, 嶋田裕之, 三村将, 岡野栄之, 岩坪威, 秋山治彦, 森啓

    Dementia Japan   32 ( 3 )   2018

  • 小胞体シャペロンをコードするCNPY3の劣性変異は早期発症てんかん性脳症を引き起こす

    才津浩智, 武藤弘樹, 加藤光広, 秋田天平, 柴田琢磨, 若本裕之, 池田浩子, 北浦弘樹, 青戸一司, 中島光子, 大場ちひろ, 宮武聡子, 三宅紀子, 柿田明美, 三宅健介, 福田敦夫, 松本直通

    日本遺伝子診療学会大会プログラム・抄録集   25th   2018

  • 統合失調症脳における慢性炎症関連分子のジェネティックニューロパソロジー

    和田明, 國井泰人, 日野瑞城, 松本純弥, 長岡敦子, 丹羽真一, 竹島明, 高橋均, 那波宏之, 柿田明美, 笠井清登, 矢部博興

    統合失調症研究   8 ( 1 )   2018

  • Gli3 INDUCES NEURONAL DIFFERENTIATION IN WNT- AND SHH-ACTIVATED MEDULLOBLASTOMA Reviewed

    Manabu Natsumeda, Hiroaki Miyahara, Junichi Yoshimura, Takanori Nozawa, Yoshihiro Tsukamoto, Takafumi Wataya, Charles Eberhart, Hitoshi Takahashi, Akiyoshi Kakita, Yukihiko Fujii

    NEURO-ONCOLOGY   19   183 - 183   2017.11

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  • Establishment of Japan Brain Bank Net

    Saito Y, Kakita A, Yoshida M, Murayama S, Iritani S, Yokota O, Terada S, Ohshima K, Yasuto K, Yabe H, Inoue Y, Tanaka N, Motoyoshi Y, Murata M, Mizusawa H

    JOURNAL OF THE NEUROLOGICAL SCIENCES   381   963-963   2017.10

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    DOI: 10.1016/j.jns.2017.08.2712

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  • MS・NMO2 視神経脊髄炎における脳室上衣の免疫学的・病理学的検討

    柳村 文寛, 佐治 越爾, 穂苅 万李子, 若杉 尚宏, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊, 小野寺 理, 河内 泉

    神経免疫学   22 ( 1 )   113 - 113   2017.10

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  • Dynamics of tissue regulatory T cells in neuromyelitis optica spectrum disorders lesions

    F. Yanagimura, E. Saji, T. Wakasugi, M. Hokari, Y. Toyoshima, A. Kakita, H. Takahashi, M. Nishizawa, O. Onodera, I. Kawachi

    MULTIPLE SCLEROSIS JOURNAL   23   492 - 492   2017.10

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  • 認知症を呈する白質脳症 病理から見た病態形成 グリア細胞の関与

    他田 真理, 高橋 均, 柿田 明美

    Dementia Japan   31 ( 4 )   531 - 531   2017.10

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  • 12年前の腎生検組織でエオジン好性核内封入体が認められた神経核内封入体病の1例

    元木 三記子, 吉本 幸世, 宇野田 喜一, 石田 志門, 中嶋 秀人, 木村 文治, 荒若 繁樹, 佐藤 朋江, 他田 真理, 柿田 明美

    臨床神経学   57 ( 10 )   657 - 657   2017.10

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  • CARASIL症候性キャリアの一例

    野崎 洋明, 伊藤 絢子, 阿部 崇, 豊島 靖子, 佐藤 晶, 橋立 英樹, 五十嵐 修一, 高橋 均, 小野寺 理, 柿田 明美

    Dementia Japan   31 ( 4 )   543 - 543   2017.10

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  • MS・NMO2 視神経脊髄炎における脳室上衣の免疫学的・病理学的検討

    柳村 文寛, 佐治 越爾, 穂苅 万李子, 若杉 尚宏, 豊島 靖子, 柿田 明美, 高橋 均, 西澤 正豊, 小野寺 理, 河内 泉

    神経免疫学   22 ( 1 )   113 - 113   2017.10

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  • The perivascular microenvironment in primary central nervous system Epstein-Barr virus-positive lymphomas: the role of PD-1 and PD-L1

    Yasuo Sugita, Takuya Furuta, Satoru Komaki, Junko Miyoshi, Koichi Ohshima, Hideyuki Abe, Yoshihiro Tsukamoto, Hitoshi Takahashi, Akiyoshi Kakita

    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY   76 ( 6 )   537 - 537   2017.6

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  • 進行性骨化性線維異形成症の1剖検例

    田中 英智, 豊島 靖子, 他田 真理, 清水 宏, 米持 洋介, 小澤 哲夫, 中島 孝, 高橋 均, 柿田 明美

    新潟医学会雑誌   131 ( 5 )   315 - 316   2017.5

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  • CADASIL姉弟剖検例の臨床病理所見

    齋藤 理恵, 豊島 靖子, 鈴木 正博, 田中 政春, 野崎 洋明, 小野寺 理, 高橋 均, 柿田 明美

    新潟医学会雑誌   131 ( 5 )   313 - 314   2017.5

  • 脳実質びまん性に認められた小型リンパ球増殖性疾患の一手術例

    塚本 佳広, 野澤 孝徳, 渡邉 潤, 佐藤 朋江, 棗田 学, 大石 誠, 高橋 均, 杉田 保雄, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   34 ( Suppl. )   138 - 138   2017.5

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  • 分子病理と分子病態 Oncogenesis and Progression WNT群、SHH群におけるGli3高発現と神経細胞分化

    棗田 学, 吉村 淳一, 宮原 弘明, 野澤 孝徳, 塚本 佳広, 綿谷 崇史, Eberhart Charles, 高橋 均, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   34 ( Suppl. )   073 - 073   2017.5

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  • H3F3A G34Rが認められたcerebral hemispheric glioblastomaの1例

    塚本 佳広, 野澤 孝徳, 伊藤 絢子, 阿部 英明, 小倉 良介, 五十川 瑞穂, 棗田 学, 青木 洋, 岡本 浩一郎, 高橋 均, 藤井 幸彦, 柿田 明美

    新潟医学会雑誌   131 ( 5 )   313 - 313   2017.5

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  • 死後脳内において高頻度にコピー数多型(CNV)が観察された統合失調症3症例の臨床的特徴について

    長岡敦子, 國井泰人, 松本純弥, 和田明, 和田明, 日野瑞城, 丹羽真一, 那波宏之, 高橋均, 柿田明美, 赤津裕康, 赤津裕康, 赤津裕康, 赤津裕康, 橋詰良夫, 橋詰良夫, 山本左近, 山本左近, 尾関祐二, 矢部博興

    統合失調症研究   7 ( 1 )   85   2017.3

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  • エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立に関する研究 肥厚性硬膜炎の診断基準・重症度分類に関する研究

    河内泉, 西澤正豊, 佐治越爾, 横関明子, 柳村文寛, 若杉尚宏, 荒川武蔵, 柳川香織, 穂苅万李子, 小野寺理, 豊島靖子, 柿田明美, 高橋均

    エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立 平成28年度 総括・分担研究報告書(Web)   50‐51 (WEB ONLY)   2017

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  • エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立に関する研究 多発性硬化症と視神経脊髄炎の臨床経過と炎症・神経変性機構に関する研究

    河内泉, 穂苅万李子, 佐治越爾, 柳村文寛, 若杉尚宏, 横関明子, 荒川武蔵, 柳川香織, 小野寺理, 豊島靖子, 柿田明美, 高橋均, 西澤正豊

    エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立 平成28年度 総括・分担研究報告書(Web)   39‐40 (WEB ONLY)   2017

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  • アルツハイマー病剖検脳を用いたRNA-seq解析

    原範和, 宮下哲典, 菊地正隆, 中谷明弘, 柿田明美, 池内健

    Dementia Japan   31 ( 4 )   2017

  • 原発性側索硬化症と診断したが、進行性核上性麻痺と病理診断された症例の臨床病理学

    米持 洋介, 飛永 雅信, 池田 哲彦, 遠藤 寿子, 大田 健太郎, 会田 泉, 中島 孝, 高原 誠, 今里 真, 小澤 哲夫, 三吉 政道, 金谷 洋, 横山 裕一, 他田 真理, 柿田 明美, 高橋 均

    臨床神経学   56 ( Suppl. )   S446 - S446   2016.12

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  • 病理診断されたGlobular Glial Tauopathyの臨床的特徴 自験2例と既報39例のまとめ

    三浦 健, 目崎 直実, 三瓶 一弘, 青木 賢樹, 竹内 亮子, 田中 英智, 豊島 靖子, 柿田 明美, 小野寺 理, 池内 健

    Dementia Japan   30 ( 4 )   542 - 542   2016.10

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  • 病理計断されたGlobular Glial Tauopathyの臨床的特徴 自験2例と既報39例のまとめ

    三浦 健, 目崎 直実, 三瓶 一弘, 青木 賢樹, 竹内 亮子, 田中 英智, 豊島 靖子, 柿田 明美, 小野寺 理, 池内 健

    Dementia Japan   30 ( 4 )   542 - 542   2016.10

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  • 視神経脊髄炎におけるtissue Tregs動態の検討

    柳村 文寛, 佐治 越爾, 穂苅 万李子, 柳川 香織, 豊島 靖子, 柿田 明美, 高橋 均, 小野寺 理, 西澤 正豊, 河内 泉

    神経免疫学   21 ( 1 )   123 - 123   2016.9

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  • 視神経脊髄炎におけるtissue Tregs動態の検討

    柳村 文寛, 佐治 越爾, 穂苅 万李子, 柳川 香織, 豊島 靖子, 柿田 明美, 高橋 均, 小野寺 理, 西澤 正豊, 河内 泉

    神経免疫学   21 ( 1 )   123 - 123   2016.9

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  • Neuromyelitis optica脳病変における神経放射線学的・神経病理学的特徴

    穂苅 万李子, 佐治 越爾, 柳村 文寛, 柳川 香織, 豊島 靖子, 柿田 明美, 高橋 均, 小野寺 理, 西澤 正豊, 河内 泉

    神経免疫学   21 ( 1 )   124 - 124   2016.9

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  • Neuromyelitis optica脳病変における神経放射線学的・神経病理学的特徴

    穂苅 万李子, 佐治 越爾, 柳村 文寛, 柳川 香織, 豊島 靖子, 柿田 明美, 高橋 均, 小野寺 理, 西澤 正豊, 河内 泉

    神経免疫学   21 ( 1 )   124 - 124   2016.9

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  • Severe neurodegeneration and unique dynamics of aquaporin-4 on astrocytes in the anterior visual pathway of neuromyelitis optica.

    I. Kawachi, M. Hokari, A. Yokoseki, M. Arakawa, E. Saji, K. Yanagawa, F. Yanagimura, Y. Toyoshima, A. Kakita, H. Takahashi, O. Onodera, M. Nishizawa

    MULTIPLE SCLEROSIS JOURNAL   22   24 - 24   2016.9

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  • Factors affecting the cardiac sympathetic denervation in autopsy confirmed dementia with Lewy bodies

    M. Takahashi, T. Uchihara, M. Yoshida, K. Wakabayashi, A. Kakita, H. Takahashi, S. Toru, T. Kobayashi, S. Orimo

    MOVEMENT DISORDERS   31   S585 - S585   2016.6

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  • 髄芽腫のmolecular分類 MAGIC分類とGli3免疫染色の対比

    吉村 淳一, 宮原 弘明, 綿谷 崇史, 清家 尚彦, 棗田 学, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   33 ( Suppl. )   096 - 096   2016.5

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  • PXA with anaplastic features with sarcomatous componentと組織診断した前頭葉腫瘍の1例

    小倉 良介, 伊藤 絢子, 塚本 佳広, 五十川 瑞穂, 齋藤 理恵, 青木 洋, 岡本 浩一郎, 藤井 幸彦, 高橋 均, 柿田 明美

    The Kitakanto Medical Journal   66 ( 2 )   172 - 173   2016.5

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  • 統合失調症患者死後脳前頭前皮質におけるAktシグナル伝達系蛋白質群の多項目同時測定

    日野瑞城, 國井泰人, 松本純弥, 和田明, 長岡敦子, 丹羽真一, 丹羽真一, 高橋均, 柿田明美, 赤津裕康, 赤津裕康, 橋詰良夫, 山本孝之, 矢部博興

    統合失調症研究   6 ( 1 )   123   2016.3

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  • 1 Anaplastic ependymomaにSarcomatous changeが生じた1例 : 全治療経過と剖検所見の検討 (Ⅰ.一般演題, 第66回新潟脳神経外科懇話会)

    阿部 英明, 三橋 大樹, 大石 誠, 鈴木 健司, 川口 正, 柿田 明美, 豊島 靖子

    新潟医学会雑誌   130 ( 3 )   208 - 208   2016.3

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    Other Link: http://search.jamas.or.jp/link/ui/2016392706

  • エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立に関する研究 視神経脊髄炎と多発性硬化症におけるグリア異常を介した神経変性機構の解析

    西澤正豊, 河内泉, 穂苅万李子, 横関明子, 佐治越爾, 荒川武蔵, 柳川香織, 柳村文寛, 豊島靖子, 柿田明美, 高橋均

    エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立に関する研究 平成27年度 総括・分担研究報告書   46‐47   2016

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  • エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立に関する研究 視神経脊髄炎と多発性硬化症における前部視覚路障害の臨床的特徴

    西澤正豊, 穂苅万李子, 河内泉, 横関明子, 佐治越爾, 荒川武蔵, 柳川香織, 柳村文寛, 豊島靖子, 柿田明美, 高橋均

    エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立に関する研究 平成27年度 総括・分担研究報告書   81‐82   2016

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  • 筋萎縮性側索硬化症におけるTDP-43に対するGPNMBの関与

    長原悠樹, 鶴間一寛, 嶋澤雅光, 伊藤絢子, 柿田明美, 原英彰

    日本病院薬剤師会東海ブロック・日本薬学会東海支部合同学術大会講演要旨集   26th-2016   2016

  • HDLS患者脳におけるミクログリアの形態学的異常 Microgliopathyとして

    他田 真理, 高橋 均, 柿田 明美

    臨床神経学   55 ( Suppl. )   S122 - S122   2015.12

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  • PINK1-ParkinによるIPAS分解が神経細胞死を抑制する

    葛西 秋宅, 鳥居 暁, 安元 研一, 柿田 明美, 十川 和博

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   88回・38回   [1P0437] - [1P0437]   2015.12

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  • 急激に高度のびまん性脳浮腫を呈した急性脳症の臨床病理学的検討

    竹腰 顕, 林 祐一, 柿田 明美, 清家 尚彦, 瀬川 一, 安西 将大, 吉倉 延亮, 原田 斉子, 香村 彰宏, 木村 暁夫, 犬塚 貴

    臨床神経学   55 ( Suppl. )   S394 - S394   2015.12

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  • 歩行障害と認知機能低下が亜急性に進行し、同心円状の造影病変を呈した炎症性脱髄性疾患の75歳女性例

    原 敦, 小別所 博, 三宅 敏彦, 松本 圭吾, 清家 尚彦, 田中 英智, 柿田 明美

    臨床神経学   55 ( 11 )   866 - 866   2015.11

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  • 多系統萎縮症におけるアストロサイト特異的タンパク質の解析

    星 明彦, 角田 綾子, 宇川 義一, 西澤 正豊, 他田 真理, 柿田 明美

    脳循環代謝   27 ( 1 )   194 - 194   2015.10

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  • The degree of cardiac MIBG uptake is correlated with that of cardiac sympathetic denervation in pathologically-verified Lewy body disease

    S. Orimo, M. Takahashi, H. Kitazono, T. Sekiguchi, A. Inaba, M. Ikemura, T. Oka, T. Uchihara, K. Wakabayashi, A. Kakita, H. Takahashi, M. Yoshida, S. Tohru, T. Kobayashi

    JOURNAL OF THE NEUROLOGICAL SCIENCES   357   E281 - E281   2015.10

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    DOI: 10.1016/j.jns.2015.08.985

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  • APP遺伝子重複による家族性アルツハイマー病および脳アミロイド血管症の1剖検例

    横山 裕一, 豊島 靖子, 鈴木 正博, 春日 健作, 橋立 英樹, 染矢 俊幸, 高橋 均, 池内 健, 柿田 明美

    Dementia Japan   29 ( 3 )   388 - 388   2015.9

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  • 拘束性換気障害を契機に76歳時に診断された球脊髄性筋萎縮症の1剖検例

    長谷川 有香, 黒羽 泰子, 谷 卓, 松原 奈絵, 他田 真理, 柿田 明美, 小池 亮子

    臨床神経学   55 ( 8 )   608 - 608   2015.8

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  • 7 繰り返す脳梗塞と動眼神経麻痺を呈したinflammatory pseudotumorの1例(Ⅰ.一般演題, 第64回新潟脳神経外科懇話会)

    藤原 秀元, 中里 真二, 近 貴志, 森田 幸太郎, 渡邉 正人, 岡本 浩一郎, 柿田 明美

    新潟医学会雑誌   129 ( 8 )   488 - 488   2015.8

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  • Relationship among degeneration of the cardiac sympathetic nerve, clinical features and neuropathological findings in dementia with Lewy bodies

    M. Takahashi, A. Nakamura, T. Uchihara, M. Yoshida, K. Wakabayashi, A. Kakita, H. Takahashi, S. Orimo

    MOVEMENT DISORDERS   30   S49 - S49   2015.6

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  • 悪性星細胞腫瘍におけるp53の発現意義

    小倉 良介, 塚本 佳広, 棗田 学, 五十川 瑞穂, 青木 洋, 小林 勉, 吉田 誠一, 高橋 均, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   32 ( Suppl. )   105 - 105   2015.5

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  • 病理診断クイックリファレンス Invited

    清水 宏, 柿田 明美

    病理と臨床(別冊、臨時増刊号)   33   334 - 334   2015.4

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  • 病理診断クイックリファレンス Invited

    清水 宏, 柿田 明美

    病理と臨床(臨時増刊号)   33   332 - 332   2015.4

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  • 死後3T MRI画像と神経病理解剖 新潟大学脳研究所の取組

    柿田 明美, 渡辺 将樹, 中田 力, 藤井 幸彦, 西澤 正豊

    法医病理   21 ( 1 )   3 - 3   2015.4

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  • 末梢神経障害と後索変性を伴った中年期発症の脊髄小脳変性症の1剖検例

    齋藤 理恵, 他田 真理, 谷 卓, 小池 亮子, 五十嵐 修一, 山崎 元義, 小野寺 理, 西澤 正豊, 高橋 均, 柿田 明美

    信州医学雑誌   63 ( 1 )   70 - 71   2015.2

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  • プリオン病及び遅発性ウイルス感染症の分子病態解明・治療法開発に関する研究 硬膜移植後Creutzfeldt‐Jakob病剖検脳におけるリン酸化タウ,リン酸化α‐シヌクレイン,リン酸化TDP‐43の沈着について

    山田正仁, 浜口毅, 谷口優, 坂井健二, 北本哲之, 岩崎靖, 吉田眞理, 高尾昌樹, 村山繁雄, 内木宏延, 清水宏, 柿田明美, 高橋均, 鈴木博義, 三條伸夫, 水澤英洋

    プリオン病及び遅発性ウイルス感染症の分子病態解明・治療法開発に関する研究 平成26年度 委託業務成果報告書   50 - 52   2015

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  • エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立に関する研究 視神経脊髄炎と多発性硬化症における神経変性機構の解析

    西澤正豊, 河内泉, 穂苅万李子, 佐治越爾, 横関明子, 荒川武蔵, 柳川香織, 豊島靖子, 柿田明美, 高橋均

    エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立に関する研究 平成26年度 総括・分担研究報告書   72‐73   2015

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  • エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立に関する研究 免疫介在性肥厚性硬膜炎の原因とその位置づけ

    西澤正豊, 河内泉, 穂苅万李子, 佐治越爾, 横関明子, 荒川武蔵, 柳川香織, 豊島靖子, 柿田明美, 高橋均

    エビデンスに基づいた神経免疫疾患の早期診断基準・重症度分類・治療アルゴリズムの確立に関する研究 平成26年度 総括・分担研究報告書   101‐102   2015

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  • プリオン病及び遅発性ウイルス感染症の分子病態解明・治療法開発に関する研究 硬膜移植後Creutzfeldt‐Jakob病剖検脳におけるアミロイドβ蛋白の沈着

    浜口毅, 谷口優, 坂井健二, 北本哲之, 岩崎靖, 吉田眞理, 高尾昌樹, 村山繁雄, 内木宏延, 清水宏, 柿田明美, 高橋均, 鈴木博義, 三條伸夫, 水澤英洋, 山田正仁

    プリオン病及び遅発性ウイルス感染症の分子病態解明・治療法開発に関する研究 平成26年度 委託業務成果報告書   46 - 49   2015

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  • 全ゲノム遺伝子多型解析による統合失調症脳内ドパミン関連タンパク質発現プロファイルの予測

    國井泰人, 松本純弥, 日野瑞城, 和田明, 丹羽真一, 那波宏之, 横山裕一, 高橋均, 柿田明美, 矢部博興

    統合失調症研究   5 ( 1 )   2015

  • 神経変性疾患におけるアクアポリンと内向き整流性カリウムチャネル4.1の解析

    星 明彦, 角田 綾子, 宇川 義一, 西澤 正豊, 他田 真理, 柿田 明美, 高橋 均

    臨床神経学   54 ( Suppl. )   S135 - S135   2014.12

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  • FIG4はピック小体、レヴィ小体と核内封入体に局在する

    今 智矢, 森 文秋, 丹治 邦和, 三木 康生, 豊島 靖子, 柿田 明美, 吉田 眞理, 佐々木 秀直, 高橋 均, 冨山 誠彦, 馬場 正之, 若林 孝一

    臨床神経学   54 ( Suppl. )   S24 - S24   2014.12

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  • 神経軸索スフェロイドを伴う白質脳症HDLS Microgliaの組織学的異常

    他田 真理, 今野 卓哉, 他田 正義, 岡崎 健一, 荒川 武蔵, 伊東 恭子, 山本 徹, 横尾 英明, 吉倉 延亮, 石原 健司, 豊島 靖子, 小野寺 理, 西澤 正豊, 池内 健, 高橋 均, 柿田 明美

    臨床神経学   54 ( Suppl. )   S214 - S214   2014.12

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  • HDLSはCSF-1Rの機能喪失で生じる シグナル伝達障害とハプロ不全

    勇 亜衣子, 今野 卓哉, 他田 正義, 他田 真理, 小山 哲秀, 野崎 洋明, 金田 大太, 田代 裕一, 山本 徹, 高橋 均, 西澤 正豊, 小野寺 理, 柿田 明美, 池内 健

    臨床神経学   54 ( Suppl. )   S8 - S8   2014.12

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  • 筋萎縮性側索硬化症のTDP-43大脳皮質組織像の多様性 臨床病理および生化学的解析

    竹内 亮子, 他田 真理, 志賀 篤, 今野 卓哉, 豊島 靖子, 小野寺 理, 西澤 正豊, 柿田 明美, 高橋 均

    臨床神経学   54 ( Suppl. )   S200 - S200   2014.12

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  • ALSでのStasimonヒトホモログmRNAのスプライシング異常の検討

    石原 智彦, 志賀 篤, 小山 哲秀, 柿田 明美, 西澤 正豊, 高橋 均, 小野寺 理

    臨床神経学   54 ( Suppl. )   S99 - S99   2014.12

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  • 多系統萎縮症でのtubulin polymerization promoting protein(TPPP)の細胞内局在変化

    太田 浄文, 大林 正人, 尾崎 心, 市野瀬 志津子, 他田 真理, 柿田 明美, 高橋 均, 石川 欽也, 水澤 英洋

    臨床神経学   54 ( Suppl. )   S197 - S197   2014.12

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  • Astrocyteにおけるタウの蓄積像に着目したPSP関連タウオパチーの連続性について

    横山 裕一, 豊島 靖子, 他田 真理, 志賀 篤, 池内 健, 長谷川 一子, 染矢 俊幸, 柿田 明美, 高橋 均

    Dementia Japan   28 ( 4 )   508 - 508   2014.10

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  • Role of meningeal lymphoid follicle-like structures in the CNS inflammatory disorders

    Izumi Kawachi, Mariko Hokari, Etsuji Saji, Yasuko Toyoshima, Akiko Yokoseki, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizaw

    JOURNAL OF NEUROIMMUNOLOGY   275 ( 1-2 )   64 - 64   2014.10

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    DOI: 10.1016/j.jneuroim.2014.08.169

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  • Upregulation of xCT in spinal cords from sporadic ALS patients

    N. Shibata, Y. Inose, M. Niida-Kawaguchi, S. Toi, A. Kakita, H. Takahashi

    BRAIN PATHOLOGY   24   60 - 60   2014.9

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  • Immunohistochemical localization of neuron derived orphan receptor-1 in neurodegenerative diseases

    T. Kon, Y. Miki, K. Tanji, F. Mori, Y. Toyoshima, A. Kakita, H. Takahashi, J. Utsumi, H. Sasaki, K. Wakabayashi

    BRAIN PATHOLOGY   24   71 - 71   2014.9

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  • The essential role of Brain Bank Committee, Japanese Society of Neuropathology, in establishing Japan Brain Net

    S. Murayama, Y. Saito, Y. Akatsu, S. Iritani, K. Oshima, A. Kakita, H. Takahashi, H. Kowa, M. Takao, M. Takanashi, S. Tanaka, H. Nishimura, S. Niwa, H. Miyata, H. Mochizuki, M. Yamada, O. Yokota, M. Yoshida

    BRAIN PATHOLOGY   24   58 - 58   2014.9

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  • Radiological and Pathological Analyses of Cortical Lesions in Inflammatory Demyelinating Diseases of the Central Nervous System

    Etsuji Saji, Musashi Arakawa, Akiko Yokoseki, Mariko Hokari, Yasuko Toyoshima, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa, Izumi Kawachi

    MULTIPLE SCLEROSIS JOURNAL   20 ( 7 )   940 - 941   2014.6

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  • Neuromyelitis Optica with Severe Progressive Cognitive and Psychiatric Impairment: Pathological Analysis of Three Autopsied Cases

    Musashi Arakawa, Etsuji Saji, Yasuko Toyoshima, Mariko Hokari, Akiko Yokoseki, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa, Izumi Kawachi

    MULTIPLE SCLEROSIS JOURNAL   20 ( 7 )   945 - 946   2014.6

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  • "Gliomatosis encephali'' as a Novel Category of Brain Tumors: The First Autopsy Case Report of Gliomatosis Cerebelli

    Asa Nakahara, Toshikazu Yoshida, Masanobu Yazawa, Takashi Ehara, Jun Nakayama, Akiyoshi Kakita, Ryosuke Ogura, Mika Asakawa, Emi Suzuki-Kouyama, Kiyomitsu Oyanagi

    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY   73 ( 6 )   632 - 632   2014.6

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  • Scientific correspondence

    F. Mori, Y. Toyoshima, K. Tanji, A. Kakita, H. Takahashi, K. Wakabayashi

    NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY   40 ( 3 )   351 - 355   2014.4

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    DOI: 10.1111/nan.12075

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  • 膠芽腫により死亡した家族性特発性両側性大脳基底核石灰化症の1剖検例

    木村 正志, 齋藤 祥二, 本道 洋昭, 三浦 健, 青木 賢樹, 今野 卓也, 池内 健, 高橋 均, 柿田 明美

    新潟医学会雑誌   128 ( 4 )   189 - 189   2014.4

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  • 7 臨床的にALS-Dと診断され, Globular glial tauopathy類似の特異な病理組織学的所見を呈した1剖検例(Ⅰ. 一般演題, 第39回上信越神経病理懇談会)

    竹内 亮子, 豊島 靖子, 三浦 健, 青木 賢樹, 西澤 正豊, 柿田 明美, 高橋 均

    新潟医学会雑誌   128 ( 4 )   191 - 192   2014.4

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  • 2 Anaplastic pilocytic astrocytomaの1剖検例(Ⅰ. 一般演題, 第39回上信越神経病理懇談会)

    小倉 良介, 塚本 佳広, 佐野 正和, 青木 洋, 吉村 淳一, 藤井 幸彦, 高橋 均, 柿田 明美

    新潟医学会雑誌   128 ( 4 )   188 - 189   2014.4

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  • プリオン病及び遅発性ウイルス感染症に関する調査研究 硬膜移植後Creutzfeldt‐Jakob病剖検脳におけるアミロイドβ蛋白の沈着

    浜口毅, 北本哲之, 岩崎靖, 吉田眞理, 高尾昌樹, 村山繁雄, 内木宏延, 清水宏, 柿田明美, 高橋均, 鈴木博義, 坂井健二, 三條伸夫, 水澤英洋, 山田正仁

    プリオン病及び遅発性ウイルス感染症に関する調査研究 平成25年度 総括・分担研究報告書   43 - 46   2014

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  • 免疫性神経疾患に関する調査研究 多発性硬化症/視神経脊髄炎 病態(1)中枢神経系自己免疫炎症における髄膜リンパ濾胞構造の解析~髄膜形態からみた視神経脊髄炎と多発性硬化症の免疫病態の相違点~

    西澤正豊, 河内泉, 佐治越爾, 穂苅万李子, 横関明子, 荒川武蔵, 豊島靖子, 柿田明美, 高橋均

    免疫性神経疾患に関する調査研究 平成25年度 総括・分担研究報告書   18 - 19   2014

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  • 統合失調症でのドパミンD2受容体遺伝子多型による線条体ドパミンシステムへの影響

    松本純弥, 國井泰人, 三浦至, 日野瑞城, 和田明, 丹羽真一, 那波宏之, 坂井美和子, 染矢俊幸, 高橋均, 柿田明美, 矢部博興

    日本生物学的精神医学会誌   2014

  • 気分障害患者死後脳におけるチトクロームc酸化酵素陰性細胞の探索

    窪田(坂下)美恵, 磯野蕗子, 柿田明美, 高橋均, 金田大太, GUSTAVO Turecki, 加藤忠史

    日本生物学的精神医学会誌   2014

  • 異常タンパク伝播仮説に基づく神経疾患の画期的治療法の開発 C9ORF72変異を有する日本人ALSの一剖検例

    高橋均, 今野卓哉, 他田真理, 志賀篤, 西澤正豊, 小野寺理, 柿田明美

    異常タンパク伝播仮説に基づく神経疾患の画期的治療法の開発 平成25年度 総括・分担研究報告書   2014

  • 神経変性疾患に関する調査研究 筋萎縮性側索硬化症の大脳皮質におけるTDP-43組織像の多様性の検討:臨床病理,および生化学的解析

    高橋均, 竹内亮子, 竹内亮子, 他田真理, 志賀篤, 今野卓哉, 豊島靖子, 小野寺理, 西澤正豊, 柿田明美

    神経変性疾患に関する調査研究 平成25年度 総括・分担研究報告書   2014

  • パーキンソン病大脳皮質におけるアクアポリン発現とα-synuclein病理の検討

    星 明彦, 角田 綾子, 宇川 義一, 西澤 正豊, 他田 真理, 柿田 明美, 高橋 均

    臨床神経学   53 ( 12 )   1590 - 1590   2013.12

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  • 筋萎縮性側索硬化症におけるGemini of coiled bodyの減少

    有泉 優子, 石原 智彦, 横関 明男, 譚 春鳳, 三木 ゆかり, 柿田 明美, 高橋 均, 西澤 正豊, 小野寺 理

    臨床神経学   53 ( 12 )   1497 - 1497   2013.12

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  • ALS患者神経組織におけるU12 snRNAの減少とスプライシング異常

    石原 智彦, 志賀 篤, 有泉 優子, 横関 明男, 譚 春鳳, 柿田 明美, 西澤 正豊, 高橋 均, 小野寺 理

    臨床神経学   53 ( 12 )   1496 - 1496   2013.12

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  • 筋萎縮性側索硬化症の大脳皮質におけるTDP-43の組織学的および生化学的解析

    竹内 亮子, 志賀 篤, 他田 真理, 今野 卓哉, 豊島 靖子, 柿田 明美, 小野寺 理, 西澤 正豊, 高橋 均

    臨床神経学   53 ( 12 )   1535 - 1535   2013.12

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  • 神経軸索スフェロイドを伴う白質脳症HDLS Microgliaの組織学的解析

    他田 真理, 今野 卓哉, 他田 正義, 岡崎 健一, 荒川 武蔵, 横尾 英明, 伊東 恭子, 吉倉 延亮, 豊島 靖子, 小野寺 理, 西澤 正豊, 池内 健, 高橋 均, 柿田 明美

    臨床神経学   53 ( 12 )   1529 - 1529   2013.12

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  • GCIを形成する多系統萎縮症のoligodendrogliaでは、TPPPが核から消失する

    太田 浄文, 石川 欽也, 大林 正人, 尾崎 心, 柿田 明美, 高橋 均, 水澤 英洋

    臨床神経学   53 ( 12 )   1495 - 1495   2013.12

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  • 神経軸索スフェロイドを伴う白質脳症HDLSの臨床・画像・遺伝学的解析

    他田 正義, 今野 卓哉, 他田 真理, 小山 哲秀, 野崎 洋明, 高橋 均, 西澤 正豊, 小野寺 理, 柿田 明美, 池内 健

    Dementia Japan   27 ( 4 )   490 - 490   2013.10

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  • 神経軸索スフェロイドを伴う白質脳症HDLSの病態解析 ハプロ不全とCSF1Rシグナル障害

    今野 卓哉, 他田 正義, 他田 真理, 小山 哲秀, 野崎 洋明, 高橋 均, 西澤 正豊, 小野寺 理, 柿田 明美, 池内 健

    Dementia Japan   27 ( 4 )   491 - 491   2013.10

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  • CNS pathology in neuromyelitis optica: region-dependent dynamics of aquaporin-4

    M. Arakawa, E. Saji, Y. Toyoshima, M. Hokari, A. Yokoseki, A. Kakita, H. Takahashi, M. Nishizawa, I. Kawachi

    MULTIPLE SCLEROSIS JOURNAL   19 ( 11 )   330 - 331   2013.10

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  • Argyrophilic Grains are Constant and Disease Specific Features in Corticobasal Degeneration

    Shinsui Tatsumi, Maya Mimuro, Yasushi Iwasaki, Akiyoshi Kakita, Hitoshi Takahashi, Mari Yoshida

    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY   72 ( 6 )   555 - 555   2013.6

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  • 興味深い所見を呈した左側頭葉グリア系腫瘍の1生検例

    "小倉 良介", "青木 洋", "小林 勉", "藤井 幸彦", "柿田 明美", "高橋 均"

    The Kitakanto medical journal   63 ( 2 )   179 - 180   2013.5

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  • 硬膜への播種性再発と腫瘍内出血を繰り返した膠肉腫の一例

    青木 洋, 小倉 良介, 塚本 佳広, 棗田 学, 小林 勉, 岡本 浩一郎, 吉田 誠一, 柿田 明美, 高橋 均, 藤井 幸彦

    Brain Tumor Pathology   30 ( Suppl. )   157 - 157   2013.5

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  • 神経膠腫摘出標本における免疫染色法を用いたIDH1 mutationの評価と予後解析

    小倉 良介, 棗田 学, 青木 洋, 小林 勉, 柿田 明美, 高橋 均, 藤井 幸彦

    新潟医学会雑誌   127 ( 3 )   172 - 172   2013.3

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  • 免疫性神経疾患に関する調査研究 多発性硬化症/視神経脊髄炎 臨床(1)本邦の中枢性炎症性脱髄疾患における認知機能障害の特徴

    西澤正豊, 佐治越爾, 河内泉, 荒川武蔵, 横関明子, 穂苅万李子, 豊島靖子, 柿田明美, 高橋均

    免疫性神経疾患に関する調査研究 平成24年度 総括・分担研究報告書   9 - 10   2013

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  • 免疫性神経疾患に関する調査研究 多発性硬化症/視神経脊髄炎 臨床(2)Neuromyelitis opticaの大脳皮質病理に関する検討

    西澤正豊, 河内泉, 荒川武蔵, 佐治越爾, 横関明子, 穂苅万李子, 豊島靖子, 柿田明美, 高橋均

    免疫性神経疾患に関する調査研究 平成24年度 総括・分担研究報告書   19 - 20   2013

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  • 上位運動ニューロンの組織変性が下位のそれに比し高度であったALS剖検例の検討

    他田 真理, 柿田 明美, 志賀 篤, 黒羽 泰子, 小池 亮子, 樋口 真也, 森 茂, 付 永娟, 豊島 靖子, 小柳 清光, 西澤 正豊, 高橋 均

    臨床神経学   52 ( 12 )   1600 - 1600   2012.12

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  • 人工呼吸器管理を要する呼吸不全を認めたパーキンソン病3症例の検討

    横関 明男, 近藤 浩, 近藤 崇, 石川 厚, 西澤 正豊, 清水 宏, 小阪 崇幸, 高橋 均, 柿田 明美, 山田 光則

    臨床神経学   52 ( 12 )   1593 - 1593   2012.12

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  • ALS患者神経組織ではスプライシング関連機能性RNAが低下する

    石原 智彦, 志賀 篤, 横尾 麻衣子, 有泉 優子, 横関 明男, 譚 春鳳, 柿田 明美, 西澤 正豊, 高橋 均, 小野寺 理

    臨床神経学   52 ( 12 )   1409 - 1409   2012.12

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  • Potential role of CCR6+T cells in inflammatory demyelinating diseases of central nervous system

    Etsuji Saji, Musashi Arakawa, Mariko Hokari, Yasuko Toyosima, Kaori Yanagawa, Akiko Yokoseki, Akiyoshi Kakita, Hitsohi Takahashi, Masatoyo Nishizawa, Izumi Kawachi

    JOURNAL OF NEUROIMMUNOLOGY   253 ( 1-2 )   76 - 77   2012.12

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  • Characteristic features of inflammatory demyelination and neurodegeneration in neuromyelitis optica spectrum disorder

    Musashi Arakawa, Yasuko Toyoshima, Etsuji Saji, Kaori Yanagawa, Akiko Yokoseki, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa, Izumi Kawachi

    JOURNAL OF NEUROIMMUNOLOGY   253 ( 1-2 )   148 - 148   2012.12

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  • パーキンソン病大脳皮質におけるアクアポリン発現の検討

    星 明彦, 角田 綾子, 宇川 義一, 西澤 正豊, 他田 真理, 柿田 明美, 高橋 均

    脳循環代謝   24 ( 1 )   222 - 222   2012.11

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  • 若年性認知症を呈する白質脳症 HDLS患者のCSF1R変異、MRI所見、臨床像、病理像の検討

    今野 卓哉, 他田 正義, 小山 哲秀, 荒川 武蔵, 岡崎 健一, 柿田 明美, 高橋 均, 西澤 正豊, 小野寺 理, 池内 健

    Dementia Japan   26 ( 4 )   472 - 472   2012.10

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  • Unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve in Parkinson's disease

    S. Orimo, T. Uchihara, Y. Itoh, A. Kakita, K. Wakabayashi, H. Takahashi

    EUROPEAN JOURNAL OF NEUROLOGY   19   289 - 289   2012.9

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  • Analysis of chromosome 19q13.42 amplification in embryonal brain tumours with ependymoblastic multi-layered rosettes

    S. Nobusawa, H. Yokoo, J. Hirato, A. Kakita, H. Takahashi, Y. Nakazato

    EUROPEAN JOURNAL OF NEUROLOGY   19   762 - 762   2012.9

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  • 大脳基底核など深部組織におけるてんかん原性の可能性についての組織学的考察(Potential epileotogenesis of deep brain structure)

    Kaido Takanobu, 大槻 泰介, 高橋 章夫, 金子 裕, 本田 涼子, 中川 栄二, 斎藤 義朗, 須貝 研司, 佐々木 征行, 柿田 明美

    てんかん研究   30 ( 2 )   344 - 344   2012.9

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  • 内服抗がん剤の副作用類似症状で発症した転移性下垂体腫瘍の1例

    岡田 正康, 神宮字 伸哉, 米岡 有一郎, 川崎 隆, 高橋 英明, 柿田 明美, 高橋 均, 藤井 幸彦

    新潟医学会雑誌   126 ( 6 )   339 - 339   2012.6

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  • Unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve in Parkinson's disease

    S. Orimo, T. Uchihara, T. Kanazawa, Y. Itoh, K. Wakabayashi, A. Kakita, H. Takahashi

    MOVEMENT DISORDERS   27   S494 - S494   2012.6

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  • 脳腫瘍病理学の新傾向 日常の病理組織診断への分子遺伝学の応用(パートII)(髄芽腫) Gli3は髄芽腫におけるニューロンおよびグリア分化に関連する(New Trends in Brain Tumor Pathology: Application of Molecular Genetics to Routine Histopathological Diagnosis(Part II)(Medulloblastoma) Gli3 is Associated with Neuronal and Glial Di

    棗田 学, 宮原 弘明, 吉村 淳一, 西山 健一, 豊島 靖子, 柿田 明美, 高橋 均, 藤井 幸彦

    Brain Tumor Pathology   29 ( Suppl. )   116 - 116   2012.5

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  • 神経膠腫におけるIDH1 mutationと予後との関連 摘出組織を用いた免疫組織化学的検討

    小倉 良介, 棗田 学, 青木 洋, 小林 勉, 高橋 均, 柿田 明美, 藤井 幸彦

    Brain Tumor Pathology   29 ( Suppl. )   190 - 190   2012.5

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  • 脳腫瘍に対する治療戦略の新しい展望 分子解析に基づく臨床試験 神経膠腫の擬似進行ではIDH1変異ではなくnegative MGMT発現が高頻度に発生する(New Horizon of Treatment Strategy for Brain Tumor: Clinical Trial Based on Molecular Analyses High Incidence of Negative MGMT Expression but not IDH1 Mutation in Pseudoprogressio

    棗田 学, 小倉 良介, 青木 洋, 小林 勉, 宇塚 岳夫, 柿田 明美, 高橋 均, 藤井 幸彦

    Brain Tumor Pathology   29 ( Suppl. )   151 - 151   2012.5

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  • 脳形成異常を主とする発達期脳障害の病因・病態と治療に関する研究 MRIによる片側巨脳症の分類と発作予後

    佐々木征行, 須貝研司, 本田涼子, 中川栄二, 斎藤義朗, 齋藤貴志, 小牧宏文, 大槻泰介, 高橋章夫, 開道貴信, 伊藤雅之, 柿田明美

    脳形成異常を主とする発達期脳障害の病因・病態と治療に関する研究 平成23年度 総括・分担研究報告書   11 - 13   2012

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  • Primary Lateral Sclerosis: An Immunohistochemical and Biochemical Study of Pathological TDP-43 in Two Cases

    Takayuki Kosaka, Fu Yong-Juan, Atsushi Shiga, Osamu Onodera, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    DEMENTIA AND GERIATRIC COGNITIVE DISORDERS   33   93 - 93   2012

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  • 免疫性神経疾患に関する調査研究 多発性硬化症/視神経脊髄炎(3)Neuromyelitis opticaにおける神経変性機構の解析

    西澤正豊, 佐治越爾, 河内泉, 荒川武蔵, 柳川香織, 横関明子, 豊島靖子, 柿田明美, 高橋均

    免疫性神経疾患に関する調査研究 平成23年度 総括・分担研究報告書   34 - 35   2012

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  • 免疫性神経疾患に関する調査研究 多発性硬化症/視神経脊髄炎(2)中枢神経系炎症性脱髄疾患におけるCCR6発現T細胞の解析

    西澤正豊, 河内泉, 佐治越爾, 柳川香織, 荒川武蔵, 横関明子, 豊島靖子, 柿田明美, 高橋均

    免疫性神経疾患に関する調査研究 平成23年度 総括・分担研究報告書   19 - 20   2012

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  • HDLSの分子病態と白質を主病変とする他疾患との異同

    池内健, 今野卓哉, 他田正義, 荒川武蔵, 岡崎健一, 小山哲秀, 酒井直子, 野崎洋明, 徳永純, 河内泉, 柿田明美, 高橋均, 西澤正豊, 小野寺理

    日本神経学会学術大会プログラム・抄録集   53rd   2012

  • A Review of Mercury Toxicity with Special Reference to Methylmercury Invited

    Mineshi Sakamoto, Katsuyuki Murata, Akiyoshi Kakita, Masanori Sasaki

    Environmental Chemistry and Toxicology of Mercury   15   501 - 516   2011.12

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    DOI: 10.1002/9781118146644.ch15

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  • ヒト疾患脳におけるポリグルタミン病重合体の検出

    高橋 俊昭, 石平 悠, 堅田 慎一, 他田 正義, 他田 真理, 佐藤 俊哉, 柿田 明美, 高橋 均, 小野寺 理, 西澤 正豊

    臨床神経学   51 ( 12 )   1272 - 1272   2011.12

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  • VEGFシグナル阻害はtPAによる血栓溶解療法後の脳出血を抑制する

    下畑 享良, 金澤 雅人, 五十嵐 博中, 高橋 哲哉, 川村 邦雄, 柿田 明美, 高橋 均, 中田 力, 西澤 正豊

    臨床神経学   51 ( 12 )   1323 - 1323   2011.12

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  • ヒストン脱アセチル化酵素6の蓄積はレビー小体およびグリア細胞質内封入体に特異的である

    三木 康生, 森 文秋, 丹治 邦和, 柿田 明美, 冨山 誠彦, 馬場 正之, 高橋 均, 若林 孝一

    臨床神経学   51 ( 12 )   1345 - 1345   2011.12

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  • 孤発性筋萎縮性側索硬化症におけるRNA編集異常のメカニズムと運動ニューロン死

    日出山 拓人, 山下 雄也, 相澤 仁志, 辻 省次, 高橋 均, 柿田 明美, 鈴木 岳史, 高橋 良輔, 三澤 日出巳, Seeburg Peter H, Higuchi Miyoko, 郭 伸

    臨床神経学   51 ( 12 )   1238 - 1238   2011.12

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  • 劇症型非ヘルペス性急性辺縁系脳炎の臨床病理学的検討

    三吉 政道, 伊藤 博明, 結城 伸泰, 會田 泉, 米持 洋介, 樋口 真也, 中島 孝, 岡崎 健一, 柿田 明美, 高橋 幸利

    臨床神経学   51 ( 12 )   1374 - 1374   2011.12

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  • VEGFシグナル阻害はtPAによる血栓溶解療法後の脳出血を抑制する

    下畑 享良, 金澤 雅人, 五十嵐 博中, 高橋 哲哉, 川村 邦雄, 柿田 明美, 高橋 均, 中田 力, 西澤 正豊

    脳循環代謝   23 ( 1 )   136 - 136   2011.11

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  • Absence of meningeal lymphoid neogenesis in neuromyelitis optica

    I. Kawachi, K. Yanagawa, Y. Toyoshima, E. Saji, M. Arakawa, A. Yokoseki, A. Kakita, H. Takahashi, M. Nishizawa

    MULTIPLE SCLEROSIS JOURNAL   17   S292 - S292   2011.10

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  • FOCUS DETECTION IN INTRACTABLE NEOCORTICAL EPILEPSY USING MAGNETOENCEPHALOGRAPHY

    H. Murakami, H. Masuda, H. Shirozu, A. Kakita, H. Takahashi, S. Kameyama

    EPILEPSIA   52   201 - 201   2011.8

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  • 効果判定のための病理診断 Pseudoprogression症例におけるMGMT発現及びオートファジー誘導の検討

    棗田 学, 青木 洋, 宮原 弘明, 宇塚 岳夫, 柿田 明美, 高橋 均, 藤井 幸彦

    Brain Tumor Pathology   28 ( Suppl. )   052 - 052   2011.5

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  • 深部白質に境界明瞭な病変を呈したPXAの一例

    青木 洋, 棗田 学, 宇塚 岳夫, 柿田 明美, 高橋 均, 藤井 幸彦

    Brain Tumor Pathology   28 ( Suppl. )   126 - 126   2011.5

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  • 髄芽腫におけるGli3の発現 神経細胞への分化と良好な患者予後との関連

    宮原 弘明, 棗田 学, 吉村 淳一, 豊島 靖子, 藤井 幸彦, 高橋 均, 柿田 明美

    Brain Tumor Pathology   28 ( Suppl. )   081 - 081   2011.5

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  • 5 椎骨脳底動脈系に線維筋異形成症をきたし, くも膜下出血を発症した全身性エリテマトーデスの1女児例(一般演題,第36回上信越神経病理懇談会)

    岡崎 健一, 柿田 明美, 大野 秀子, 西平 靖, 小池 俊朗, 高橋 均

    新潟医学会雑誌   125 ( 4 )   238 - 239   2011.4

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  • SLC1A1遺伝子多型と統合失調症との関連解析

    飯田周平, 堀内泰江, 飯嶋良味, 石黒浩毅, 稲田俊也, 渡部雄一郎, 染矢俊幸, 氏家寛, 岩田仲生, 尾崎紀夫, 功刀浩, 栃木衛, 糸川昌成, 新井誠, 新里和弘, 入谷修司, 柿田明美, 高橋均, 那波宏之, 有波忠雄

    日本人類遺伝学会大会プログラム・抄録集   56th   173   2011

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  • 免疫性神経疾患に関する調査研究 MS/NMO 画像・高次脳機能 高次脳機能評価とスペクトラルドメイン光干渉断層計を使ったNMO病態の解析

    西澤正豊, 佐治越爾, 河内泉, 柳川香織, 横関明子, 豊島靖子, 高木峰夫, 柿田明美, 高橋均

    免疫性神経疾患に関する調査研究 平成22年度 総括・分担研究報告書   33 - 34   2011

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  • Involvement of EphA4/gamma-secretase signaling in pathogenesis of Alzheimer's disease

    Eiji Inoue, Chiyuki Matsui, Akiyoshi Kakita, Kohei Arita, Aki Togawa, Maki Tawarada, Akio Yamada, Hitoshi Takahashi

    NEUROSCIENCE RESEARCH   71   E186 - E186   2011

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    DOI: 10.1016/j.neures.2011.07.802

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  • 免疫性神経疾患に関する調査研究 MS/NMO 病理 髄膜形態からみたneuromyelitis opticaの病態形成メカニズム解析

    西澤正豊, 河内泉, 柳川香織, 佐治越爾, 横関明子, 豊島靖子, 柿田明美, 高橋均

    免疫性神経疾患に関する調査研究 平成22年度 総括・分担研究報告書   22 - 23   2011

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  • ヒト脳組織中のポリグルタミン蛋白質オリゴマーの検出 ポリグルタミン病の分子病態(Detection of oligomers of polyglutamine protein in human brain tissues: implication for molecular parthenogenesis of polyglutamine diseases)

    石平 悠, 高橋 俊昭, 堅田 慎一, 佐藤 俊哉, 柿田 明美, 高橋 均, 西澤 正豊, 小野寺 理

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   83回・33回   2P - 0926   2010.12

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  • 筋萎縮性側索硬化症におけるsnRNAの変化(Alteration of snRNAs in amyotrophic lateral sclerosis)

    石原 智彦, 志賀 篤, 柿田 明美, 横関 明男, 西澤 正豊, 高橋 均, 小野寺 理

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   83回・33回   2P - 0917   2010.12

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  • 急性脳虚血によるTDP43の限定分解と神経細胞内局在変化

    下畑 享良, 金澤 雅人, 柿田 明美, 五十嵐 博中, 高橋 哲哉, 高橋 均, 中田 力, 西澤 正豊

    臨床神経学   50 ( 12 )   1171 - 1171   2010.12

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  • 孤発性筋萎縮性側索硬化症とRNA編集異常

    日出山 拓人, 山下 雄也, 相澤 仁志, 柿田 明美, 高橋 均, 辻 省次, 郭 伸

    臨床神経学   50 ( 12 )   1160 - 1160   2010.12

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  • 脳虚血・基礎・メカニズム 急性脳虚血によるTDP-43の生化学的・組織学的変化の検討

    下畑 享良, 金澤 雅人, 柿田 明美, 五十嵐 博中, 高橋 哲哉, 川村 邦雄, 高橋 均, 中田 力, 西澤 正豊

    脳循環代謝   22 ( 1 )   69 - 69   2010.11

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  • Potential role of cellular immunity in neuromyleitis optica

    Kawachi Izumi, Toyoshima Yasuko, Yanagawa Kaori, Saji Etsuji, Kakita Akiyoshi, Takahashi Hitoshi, Nishizawa Masatoyo

    JOURNAL OF NEUROIMMUNOLOGY   228 ( 1-2 )   138 - +   2010.11

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  • アルツハイマー病脳組織におけるSORL1の遺伝子発現解析

    温雅楠, 宮下哲典, 月江珠緒, 齊藤祐子, 初田裕幸, 村山繁雄, 柿田明美, 高橋均, 北村信隆, 赤澤宏平, 井原康夫, 桑野良三

    Dement Jpn   24 ( 3 )   191   2010.9

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  • Immunocytochemical localization of histone deacetylase 6 in neurodegenerative disorders

    Y. Miki, F. Mori, K. Tanji, A. Kakita, H. Takahashi, K. Wakabayashi

    BRAIN PATHOLOGY   20   27 - 27   2010.9

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  • Disequilibrium in MSA phenotype distribution between populations: genetics or environment?

    T. Ozawa, J. L. Holton, D. Paviour, A. J. Lees, M. Tada, A. Kakita, O. Onodera, K. Wakabayashi, H. Takahashi, M. Nishizawa, T. Revesz

    BRAIN PATHOLOGY   20   29 - 29   2010.9

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  • Relationship between Bunina bodies and TDP-43 inclusions in spinal anterior horn in amyotrophic lateral sclerosis

    F. Mori, K. Tanji, Y. Miki, A. Kakita, H. Takahashi, K. Wakabayashi

    BRAIN PATHOLOGY   20   32 - 33   2010.9

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  • ALS of Guam: neuropathological reevaluation in comparison with the parkinsonism-dementia complex, frontotemporal lober degeneration and classic ALS

    K. Oyanagi, T. Hashimoto, M. Yamazaki, M. Hasegawa, T. Arai, H. Akiyama, K. Tsuchiya, T. Morita, T. Mizutani, A. Kakita, H. Takahashi

    BRAIN PATHOLOGY   20   34 - 34   2010.9

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  • Distribution of TDP-43-immunoreactive neuronal and glial cytoplasmic inclusions in sporadic amyotrophic lateral sclerosis

    Y. Nishihira, C. F. Tan, Y. Toyoshima, M. Yamada, H. Takahashi, O. Onodera, T. Morita, M. Nishizawa, A. Kakita

    BRAIN PATHOLOGY   20   32 - 32   2010.9

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  • An autopsy case of familial Alzheimer&apos;s disease with an L381V substitution in the presenilin 1 gene

    T. Kosaka, Y. J. Fu, A. Ishikawa, T. Ikeuchi, A. Miyashita, R. Kuwano, A. Kakita, H. Takahashi

    BRAIN PATHOLOGY   20   17 - 17   2010.9

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  • Immunohistochemical study of microglia in the Nasu-Hakola diseased brain

    A. Sasaki, A. Kakita, S. Hayashi, T. Kondo, H. Matsuo, H. Takahashi

    BRAIN PATHOLOGY   20   42 - 42   2010.9

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  • Existence of pre-synaptic proteinase K-resistant alpha-synuclein in human Lewy body disease and A53T alpha-synuclein transgenic mice

    K. Tanji, F. Mori, A. Kakita, H. Takahashi, K. Wakabayashi

    BRAIN PATHOLOGY   20   27 - 27   2010.9

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  • アルツハイマー病脳組織におけるSORL1の遺伝子発現解析

    温 雅楠, 宮下 哲典, 月江 珠緒, 齊藤 祐子, 初田 裕幸, 村山 繁雄, 柿田 明美, 高橋 均, 北村 信隆, 赤澤 宏平, 井原 康夫, 桑野 良三

    Dementia Japan   24 ( 3 )   389 - 389   2010.9

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  • Renal sclerosing peritubular nodules in a patient with neurofibromatosis type 2: A case report with immunohistochemical and electron microscopic studies

    Takashi Morita, Kakuhei Kimura, Akiyoshi Kakita

    HUMAN PATHOLOGY   41 ( 7 )   1051 - 1052   2010.7

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    DOI: 10.1016/j.humpath.2010.01.020

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  • 悪性神経膠腫症例におけるオートファジーモニタリングと治療抵抗性獲得の検討

    棗田 学, 青木 洋, 宮原 弘明, 宇塚 岳夫, 豊島 靖子, 柿田 明美, 高橋 均, 藤井 幸彦

    Brain Tumor Pathology   27 ( Suppl. )   101 - 101   2010.5

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  • 脳腫瘍における術中迅速免疫組織化学的診断の有用性

    宇塚 岳夫, 棗田 学, 青木 洋, 宮原 弘明, 柿田 明美, 高橋 均, 藤井 幸彦

    Brain Tumor Pathology   27 ( Suppl. )   71 - 71   2010.5

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  • 免疫性神経疾患に関する調査研究 視神経脊髄炎・臨床 リンパ球浸潤形態からみたneuromyelitis opticaの脊髄病変

    西澤正豊, 河内泉, 柳川香織, 佐治越爾, 豊島靖子, 柿田明美, 高橋均

    免疫性神経疾患に関する調査研究班 平成21年度 総括・分担研究報告書   17 - 18   2010

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  • The effect of prenatal stress on the maturation of dentate granule cells

    Makoto Tamura, Akiyoshi Kakita, Norio Matsuki, Ryuta Koyama

    JOURNAL OF PHARMACOLOGICAL SCIENCES   112   98P - 98P   2010

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  • Accumulation of presynaptic proteinase K-resistant alpha-synuclein in Parkinson's disease

    Kunikazu Tanji, Fumiaki Mori, Akiyoshi Kakita, Hitoshi Takahashi, Koichi Wakabayashi

    NEUROSCIENCE RESEARCH   68   E192 - E192   2010

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    DOI: 10.1016/j.neures.2010.07.2421

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  • 免疫性神経疾患に関する調査研究 視神経脊髄炎・臨床 Neuromyelitis optica spectrum disorderの高次脳機能障害

    西澤正豊, 佐治越爾, 河内泉, 柳川香織, 豊島靖子, 柿田明美, 高橋均

    免疫性神経疾患に関する調査研究班 平成21年度 総括・分担研究報告書   19 - 20   2010

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  • 日本人MSA剖検例の表現型スペクトラム 英国の結果と対比して

    小澤 鉄太郎, 他田 真理, 小野寺 理, 柿田 明美, 高橋 均, 西澤 正豊

    臨床神経学   49 ( 12 )   1133 - 1133   2009.12

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  • IMMUNOHISTOCHEMICAL ASSESSMENT OF O-6-METHYLGUANINE-DNA METHYLTRANSFERASE FOR GLIOBLASTOMAS: A REAPPRAISAL Reviewed

    Manabu Natsumeda, Akiyoshi Kakita, Takeo Uzuka, Yukihiko Fujii, Hitoshi Takahashi

    NEURO-ONCOLOGY   11 ( 6 )   945 - 945   2009.12

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  • ラット中大脳動脈閉塞再灌流モデルにおけるcaspase-3依存性TDP-43切断

    金澤 雅人, 柿田 明美, 五十嵐 博中, 高橋 哲哉, 高橋 均, 西澤 正豊, 中田 力, 下畑 享良

    臨床神経学   49 ( 12 )   1037 - 1037   2009.12

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  • TDP-43は急性脳虚血により限定分解され、細胞内局在が変化する

    金澤 雅人, 柿田 明美, 五十嵐 博中, 高橋 哲哉, 高橋 均, 中田 力, 西澤 正豊, 下畑 享良

    脳循環代謝   21 ( 1 )   116 - 116   2009.11

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  • MAGNETOENCEPAHLOGRAPHY-DIRECTED EPILEPSY SURGERY IN CHILDREN: CAN INVASIVE INTRACRANIAL ELECTRODE MONITORING BE AVOIDED?

    H. Murakami, S. Kameyama, H. Masuda, N. Saito, N. Akasaka, J. Tohyama, A. Kakita, H. Takahashi

    EPILEPSIA   50   116 - 116   2009.10

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  • レビー小体病の大脳皮質におけるαシヌクレイン蓄積とSNCA mRNA発現量の検討

    野崎 洋明, 石平 悠, 金子 博之, 豊島 靖子, 柿田 明美, 高橋 均, 小野寺 理, 西澤 正豊, 池内 健

    Dementia Japan   23 ( 2 )   181 - 181   2009.8

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  • 脳低温療法は局所脳虚血に伴うTDP43の機能障害を抑制する

    下畑 享良, 金澤 雅人, 柿田 明美, 五十嵐 博中, 高橋 哲哉, 高橋 均, 中田 力, 西澤 正豊

    日本脳低温療法学会プログラム・抄録集   12回   45 - 45   2009.7

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  • 神経膠芽腫におけるbiomarkerとしてのMGMT免疫染色法確立の試み

    棗田 学, 柿田 明美, 青木 洋, 宇塚 岳夫, 高橋 均, 藤井 幸彦

    Brain Tumor Pathology   26 ( Suppl. )   63 - 63   2009.5

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  • 免疫性神経疾患に関する調査研究 視神経脊髄炎(NMO)の病態 視神経炎病変を伴わないlimited form of neuromyelitis opticaの臨床病理学的特徴

    西澤正豊, 柳川香織, 河内泉, 横関明子, 豊島靖子, 柿田明美, 高橋均

    免疫性神経疾患に関する調査研究班 平成20年度 総括・分担研究報告書   38 - 39   2009

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  • Reduced cardiac MIBG uptake is a potential biomarker for the presence of Lewy bodies

    S. Orimo, T. Uchihara, A. Nakamura, A. Kakita, K. Wakabayashi, H. Takahashi

    MOVEMENT DISORDERS   24   S206 - S207   2009

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  • Prenatal stress impairs the dendritic maturation of dentate granule cells

    Makoto Tamura, Akiyoshi Kakita, Norio Matsuki, Ryuta Koyama

    NEUROSCIENCE RESEARCH   65   S254 - S255   2009

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    DOI: 10.1016/j.neures.2009.09.1450

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  • The spectrum of pathological involvement in Japanese patients with multiple system atrophy: A population-bound phenotype distribution

    T. Ozawa, M. Tada, O. Onodera, A. Kakita, T. Shimohata, H. Takahashi, N. Nishizawa

    MOVEMENT DISORDERS   24   S416 - S417   2009

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  • Bunina小体を認める家族性ALSに認めたTDP43ミスセンス変異

    横関 明男, 志賀 篤, 金子 博之, 田川 朝子, 譚 春鳳, 柿田 明美, 高橋 均, 西澤 正豊, 小野寺 理

    臨床神経学   48 ( 12 )   1122 - 1122   2008.12

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  • プレセニリン1変異による難溶性αシヌクレイン蓄積の分子機序

    池内 健, 金子 博之, 柿田 明美, 春日 健作, 野崎 洋明, 石川 厚, 高橋 均, 小野寺 理, 西澤 正豊

    臨床神経学   48 ( 12 )   1244 - 1244   2008.12

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  • ラット中大脳動脈塞栓モデルにおける血管内皮細胞のVEGF発現

    金澤 雅人, 五十嵐 博中, 柿田 明美, 高橋 均, 西澤 正豊, 下畑 享良

    臨床神経学   48 ( 12 )   1180 - 1180   2008.12

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  • Sex differences in dendritic maturation of hippocampal granule cells after prenatal stress

    M. Tamura, S. Nakahara, A. Kakita, N. Matsuki, R. Koyama

    INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE   26 ( 8 )   858 - 858   2008.12

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    DOI: 10.1016/j.ijdevneu.2008.09.101

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  • O2-62 Comparison of the pathological classification with magnetoencephalogram in focal cortical dysplasia(The 42^<nd> Congress of the Japan Epilepsy Society)

    Journal of the Japan Epilepsy Society   26 ( 2 )   325 - 325   2008.9

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  • 免疫組織化学的手法を用いた片側巨脳症患者の介在神経細胞の検討 Reviewed

    齋藤貴志, 中川栄二, 佐久間啓, 小牧宏文, 斎藤義朗, 須貝研司, 佐々木征行, 有馬邦正, 柿田明美, 大槻泰介, 伊藤雅之

    てんかん研究   26 ( 2 )   347 - 347   2008.9

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  • 5. 皮質形成異常の診断と治療(ES1-1 器質性病変を持つてんかんに対する外科的治療〜てんかん外科を始めるために必要な知識〜,イブニング教育セミナー,脳神経外科の夢と志,第28回日本脳神経外科コングレス総会)

    増田 浩, 亀山 茂樹, 村上 博淳, 柿田 明美

    脳神経外科ジャーナル   17   65 - 65   2008.4

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  • Axonal alpha-synuclein (alpha S) aggregates herald centripetal degeneration of cardiac sympathetic nerve in Parkinson's disease (PD)

    S. Orimo, T. Uchihara, A. Nakamura, F. Mori, A. Kakita, K. Wakabayashi, H. Takahashi

    MOVEMENT DISORDERS   23 ( 1 )   S19 - S19   2008

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  • Human granule cell dispersion associated with hippocampal sclerosis: Identification of neural progenitors and neurogenesis

    Masae Ryufuku, Yasuko Toyoshima, Yingiun Zheng, Hiroki Kitaura, Shigeki Kameyama, Hitoshi Takahashi, Akiyoshi Kakita

    NEUROSCIENCE RESEARCH   61   S127 - S127   2008

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  • ErbBI receptor ligands attenuate presynaptic maturation in neocortical neurons

    Hiroyuki Nawa, Nobuyuki Takei, Akiyoshi Kakita, Hitoshi Takahashi, Daisaku Yokomaku

    NEUROSCIENCE RESEARCH   61   S37 - S37   2008

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  • Prenatal stress disrupts dendritic maturation of dentate granule cells

    Makoto Tamura, Soichiro Nakahara, Akiyoshi Kakita, Norio Matsuki, Ryuta Koyama

    NEUROSCIENCE RESEARCH   61   S91 - S91   2008

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  • 進行性核上性麻痺の臨床病型の検討

    金澤 雅人, 下畑 享良, 柿田 明美, 豊島 靖子, 他田 真理, 森田 俊, 高橋 均, 西澤 正豊

    臨床神経学   47 ( 12 )   1059 - 1059   2007.12

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  • 認知症を伴う遺伝性パーキンソニズムにおけるα-synuclein遺伝子(SNCA)重複

    池内 健, 春日 健作, 志賀 篤, 金子 博之, 柿田 明美, 内山 剛, 大橋 寿彦, 石川 厚, 高橋 均, 西澤 正豊, 小野寺 理

    臨床神経学   47 ( 12 )   1125 - 1125   2007.12

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  • Loss of aquaporin 4 and astroglial changes in lesions of neuromyelitis optica: distinction from multiple sclerosis

    T. Misu, K. Fujihara, A. Kakita, H. Konno, M. Nakamura, S. Watanabe, T. Takahashi, I. Nakashima, H. Takahashi, Y. Itoyama

    MULTIPLE SCLEROSIS   13   S143 - S143   2007.10

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  • P2-19 Usefulness of MEG in epilepsy surgery for congenital bilateral/unilateral perisylvian syndrome(The 41^<st> Congress of the Japan Epilepsy Society)

    Journal of the Japan Epilepsy Society   25 ( 3 )   356 - 356   2007.9

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  • P2-18 Resection of epileptogenic focus around the anterior striatum(The 41^<st> Congress of the Japan Epilepsy Society)

    Journal of the Japan Epilepsy Society   25 ( 3 )   355 - 355   2007.9

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  • O1-39 Comparison of MEG with post-surgical seizure outcome of non-lesional neocortical epilepsy(The 41^<th> Congress of the Japan Epilepsy Society)

    Journal of the Japan Epilepsy Society   25 ( 3 )   272 - 272   2007.9

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  • 線条体前方部切除により発作が消失した前頭葉てんかんの一例(第1回日本てんかん学会関東・甲信越地方会)

    開道 貴信, 大槻 泰介, 仲間 秀幸, 金子 裕, 柿田 明美

    てんかん研究   25 ( 2 )   129 - 130   2007.8

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  • MEGガイド下てんかん外科の可能性(第1回日本てんかん学会関東・甲信越地方会)

    村上 博淳, 杉山 一郎, 増田 浩, 亀山 茂樹, 齋藤 なか, 赤坂 紀幸, 遠山 潤, 柿田 明美, 高橋 均

    てんかん研究   25 ( 2 )   132 - 133   2007.8

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  • Alteration of RNA editing and neuronal death in motor neuron diseases

    T. Hideyama, Y. Nishimoto, T. Yamashita, S. Tsuji, H. Takahashi, A. Kakita, T. Suzuki, S. Kwak

    JOURNAL OF NEUROLOGY   254   53 - 53   2007.5

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  • Multiple system atrophy: Morphometric evaluation of the CNS autonomic nuclei in patients with sudden deaths

    Mari Tada, Akiyoshi Kakita, Osamu Onodera, Masatoyo Nishizawa, Hitoshi Takahashi

    NEUROLOGY   68 ( 12 )   A50 - A50   2007.3

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  • 10 Perisylvian syndromeに伴う側頭葉てんかんの外科治療(一般演題,第47回新潟脳神経外科懇話会)

    亀山 茂樹, 増田 浩, 藤本 礼尚, 村上 博淳, 柿田 明美, 高橋 均

    新潟医学会雑誌   121 ( 3 )   180 - 180   2007.3

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  • 18 大脳半球剔除術後45年のCT像と剖検脳 : 剔除脳と剖検脳の再会(第47回新潟脳神経外科懇話会)

    高橋 英明, 田中 隆一, 柿田 明美, 高橋 均

    新潟医学会雑誌   121 ( 3 )   184 - 184   2007.3

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    Other Link: http://search.jamas.or.jp/link/ui/2007306281

  • Utilities of MRI scoring and pathological grading systems for hippocampal sclerosis in mesial temporal lobe epilepsy

    H. Murakami, A. Fujimoto, Sugiyama, I, H. Masuda, S. Kameyama, A. Kakita, H. Takahashi

    EPILEPSIA   48   133 - 134   2007

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  • Magnetic resonance images and pathology in focal cortical dysplasia

    S. Kameyama, A. Kakita, H. Masuda, H. Murakami, Sugiyama, I, H. Takahashi

    EPILEPSIA   48   120 - 120   2007

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  • Degeneration of cardiac sympathetic nerve can occur in multiple system atrophy

    S. Orimo, T. Kanazawa, A. Nakamura, T. Uchihara, F. Mori, A. Kakita, K. Wakabayashi, H. Takahashi

    MOVEMENT DISORDERS   22   S4 - S4   2007

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  • 多系統萎縮症早期死亡例の臨床病理学的検討

    他田 真理, 柿田 明美, 小野寺 理, 西澤 正豊, 高橋 均

    臨床神経学   46 ( 12 )   1134 - 1134   2006.12

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  • 運動ニューロン病におけるRNA編集異常の検討

    日出山 拓人, 西本 祥仁, 伊藤 杏子, 柿田 明美, 高橋 均, 辻 省次, 郭 伸

    臨床神経学   46 ( 12 )   1088 - 1088   2006.12

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  • 進行性核上性麻痺(PSP)及び皮質基底核変性症(CBD)とタウ遺伝子(MAPT)

    高野 弘基, 西澤 正豊, 高橋 均, 柿田 明美, 小野寺 理

    臨床神経学   46 ( 12 )   1119 - 1119   2006.12

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  • DMRVの筋障害分布を規定する要因の研究

    田中 惠子, 荒木 恵子, 柿田 明美, 西澤 正豊

    臨床神経学   46 ( 12 )   1052 - 1052   2006.12

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  • Degeneration of cardiac sympathetic nerve begins in the early process of Parkinson's disease

    S. Orimo, T. Kanazawa, T. Kojo, A. Nakamura, T. Uchihara, K. Wakabayashi, A. Kakita, H. Takahashi

    EUROPEAN JOURNAL OF NEUROLOGY   13   201 - 202   2006.9

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  • Pathological studies of all human autopsy cases concerned with Minamata disease in Japan compared with those of other countries until 2005

    Akira Yasutake, Hitoshi Takahashi, Akiyoshi Kakita, Masumi Sawada, Hidehiro Tokunaga

    MODERN PATHOLOGY   19   51 - 52   2006.9

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  • O1-58 Neuropatnological analysis of non-lesional neocortical epilepsy in MRI(The 40th Congress of the Japan Epilepsy Society)

    Journal of the Japan Epilepsy Society   24 ( 3 )   207 - 207   2006.8

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  • α-Synuclein遺伝子重複を認めた遺伝性Lewy小体病の分子遺伝学および生化学的解析

    志賀 篤, 池内 健, 春日 健作, 金子 博之, 譚 春鳳, 柿田 明美, 高橋 均, 西澤 正豊, 小野寺 理, 石川 厚

    Dementia Japan   20 ( 2 )   169 - 169   2006.8

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  • 遺伝性Lewy小体病を表現型としたpresenilin-1変異(ΔT440)によるin vivoおよびin vitroにおけるα-synuclein蓄積の検討

    金子 博之, 池内 健, 石川 厚, 柿田 明美, 宮下 哲典, 桑野 良三, 伊藤 弦太, 岩坪 威, 高橋 均, 西澤 正豊, 小野寺 理

    Dementia Japan   20 ( 2 )   168 - 168   2006.8

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  • Activity report from the Brain Bank Committee, the Japanese Association of Neuropathology

    S Murayama, K Arima, H Akatsu, A Kakita, T Kitamoto, S Suzuki, T Makibuchi, H Miyata, M Yoshida, N Arai

    JOURNAL OF NEURAL TRANSMISSION   113 ( 6 )   IV - IV   2006.6

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  • Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are associated with the 5 ' region of the tau gene in Japanese, an H1 only population

    H Takano, M Nishizawa, O Onodera, A Kakita, H Takahashi

    NEUROLOGY   66 ( 5 )   277 - 277   2006.3

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  • Corticobasal degeneration with focal, massive tau accumulation in the subcortical white matter astrocytes

    K. Sakai, Y. Piao, K. Kikugawa, S. Ohara, M. Hasegawa, H. Takano, M. Fukase, M. Nishizawa, A. Kakita, H. Takahashi

    MOVEMENT DISORDERS   21   S524 - S524   2006

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  • Multiple system atrophy: Morphometric evaluation of the CNS autonomic nuclei in patients with sudden deaths

    M. Tada, A. Kakita, O. Onodera, M. Nishizawa, H. Takahashi

    MOVEMENT DISORDERS   21   S535 - S535   2006

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  • Negative influence on postsynaptic development by ErbB1 receptor ligands in rat neocortex

    Daisaku Yokomaku, Hussain Jourdi, Akiyoshi Kakita, Tadasato Nagano, Hitoshi Takahashi, Nobuyuki Takei, Hiroyuki Nawa

    NEUROSCIENCE RESEARCH   55   S78 - S78   2006

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  • 進行性核上性麻痺PSPとタウ遺伝子の関連

    高野 弘基, 西澤 正豊, 高橋 均, 柿田 明美, 小野寺 理

    臨床神経学   45 ( 12 )   1099 - 1099   2005.12

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  • A comparative neuropathological analysis of Japanese cases of neuromyelitis optica and multiple sclerosis

    T Misu, A Kakita, K Fujihara, Nakashima, I, H Takahashi, Y Itoyama

    NEUROLOGY   64 ( 6 )   A39 - A39   2005.3

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  • Pathological findings of mesial temporal lobe epilepsy.

    H Masuda, S Kameyama, J Homma, A Fujimoto, A Kakita, H Takahashi

    EPILEPSIA   46   25 - 25   2005

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  • Audiogenic seizures visualised with transcranial autofluorescence imaging in the sensorimotor cortex of DBA/2 mice

    T Takao, H Murakami, M Fukuda, T Kawaguchi, A Kakita, H Takahashi, R Tanaka, K Shibuki

    EPILEPSIA   46   362 - 362   2005

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  • Pathological findings of mesial temporal lobe epilepsy

    H Masuda, S Kameyama, J Homma, A Fujimoto, A Kakita, H Takahashi

    EPILEPSIA   46   317 - 317   2005

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  • Focal cortical dysplasia and tuberous sclerosis have different types of epileptogenicity

    S Kameyama, H Masuda, J Homma, M Oishi, T Ueno, M Sasagawa, O Kanazawa, J Tohyama, A Kakita, H Takahashi

    EPILEPSIA   46   6 - 6   2005

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  • 多系統萎縮症(MSA)におけるsynuclein関連遺伝子の一塩基多型(SNP)解析

    大竹 弘哲, 小野寺 理, 柿田 明美, 長谷川 有香, 五十嵐 修一, 小澤 鉄太郎, 奥泉 薫, 高橋 均, 辻 省次, 西澤 正豊

    新潟医学会雑誌   118 ( 12 )   714 - 714   2004.12

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  • 多系統萎縮症(MSA)におけるsynuclein関連遺伝子の一塩基多型(SNP)解析

    大竹 弘哲, 小野寺 理, 柿田 明美, 長谷川 有香, 五十嵐 修一, 小澤 鉄太郎, 奥泉 薫, 辻 省次, 高橋 均, 西澤 正豊

    臨床神経学   44 ( 12 )   1157 - 1157   2004.12

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  • 進行性核上麻痺とタウ遺伝子領域の関連

    高野 弘基, 小野寺 理, 柿田 明美, 高橋 均, 西澤 正豊

    臨床神経学   44 ( 12 )   1152 - 1152   2004.12

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  • 孤発性純粋タウオパチーとタウ遺伝子領域の関連

    高野 弘基, 西澤 正豊, 小野寺 理, 柿田 明美, 高橋 均

    新潟医学会雑誌   118 ( 12 )   713 - 714   2004.12

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  • 白血病阻害因子の脳内投与によるドパミン・シグナルおよび潜在制止の異常(Central Administration of Leukemia Inhibitory Factor Disrupts Dopaminergic Signaling and Latent Inhibition)

    渡部 雄一郎, 武井 延之, 柿田 明美, 染矢 俊幸, 那波 宏之

    神経化学   43 ( 2-3 )   490 - 490   2004.8

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  • パーキンソン病線条体におけるEGF/EGFレセプターシグナルの変化(Decreased EGF/ErbB1 receptor signal in the brain of patients with Parkinsons disease)

    岩倉 百合子, 柿田 明美, 朴 英善, 武井 延之, 那波 宏之

    神経化学   43 ( 2-3 )   529 - 529   2004.8

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  • 1 画像診断上,悪性リンパ腫を思わせたglioblastomaの1剖検例(I.一般演題,第47回新潟画像医学研究会)

    登木口 進, 関 雅也, 小松 憲章, 岡本 浩一郎, 稲永 親憲, 高橋 均, 柿田 明美

    新潟医学会雑誌   118 ( 4 )   234 - 234   2004.4

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  • 重篤な多発性単ニューロパチーを呈し,C型肝炎ウィルス感染に関連した混合型クリオグロブリン血症をみとめた全身性血管炎の1剖検例

    他田真理, 成瀬 聡, 新井 亜希, 佐藤 晶, 田中惠子, 朴 月善, 柿田明美, 高橋 均, 西澤正豊, 辻 省次

    臨床神経   44   686 - 690   2004

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  • Lewy小体型痴呆(DLB)患者におけるbeta-及びgamma-synuclein(SNCB,SNCG)遺伝子変異

    大竹 弘哲, 小野寺 理, 五十嵐 修一, 斎藤 正明, 柿田 明美, 高橋 均, 石川 厚, 出塚 次郎, 若林 允甫, 戸田 達史, 辻 省次

    臨床神経学   43 ( 12 )   923 - 923   2003.12

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  • 家族性多系統萎縮症の臨床像と連鎖解析

    原 賢寿, 宮下 哲典, 桑野 良三, 柿田 明美, 高橋 均, 登木口 進, 平澤 基之, 水野 美邦, 後藤 順, 辻 省次

    臨床神経学   43 ( 12 )   933 - 933   2003.12

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  • The analysis of polymorphisms of synuclein family genes in multiple system atrophy (MSA).

    H Ohtake, O Onodera, A Kakita, A Hasegawa, S Igarashi, T Ozawa, K Okuizumi, H Takahashi, S Tsuji, M Nishizawa

    AMERICAN JOURNAL OF HUMAN GENETICS   73 ( 5 )   469 - 469   2003.11

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  • 多系統萎縮症(MSA)の疾患遺伝子同定へのアプローチ

    原 賢寿, 福島 隆男, 下畑 光輝, 寺島 健史, 宮下 哲典, 桑野 良三, 柿田 明美, 高橋 均, 若林 孝一, 登木口 進, 平澤 基之, 水野 美邦, 後藤 順, 辻 省次

    新潟医学会雑誌   117 ( 10 )   602 - 602   2003.10

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  • Patterns and Dynamics of Progenitor Migration in the Developing Brain

    KAKITA Akiyoshi

    28 ( 3 )   187 - 187   2003.6

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  • 異所性小脳組織とモノアミン作動性神経細胞を認めた頭蓋内前方部の発生異常脳

    豊島 靖子, 柿田 明美, 山田 光則, 佐藤 元, 森 宏, 田中 隆一, 岡本 浩一郎, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   23   148 - 148   2003.5

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  • 孤発性筋萎縮性側索硬化症 : 102剖検例の臨床病理学的研究

    朴 月善, 若林 孝一, 柿田 明美, 山田 光則, 林 森太郎, 森田 俊, 生田 房弘, 小柳 清光, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   23   98 - 98   2003.5

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  • 神経原線維変化と皮質型レビー小体の広範な出現を伴い、左右差のある前頭側頭葉葉性萎縮を示した初老期痴呆の一剖検例

    譚 春鳳, 柿田 明美, 登木口 進, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   23   139 - 139   2003.5

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  • 視床に海綿状変化が確認されたsporadic fatal insomnia (SFI)の一剖検例

    朴 月善, 柿田 明美, 渡辺 浩之, 北本 哲之, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   23   47 - 47   2003.5

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  • α-Synucleinopathiesの小脳Bergmann gliaにおけるα-synucleinの異常蓄積

    朴 月善, 森 文秋, 林 森太郎, 丹治 邦和, 吉本 真, 柿田 明美, 若林 孝一, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   23   182 - 182   2003.5

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  • 原発性側索硬化症とは? : 上位運動ニューロン優位の変性と前頭側頭葉萎縮を示した一剖検例

    譚 春鳳, 柿田 明美, 朴 月善, 菊川 公紀, 田中 正美, 岡本 幸市, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   23   211 - 211   2003.5

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  • C-26 限局性皮質形成異常と結節性硬化症のてんかん原性の相違について

    亀山 茂樹, 増田 浩, 本間 順平, 大石 誠, 笹川 睦男, 金澤 治, 遠山 潤, 柿田 明美, 高橋 均

    日本てんかん学会プログラム・予稿集   ( 37 )   146 - 146   2003

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  • 進行性核上性麻痺および大脳皮質基底核変性症の小脳皮質におけるタウの免疫組織化学的・免疫電顕的検討

    朴 月善, 林 森太郎, 若林 孝一, 柿田 明美, 会田 泉, 山田 光則, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   22   105 - 105   2002.5

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  • Bilateral periventricular nodular heterotopiaの1剖検例

    柿田 明美, 林 森太郎, 小澤 常徳, 小野 晃嗣, 亀山 茂樹, WALSH C.A., 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   22   210 - 210   2002.5

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  • Migration Pathways and Behavior of Progenitors in the Developing Forebrain

    KAKITA Akiyoshi

    Niigata medical journal   116 ( 3 )   105 - 111   2002.3

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    The great majority of glial cells are generated in the perinatal period from progenitors in the subventricular zone (SVZ). We investigated the migration of progenitors from the neonatal (postnatal day 0,P0) rat forebrain SVZ by labeling them in vivo with a retrovirus encoding green fluorescent protein gene, and monitoring their movements by time-lapse video microscopy in P3 slice preparations. Cells migrated radially and tangentially after emigration into white matter, cortex, and striatum. During migration, elongation of the leading process and nuclear translocation were independent or linked. Orthogonal turning involved either cessation of the cell body movement and formation of a new leading process, or continuous cell body movement and bending of the leading process. Some cells migrated tangentially through the corpus callosum along the unmyelinated axon fascicules, rather than the radial fibers. The dynamic behavior of progenitors may reflect local tissue architecture and contribute to the widespread distribution of glia.

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  • 13)てんかんを主症状とした左側頭葉oligoastrocytomaの1例(一般演題, 第37回新潟脳神経外科懇話会)

    亀山 茂樹, 師田 信人, 富川 勝, 大石 誠, 高橋 均, 柿田 明美

    新潟医学会雑誌   115 ( 10 )   541 - 541   2001.10

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  • グリア芽細胞の一部は脳梁を通って対側大脳半球に移動する

    柿田 明美, ZERLIN Marielba, 高橋 均, GOLDMAN James E.

    Neuropathology : official journal the Japanese Society of Neuropathology   20   62 - 62   2000.6

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  • 孤発性筋萎縮性側索硬化症の線条体におけるユビキチン陽性神経細胞内封入体の出現

    若林 孝一, 朴 月善, 林 森太郎, 柿田 明美, 山田 光則, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   20   208 - 208   2000.6

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  • Leptomeningeal glioneuronal heterotopia : 経胎盤的メチル水銀投与により惹起されたラット大脳側頭部の皮質異形成症

    柿田 明美, 若林 孝一, 蘇 牧, 朴 月善, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   20   163 - 163   2000.6

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  • B-33 脳腫瘍によるてんかん症例の外科治療

    亀山 茂樹, 福多 真史, 師田 信人, 富川 勝, 大石 誠, 柿田 明美, 高橋 均

    日本てんかん学会プログラム・予稿集   ( 34 )   126 - 126   2000

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  • Lewy body disordersとmultiple system atrophyに共通するα-synuclein/NACPの異常蓄積

    若林 孝一, 林 森太郎, 柿田 明美, 山田 光則, 豊島 靖子, 吉本 真, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   19   213 - 213   1999.6

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  • Dynamics of SVZ cell migration in the postnatal forebrain.

    A Kakita, JE Goldman

    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY   58 ( 5 )   518 - 518   1999.5

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  • Polyglutamine aggregates: a possible component of eosinophilic intranuclear inclusions in the hippocampal pyramidal neurons of a patient with amyotrophic lateral sclerosis? Reply

    A Kakita, H Takahashi

    ACTA NEUROPATHOLOGICA   97 ( 1 )   103 - 104   1999.1

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  • てんかん原性病巣としてのcortical dysplasiaにおける結節性硬化症原因遺伝子蛋白tuberinの発現

    柿田 明美, 水口 雅, 高嶋 幸男, 亀山 茂樹, 福多 真史, 田中 隆一, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   18   314 - 314   1998.5

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  • 歯状核赤核淡蒼球ルイ体萎縮症(DRPLA)の歯状核神経細胞胞体内にみられたubiquitin陽性filamentous inclusion

    林 靖子, 柿田 明美, 山田 光則, 江川 重公, 小柳 新策, 内藤 明彦, 辻 省次, 高橋 均

    NEUROPATHOLOGY   18 ( Suppl. )   214 - 214   1998.5

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  • An autopsy case of hypoplasia of the dorsal spinal tracts with hydranencephaly

    M Yamadal, H Shibuya, A Kakita, H Takahashi

    BRAIN PATHOLOGY   7 ( 4 )   1101 - 1101   1997.9

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  • 中枢神経系の病巣修復 : シナプス再生に関する検討

    山田 光則, 林 森太郎, 柿田 明美, 若林 孝一, 後藤 潤, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   17   50 - 50   1997.5

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  • てんかん原性病変としてのcortical dysplasia : 神経細胞の配列異常に加えballooned eosinophilic cellの認められた2切除例

    柿田 明美, 福多 真史, 亀山 茂樹, 長谷川 精一, 鈴木 健司, 川口 正, 田中 隆一, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   17   112 - 112   1997.5

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  • パーキンソン病におけるApoE遺伝子型と皮質型レビー小体の増加

    若林 孝一, 柿田 明美, 林 森太郎, 奥泉 薫, 田中 一, 石川 厚, 辻 省次, 高橋 均

    NEUROPATHOLOGY   17 ( Suppl. )   136 - 136   1997.5

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  • 大脳白質の広範な淡明化に加え,視床・橋にも対称性の病変を認めた歯状核赤核淡蒼球ルイ体萎縮症(DRPLA)の1剖検例

    柿田 明美, 登木口 進, 池内 健, 辻 省次, 高橋 均

    NEUROPATHOLOGY   17 ( Suppl. )   82 - 82   1997.5

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  • 網膜色素変性症を伴う多系統萎縮症の一剖検例

    若林 孝一, 柿田 明美, 登木口 進, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   16   98 - 98   1996.5

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  • 脊髄後索低形成を合併した水無脳症の1剖検例

    山田 光則, 渋谷 宏行, 柿田 明美, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   16   231 - 231   1996.5

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  • Pick病脳におけるapolipoprotein Eの免疫組織化学的検討

    林 森太郎, 若林 孝一, 岩永 圭介, 柿田 明美, 関 耕治, 田中 政春, 奥泉 薫, 小野寺 理, 田中 一, 辻 省次, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   16   241 - 241   1996.5

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  • 経胎盤的メチル水銀投与により惹起されたラット胎児の中枢神経病変

    柿田 明美, 若林 孝一, 蘇 牧, 高橋 均, 生田 房弘

    Neuropathology : official journal the Japanese Society of Neuropathology   16   191 - 191   1996.5

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  • 神経芽細胞発生期におけるラット胎仔大脳の組織修復 : 神経上皮細胞のcell cycleについて

    小柳 清光, 山田 光則, 柿田 明美, 林 森太郎, 高橋 均, 生田 房弘

    Neuropathology : official journal the Japanese Society of Neuropathology   16   155 - 155   1996.5

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  • メチル水銀投与ラットにおける脊髄後根神経節細胞の変化 : 胞体, 中枢側軸索ならびにシナプス終末の経時的観察

    蘇 牧, 柿田 明美, 若林 孝一, 山田 光則, 高橋 均, 生田 房弘

    Neuropathology : official journal the Japanese Society of Neuropathology   16   192 - 192   1996.5

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  • 側頭葉難治てんかん : Cortical dysplasiaの7切除例

    柿田 明美, 鈴木 健司, 亀山 茂樹, 田中 隆一, 高橋 均

    Neuropathology : official journal the Japanese Society of Neuropathology   16   291 - 291   1996.5

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  • Degeneration of the synaptic boutons of parallel fibers in ratstreated with methylmercury: Chronological observations

    Mu Su, Akiyoshi KAKITA, Mitsunori YAMADA

    Annual report, Brain Research Institute, Niigata University   29   37 - 37   1996

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  • TEMPORARY USE OF PERITONEOVENOUS SHUNTING FOR TREATMENT OF TENSE ASCITES FOLLOWING A WHIPPLE PROCEDURE

    T TAKAHASHI, A KAKITA

    DIGESTIVE DISEASES AND SCIENCES   40 ( 9 )   1946 - 1950   1995.9

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  • 神経芽細胞発生期の細胞障害に基づくラット大脳皮質の構築異常について

    小〓 清光, 山田 光則, 柿田 明美, 川崎 浩一, 林 森太郎, 生田 房弘

    Neuropathology : official journal the Japanese Society of Neuropathology   15   243 - 243   1995.6

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  • 単眼症の1剖検例 : 眼球及び中枢神経系の病理形態学的所見

    柿田 明美, 若林 孝一, 関塚 直人, 生田 房弘

    Neuropathology : official journal the Japanese Society of Neuropathology   15   194 - 194   1995.6

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  • 中枢神経系の病巣修復 : 神経細胞樹状突起棘シナプスの再生

    山田 光則, 林 森太郎, 柿田 明美, 若林 孝一, 川崎 浩一, 高橋 均, 生田 房弘

    Neuropathology : official journal the Japanese Society of Neuropathology   15   296 - 296   1995.6

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  • パーキンソン病における皮質型レビー小体と老人斑に関する定量形態的検討

    岩林 孝一, 柿田 明美, 高橋 均, 林 森太郎, 生田 房弘

    Neuropathology : official journal the Japanese Society of Neuropathology   15   268 - 268   1995.6

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  • メチル水銀投与ラットにおける小脳顆粒細胞の経時的観察 : Parallel fiber のシナプス変性について

    蘇 牧, 柿田 明美, 高橋 均, 山田 光則, 生田 房弘

    Neuropathology : official journal the Japanese Society of Neuropathology   15   274 - 274   1995.6

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  • 主症状(muco-cutaneo-ocular symptoms)を欠き精神神経症状を主体とした神経Behcet病の1剖検例

    林 森太郎, 柿田 明美, 高橋 均, 川崎 浩一, 生田 房弘, 遠藤 耕太郎, 石川 厚

    Neuropathology : official journal the Japanese Society of Neuropathology   15   127 - 127   1995.6

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  • 単眼症の1剖検例 : 眼球及び中枢神経系の病理形態学的所見

    柿田 明美, 若林 孝一, 関塚 直人[他]

    新潟大学脳研究所業績集   28   39 - 39   1995

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  • A Defect in DNA Repair and Neuronal Cell Death Xeroderma Pigmentosum with Neurological Abnormalities

    Takahashi Hitoshi, Kakita Akiyoshi, Ikuta Fusahiro

    108 ( 7 )   481 - 484   1994.7

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  • Pleomorphic xanthoastrocytoma in a 58-year-old woman with a 36-year history of epileptic seizure

    Takahashi Hitoshi, Kakita Akiyoshi, Ikuta Fusahiro

    Annual report, Brain Research Institute, Niigata University   27   24 - 24   1994

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  • Lewy bodies in the cerebellar dentate nucleus of a patient with Parkinson's disease

    Kakita Akiyoshi, Takahashi Hitoshi, Honma Yoshiaki

    Annual report, Brain Research Institute, Niigata University   27   17 - 17   1994

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  • 頭蓋内 clear cell tumor の 2 生検例 : 髄膜腫と上衣腫のclear cell variants

    柿田 明美, 高橋 均, 伏島 徹[他]

    新潟大学脳研究所業績集   27   25 - 25   1994

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  • 12. De Sanctis-Cacchione症候群の1剖検例(第18回上信越神経病理懇談会記録)

    柿田 明美, 鈴木 裕, 高橋 均, 生田 房弘, 相川 啓子

    新潟医学会雑誌   107 ( 9 )   850 - 852   1993.9

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  • 神経学的異常を伴う色素性乾皮症--剖検脳が示す神経細胞数減少のパタ-ン (老化分子生物学と神経疾患<特集>)

    高橋 均, 柿田 明美, 生田 房弘

    モレキュラ-メディシン   30 ( 9 )   p1174 - 1181   1993.8

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    Other Link: http://search.jamas.or.jp/link/ui/1994048100

  • Specific expression of 1,4,5-trisphosphate 3-kinase in dendriticspines

    Mitsunori YAMADA, Akiyoshi KAKITA, Masashi MIZUGUCHI

    Annual report, Brain Research Institute, Niigata University   26   17 - 17   1993

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Presentations

  • 中枢神経病理:コアイメージ・キーワード Invited

    柿田 明美

    日本神経学会  2019.5 

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    Venue:大阪  

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  • 脳神経神経変性疾患:病理学的解析のポイント Invited

    柿田 明美

    日本病理学会  2019.5 

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    Venue:東京  

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  • てんかん原性脳病巣の病態病理:外科標本の解析から Invited

    柿田 明美

    第42回日本てんかん外科学会  2019.1 

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  • 難治てんかん原性病巣の病態病理:外科手術標本を用いた解析 Invited

    柿田 明美

    大阪大学セミナー  2018.11 

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    Venue:大阪  

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  • PATHOLOGIC FEATURES OF GLIA IN PATIENTS WITH DEMENTIA: Invited International conference

    KAKITA Akiyoshi

    KBRI-NBRI symposium  2018.11 

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  • てんかん原性脳病巣の病態病理:臨床に役立つ知見 Invited

    柿田 明美

    第11回さいたま神経生理てんかん研究会  2018.11 

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    Venue:大宮  

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  • Pathologic features of glia in patients with dementia:experience at the Niigata Brain Bank Invited International conference

    KAKITA Akiyoshi

    The 16th Asian and Oceanian Congress of Neurology (AOCN)  2018.11 

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    Venue:Seoul  

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  • てんかんの病理 Invited

    柿田 明美

    西新潟中央病院てんかんセンター 夏季セミナー  2018.8 

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    Venue:新潟市  

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  • てんかん原性脳病巣の病態病理 Invited

    柿田 明美

    第3回 東海生理懇談会  2018.5 

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    Venue:名古屋  

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  • てんかん原性脳病巣の病態病理:臨床に役立つ知見 Invited

    柿田 明美

    第59回 京滋奈良てんかん懇話会  2018.3 

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    Venue:京都  

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  • 白質脳症の病理 Invited

    柿田 明美

    愛知医科大学 加齢医科学研究所 セミナー  2018.2 

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  • てんかん原性脳病巣の病態病理:臨床に役立つ知見 Invited

    柿田 明美

    熊本神経病理研究会  2017.12 

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    Venue:熊本  

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  • 神経変性疾患・プロテイノパチーの実際:神経病理学の立場から Invited

    柿田 明美

    武田薬品工業株式会社 湘南研究所 神経変性セミナー  2017.11 

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  • 認知症をきたす白質脳症の病理 Invited

    柿田 明美

    大阪大学 神経内科セミナー  2017.10 

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  • てんかん原性脳病巣の病態病理:臨床に役立つ知見 Invited

    柿田 明美

    Epilepsy forum in Nagaoka  2017.9 

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    Venue:長岡  

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  • Pathologic features of glia in non-AD degenerative dementias Invited International conference

    KAKITA Akiyoshi

    XXIII World Congress of Neurology  2017.9 

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    Venue:Kyoto  

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  • Alterations of glial cells in epileptogenic regions of the brain: a pathophysiological study Invited

    Kakita A, Kitaura H

    2017.9 

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  • てんかんの病理 Invited

    柿田 明美

    国立西新潟中央病院てんかんセンター 夏期セミナー  2017.8 

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    Venue:新潟  

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  • Pathologic features of neurons and glia in tauopathies Invited

    柿田 明美

    国際タウシンポジウム  2017.7 

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  • 疾患脳におけるグリア:神経病理学の視点から Invited

    柿田 明美

    新学術領域 グリアアセンブリ 夏のワークショップ  2017.7 

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  • 医学科学生を対象とした神経病理学教育:新潟大学脳研究所の取り組み

    柿田明美, 高橋 均, 生田房弘

    第58回日本神経病理学会  2017.6 

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    Venue:東京  

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  • Histopathologic features indicating possible pathomechanisms underlying neurological disorders of infants and children Invited International conference

    KAKITA Akiyoshi

    AOCCN: Asian Oceanian Congress of Child Neurology  2017.5 

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  • 神経病理って何? Invited

    柿田 明美

    神経病理って何?  2017.1 

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  • 結節性硬化症の病態病理:手術標本を用いた解析 Invited

    柿田 明美

    結節性硬化症の治療を考える会  2016.11 

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    Venue:大阪  

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  • てんかんの病理:ビジュアルプラクティス Invited

    柿田 明美

    第128回 宮城神経放射線カンファレンス  2016.11 

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    Venue:仙台  

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  • 成人発症の白質脳症の病理:病態形成におけるグリア細胞の関与 Invited

    柿田 明美

    第34回日本神経治療学会  2016.11 

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    Venue:米子  

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  • ヒトてんかん原性脳病巣の病態を知るための病理学的アプローチ Invited

    柿田 明美

    第50回日本てんかん学会  2016.10 

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    Venue:静岡  

    シンポジウムてんかん原性についての基礎研究:臨床に役立つ知見

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  • Neuro-CPC Invited International conference

    KAKITA Akiyoshi

    Brain Bank Symposium + CPC conference  2016.9  Seoul National University Hospital

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    Venue:Seoul  

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  • Introduction of Brainbanks of Niigata and Japan Invited International conference

    KAKITA Akiyoshi

    Intelligent Brain 2016: The 19th Korean Society for Brain and  2016.9 

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    Venue:Seoul  

    Symposium: Human Brain Research & Brain Bank

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  • 新潟大学脳研究所 Invited

    柿田 明美

    第16回ブレインバンク市民講演会  2016.9 

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    Venue:小平、東京  

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  • てんかん原性脳病巣の病理 Invited

    柿田 明美

    第8回日本神経病理学会 東海北陸地方会  2016.9 

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  • てんかんの病理 Invited

    柿田 明美

    西新潟中央病院てんかんセンター 夏季セミナー 2016  2016.8 

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    Venue:新潟  

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  • 精神疾患研究の今後の展望 Invited

    柿田 明美

    精神科学術講演会  2016.7 

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    Venue:新潟  

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  • 若年性パーキンソニズムと白質脳症の病理 Invited

    柿田 明美

    第19回 兵庫県臨床神経病理カンファレンス  2016.7 

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    Venue:神戸  

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  • アストロサイト:病態における形態変化 Invited

    柿田 明美

    第57回日本神経病理学会  2016.6 

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    Venue:弘前  

    シンポジウム「グリア細胞と神経病理」

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  • Gift of Hope:精神疾患患者さんを対象とした病理解剖実施 Invited

    柿田 明美

    病理解剖説明会 精神科同窓会  2016.5 

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  • バイオリソース Invited

    柿田 明美

    脳科学の新しい推進プログラムに関する検討会  2015.11  日本脳科学関連学会連合

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    Venue:東京  

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  • てんかんの病理 Invited

    柿田 明美

    西新潟中央病院てんかんセンター 夏季セミナー  2015.7 

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    Venue:新潟  

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  • 病理解剖について:新潟大学脳研究所の取組み Invited

    柿田 明美

    NPO法人精神疾患死後脳・DNAバンク運営委員会  2015.6 

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  • てんかんの病態病理 Invited

    柿田 明美

    信州大学 第6回神経病理学セミナー 「てんかん」  2015.1 

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  • マラソン教育レクチャー14 「てんかん焦点の病理」 Invited

    柿田 明美

    第48回日本てんかん学会  2014.10 

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    Venue:東京  

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  • 死後3T MRI 画像と神経病理解剖 Invited

    柿田 明美

    第21回 法医病理夏期セミナー  2014.8 

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    Venue:新潟  

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  • 私たちの脳を見る、知る、そして考える. Invited

    柿田 明美

    新発田高校スーパーサイエンスハイスクール  2014.8 

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  • てんかんの病理 Invited

    柿田 明美

    西新潟中央病院てんかんセンター 夏季セミナー  2014.7 

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    Venue:新潟  

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  • ヒトてんかん病巣におけるグリア細胞の病理組織学的所見 Invited

    柿田 明美

    第55回日本神経学会  2014.5 

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    Venue:福岡  

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  • 老年脳神経外科診療のための画像と病理. Invited

    柿田 明美

    第27回日本老年脳神経外科学会  2014.4 

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    Venue:新潟  

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  • てんかんの病理 Invited

    柿田 明美

    第37回日本てんかん外科学会  2014.2 

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    Venue:大阪  

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  • てんかんの神経病理 Invited

    柿田 明美

    京都府立医科大学 病理学講義、大学院特別講義  2013.10  京都府立医科大学

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    Venue:京都  

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  • 難治てんかん原性病巣の病態病理:外科標本の解析 Invited

    柿田 明美

    奈良てんかん懇話会  2013.9 

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    Venue:奈良  

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  • わたくしたちの脳を知る.―ニューロサイエンス・メディカルサイエンスの入口― Invited

    柿田 明美

    柏崎高校スーパーサイエンスハイスクール  2013.8 

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  • てんかんの病理 Invited

    柿田 明美

    西新潟中央病院てんかんセンター 夏季セミナー  2013.7 

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    Venue:新潟  

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  • てんかん外科病理学の実際 ―ビジュアルにみる― Invited

    柿田 明美

    第9回 日本てんかん学会近畿地方会  2013.7 

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    Venue:大津  

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  • Surgical pathologic features of epileptogenic brain lesions in infants and children Invited

    KAKITA Akiyoshi

    2013.5 

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  • 脱髄・髄鞘障害性疾患 Invited

    柿田 明美

    第54回日本神経病理学会  2013.4 

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    Venue:東京  

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  • Surgical pathologic features of focal cortical dysplasia and related conditions in infants and children. Invited International conference

    KAKITA Akiyoshi

    Cortical Dysplasia Symposium  2013.1  Children’s Epilepsy Association of Taiwan

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    Venue:Tainan(Taiwan)  

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  • てんかんの病理 Invited

    柿田 明美

    西新潟中央病院てんかんセンター 夏季セミナー  2012.7 

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    Venue:新潟  

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  • てんかん外科病理学の実際 Invited

    柿田 明美

    第7回 日本てんかん学会九州地方会  2012.6 

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    Venue:大分  

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  • ヒトてんかん病巣の病態病理:外科標本の解析 Invited

    柿田 明美

    第1回 トランスレーショナルてんかん研究会  2012.6 

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    Venue:新潟  

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  • てんかん外科病理学の実際 Invited

    柿田 明美

    第676回 新潟医学会  2012.5 

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  • わたくしたちの脳を知る Invited

    柿田 明美

    世界脳週間・サイエンスキャンプ  2012.3  新潟大学脳研究所

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    Venue:新潟  

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  • 難治てんかん原性病巣の神経病理 Invited

    柿田 明美

    第39回 東北てんかん談話会  2012.3 

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    Venue:秋田  

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  • Surgical Pathologic Features of the Epileptogenic Lesions. Invited International conference

    KAKITA Akiyoshi

    2012.3 

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  • Surgical pathologic features of focal cortical dysplasia and related conditions in infants. Invited International conference

    KAKITA Akiyoshi

    The 14th Annual Meeting of ISS  2012.2 

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    Venue:Tokyo  

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  • 小児てんかん原性病巣の外科病理 Invited

    柿田 明美

    第60回大阪小児てんかん研究会  2011.11 

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    Venue:大阪  

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  • 脳のできかたの妙を探る Invited

    柿田 明美

    第20回 新潟脳外科病院 院内研究会  2011.11  新潟脳外科病院

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    Venue:新潟  

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  • Pathologic features of epileptogenic lesions. Invited International conference

    KAKITA Akiyoshi

    The 2nd Congress of Asian Society of Neuropathology  2011.11 

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    Venue:Beijing, China  

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  • 動脈管開存の既往があり、難治性てんかんを示した女性例 Invited

    遠山 潤, 柿田 明美

    第41回 小児神経学セミナー  2011.9 

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    Venue:大阪  

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  • 精神疾患病態解明のための死後脳研究の進め方 新潟大学の脳リソースとそれを用いた実験手技の実際 Invited

    柿田 明美

    包括型脳科学研究推進支援ネットワーク 精神疾患拠点チュートリアル  2011.8 

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    Venue:神戸  

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  • 脳神経疾患の診断に必須な組織染色 Invited

    柿田 明美

    第32回 新潟病理技術研究会  2011.7 

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    Venue:新潟  

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  • 脱髄・髄鞘障害性病態 Invited

    柿田 明美

    第52回 日本神経病理学会  2011.6 

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    Venue:京都  

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  • 脳形成異常を基盤としたてんかん原性病巣の病態病理学的研究 Invited

    柿田 明美

    厚生労働省精神・神経疾患研究開発費 発達障害関係研究班合同シンポジウム  2010.11 

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  • てんかんの病理 Invited

    柿田 明美

    国立西新潟中央病院てんかんセンター 夏期セミナー  2010.8 

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    Venue:新潟  

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  • てんかん原性病巣における分子細胞病理 ―病態形成への関与― Invited

    柿田 明美

    東京都神経科学総合研究所 神経科学セミナー 先端研究セミナー  2010.1 

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  • てんかん外科病理学の実際:異形成と腫瘍性病変 Invited

    柿田 明美

    第38回埼玉脳腫瘍病理懇話会  2009.11 

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    Venue:大宮  

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  • すこやか脳、病める脳 Invited

    柿田 明美

    新潟大学公開講座  2009.9 

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  • てんかん外科病理学の実際 Invited

    柿田 明美

    第35回静岡県神経病理懇談会  2009.9 

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    Venue:浜松  

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  • てんかんの病理 Invited

    柿田 明美

    国立西新潟中央病院てんかんセンター 夏期セミナー  2009.8 

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    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:新潟  

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  • Nasu-Hakola病脳の組織病理所見 Invited

    柿田 明美

    第3回川棚神経科学の会  2008.11  長崎神経医療センター

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    Venue:長崎  

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  • てんかん焦点の分子病理 Invited

    柿田 明美

    第38回新潟脳神経夏期セミナー 精神神経疾患を分子で斬る  2008.8 

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  • てんかんの病理 Invited

    柿田 明美

    国立西新潟中央病院てんかんセンター 夏期セミナー  2008.8 

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    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:新潟  

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  • Nasu-Hakola病 Invited

    柿田 明美

    第49回日本神経病理学会  2008.5 

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    Venue:東京  

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  • てんかんの病理 Invited

    柿田 明美

    国立西新潟中央病院てんかんセンター 夏期セミナー  2007.8 

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    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:新潟  

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  • てんかんの分子細胞病理 Invited

    柿田 明美

    第48回日本神経病理学会  2007.5 

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    Venue:東京  

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  • 中枢神経系の発生とその異常 Invited

    柿田 明美

    第36回小児神経学セミナー  2006.10 

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    Venue:葉山  

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  • てんかん原性病巣における分子細胞病理 ―病態形成への関与― Invited

    柿田 明美

    第40回日本てんかん学会  2006.9 

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    Venue:金沢  

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  • てんかんの病理 Invited

    柿田 明美

    国立西新潟中央病院てんかんセンター 夏期セミナー  2006.8 

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    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:新潟  

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  • 発生期脳における未分化細胞の移動障害:意外に身近な”Migration Disorders” Invited

    柿田 明美

    信州大学医学部第三内科同窓会  2006.6 

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    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:松本  

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  • Migration disordersの病理 Invited

    柿田 明美

    第16回東海ニューロサイエンス研究会  2006.4 

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    Venue:名古屋  

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  • 脳のかたちとそのできかたの妙をさぐる Invited

    柿田 明美

    平成17年度後期新潟大学公開講座 脳研究所公開講座「脳と心を科学する」  2005.10 

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  • てんかんの病理 Invited

    柿田 明美

    国立西新潟中央病院てんかんセンター 夏期セミナー  2005.8 

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    Venue:新潟  

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  • 側頭葉脳表部の脂肪腫とこれに連続する大脳皮質:発生異常に関連した組織所見 Invited

    柿田明美, 稲永親憲, 亀山茂樹, 増田 浩, 上野武彦, 本間順平, 下畑光輝, 高橋均

    第46回日本神経病理学会  2005.5 

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    Language:Japanese   Presentation type:Poster presentation  

    Venue:宇都宮  

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  • Lysosomal and peroxisomal disorderの神経病理 Invited

    柿田 明美

    第46回日本神経病理学会  2005.5 

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    Venue:宇都宮  

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  • 脳の発達障害の神経病理 Invited

    柿田 明美

    第94回日本病理学会  2005.4 

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    Venue:横浜  

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  • 発生期脳におけるグリア芽細胞の移動経路と動態 Invited

    柿田 明美

    グリア研究会特別講演会・グリア講演会  2005.3  東北大学神経内科

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    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:仙台  

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  • てんかんの病理 Invited

    柿田 明美

    国立西新潟中央病院てんかんセンター 夏期セミナー  2004.8 

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    Venue:新潟  

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  • 難治てんかん症例の切除脳組織に見られたcortical dysplasia Invited

    柿田明美, 亀山茂樹, 高橋 均

    第45回日本神経病理学会  2004.5 

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    Venue:前橋  

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  • てんかんの病理 Invited

    柿田 明美

    2004.5.20-21 第22回日本脳腫瘍病理学会  2004.5 

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    Venue:新潟  

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  • Cortical dysplasia / microgysgenesis: 組織所見をどう見ているか Invited

    柿田明美, 亀山茂樹, 高橋 均

    第27回日本てんかん外科学会  2004.4 

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    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:奈良  

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  • Neuropathology of NMD and epileptogenic cortical dysplasia Invited International conference

    KAKITA Akiyoshi

    VIIth Annual Meeting of the Infantile Seizure Society International Symposium on Neuronal Migration Disorders and Childhoot  2004.4 

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    Venue:Tokyo  

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▶ display all

Research Projects

  • アルツハイマー病の進行期におけるUSP10を介した神経細胞死の制御機構の解明

    Grant number:25K02461

    2025.4 - 2028.3

    System name:科学研究費助成事業

    Research category:基盤研究(B)

    Awarding organization:日本学術振興会

    藤井 雅寛, 長谷川 成人, 柿田 明美

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    Grant amount:\18590000 ( Direct Cost: \14300000 、 Indirect Cost:\4290000 )

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  • 認知症治療標的としてのミクログリアによるアストロサイト制御機構に剖検脳から迫る

    Grant number:23K24256

    2024.4 - 2025.3

    System name:科学研究費助成事業

    Research category:基盤研究(B)

    Awarding organization:日本学術振興会

    他田 真理, 池内 健, 竹林 浩秀, 加藤 隆弘, 柿田 明美

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    Grant amount:\3900000 ( Direct Cost: \3000000 、 Indirect Cost:\900000 )

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  • ひとてんかん原性病態機序を知りこれを制御する

    Grant number:23H00434

    2023.4 - 2026.3

    System name:科学研究費助成事業

    Research category:基盤研究(A)

    Awarding organization:日本学術振興会

    柿田 明美, 他田 真理, 北浦 弘樹, 田井中 一貴, 池田 昭夫

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    Grant amount:\47320000 ( Direct Cost: \36400000 、 Indirect Cost:\10920000 )

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  • 自己免疫性グリア病における免疫細胞由来「細胞外DNAトラップ」の生物学的意義の解明

    Grant number:23K06923

    2023.4 - 2026.3

    System name:科学研究費助成事業

    Research category:基盤研究(C)

    Awarding organization:日本学術振興会

    河内 泉, 佐治 越爾, 五十嵐 博中, 柿田 明美

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    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

    視神経脊髄炎 (NMOSD) と多発性硬化症 (MS) は異なる免疫特性を持つ自己免疫性グリア病である. 本研究は「細胞外DNAトラップ」に着目し, その生物学的意義を確立するため, 下記の3つの主要な目的を立てた. 第一に, NMOとMSの脳脊髄病変への「細胞外DNAトラップ」集積とその由来免疫細胞を証明する. 第二に, 「細胞外DNAトラップ」が炎症を惹起し, 血液脳関門 (BBB) の透過性を亢進させ, 神経変性を発動する可能性を探索する. 第三に, 「細胞外DNAトラップ」の解析から, 疾患活動を反映する血液バイオマーカーとしての意義を確立する.
    初年度 (2023年度) は、細胞外DNAトラップの集積とその局在, 由来免疫細胞の同定を行った. 具体的には, 脳・脊髄病変を時空間的な4つのステージ (初期病変 [I], 初期活動性病変 [EA], 後期活動性病変 [LA], 非活動性病変 [IA]) に分類した上で, 免疫組織化学法 (IH) を用い, 脳・脊髄剖検標本において, NMOSDのI/EA病変で多数のシトルリン化ヒストン及びmyeloperoxidase陽性の細胞外DNAトラップの集積とその局在を明らかにした. 細胞外DNAトラップは, 好中球マーカー陽性並びに単球マーカー陰性・ミクログリアマーカー陰性であるため, 好中球由来であると推定された. 好中球由来細胞外DNAトラップは, MSでは認めなかった. これらの研究結果を論文として報告した. これらの実績から, 第一の目的に到達したと考えた. 2年度 (2024年度) 以降, 第二及び第三の目的の到達に向けて, 研究を行う計画である.

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  • 神経病原性蛋白質オリゴマーの神経毒性を抑制する分子メカニズム

    Grant number:22H02829

    2022.4 - 2025.3

    System name:科学研究費助成事業

    Research category:基盤研究(B)

    Awarding organization:日本学術振興会

    藤井 雅寛, 長谷川 成人, 柿田 明美

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    Grant amount:\17290000 ( Direct Cost: \13300000 、 Indirect Cost:\3990000 )

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  • 認知症治療標的としてのミクログリアによるアストロサイト制御機構に剖検脳から迫る

    Grant number:22H02995

    2022.4 - 2025.3

    System name:科学研究費助成事業

    Research category:基盤研究(B)

    Awarding organization:日本学術振興会

    他田 真理, 池内 健, 竹林 浩秀, 加藤 隆弘, 柿田 明美

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    Grant amount:\17680000 ( Direct Cost: \13600000 、 Indirect Cost:\4080000 )

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  • Chemo-sensitization of brain tumors by manipulation of SLFN11

    Grant number:21KK0156

    2021.10 - 2025.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Fund for the Promotion of Joint International Research (Fostering Joint International Research (B))

    Awarding organization:Japan Society for the Promotion of Science

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    Grant amount:\18980000 ( Direct Cost: \14600000 、 Indirect Cost:\4380000 )

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  • Visualization of microenvironments of malignant glioma utilizing 7T-MRI and 3D tissue clearing technology

    Grant number:21H03042

    2021.4 - 2024.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

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    Grant amount:\17420000 ( Direct Cost: \13400000 、 Indirect Cost:\4020000 )

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  • 自己免疫性グリア病における時空間的免疫制御によるneural repairの研究

    Grant number:20K07899

    2020.4 - 2023.3

    System name:科学研究費助成事業

    Research category:基盤研究(C)

    Awarding organization:日本学術振興会

    河内 泉, 柿田 明美, 五十嵐 博中

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    Grant amount:\4420000 ( Direct Cost: \3400000 、 Indirect Cost:\1020000 )

    多発性硬化症と視神経脊髄炎は, 異なる2つの特性「自己免疫」と「神経回路破壊」を特徴とする自己免疫性グリア病である. 重篤な運動・認知機能障害に対して有効な治療法がないため, 神経修復に向けた創薬はunmet medical needsの高い重要な領域となっている. 本研究では, 神経修復能を持つ「脳特異的な制御性・修復向性免疫細胞」のヒトホモログを同定し, 自己免疫性グリア病における脳の恒常性維持と神経回路修復のプロセスを探索する. 初年度 (2020年度) および二年度 (2021年度) は, 多発性硬化症, 視神経脊髄炎, その他の炎症性中枢神経系疾患における時空間依存的な免疫細胞動態の検討を行った. 脳病変を時空間的な4ステージ (初期病変 [I], 初期活動性病変 [EA], 後期活動性病変 [LA], 非活動性病変 [IA]) に分類し, 免疫細胞を解析した. 免疫組織化学 (IH) 法及びin situ hybridization (ISH) 法を用い, (a) 細胞表面分子 (CD3, CD20など), (b) マスターレギュレーター分子 (Foxp3, T-betなど), (c) サイトカイン分子 (IL-10, IL-6, IL-17な ど) の発現パターンから, 免疫細胞を自然免疫系列 (マクロファージ, 顆粒球など) と獲得免疫系列 (T, B細胞) に分類した. EAステージおよびneural repairが盛んと考えられるLAステージで, 特に自然免疫系列であるマクロファージと顆粒球に着目し, IH法等を使い, 検討を進めた. さらに「脳特異的な修復向性免疫細胞」の血液・髄液での挙動を探索の準備を開始した. 多発性硬化症, 視神経脊髄炎, その他の炎症性中枢神経系疾患の炎症制御性・組織修復向性・脳特異性プロファイルの検証を進めた.

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  • Digital 3D Neuropathology: Methodological Platform Creation

    Grant number:20K20468

    2020.4 - 2022.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Challenging Research (Pioneering)

    Awarding organization:Japan Society for the Promotion of Science

    Kakita Akiyoshi

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    Grant amount:\25870000 ( Direct Cost: \19900000 、 Indirect Cost:\5970000 )

    The brain is a complex structure, and its functional units are especially three-dimensional. In this study, we developed a technological platform to capture the arrangement and network of neurons and glial cells, as well as the distribution of microvessels, in three dimensions by using transparency of human brain tissue and 3D imaging technology. First, we overcame the biggest optical challenges in human brain tissue, autofluorescence and browning, and succeeded in developing transparency reagents specifically for human brain tissue. Next, we established various general fluorescent staining and whole-mount immunostaining techniques for 3D. As a result, we have established an imaging platform for whole-mount visualization of many types of structures, including neurons, glial cells, microvessels, myelin sheaths, and senile plaques.

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  • Comprehensive epileptic network analysis in human brain by neuron and glia

    Grant number:19H03574

    2019.4 - 2022.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

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    Grant amount:\17680000 ( Direct Cost: \13600000 、 Indirect Cost:\4080000 )

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  • Microglia-astrocyte crosstalk in leukoencephalopathies

    Grant number:19K07972

    2019.4 - 2022.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    Tada Mari

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    Grant amount:\4420000 ( Direct Cost: \3400000 、 Indirect Cost:\1020000 )

    We have previously reported that in the brains of patients with adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP), an inherited leukoencephalopathy caused by mutations in the colony stimulating factor 1 receptor (CSF1R) gene, the increase of inflammatory microglia is small in number and restricted in area relative to the degree of widespread white matter degeneration, whereas the decrease of homeostatic microglia is significant. In this study, we examined the correlation between the distribution of astrocytes and microglia in the cerebral white matter of ALSP. Our findings support the hypothesis that disruption of microglial control over astrocytes due to microglial dysfunction induces abnormal activation of astrocytes, leading to accelerated white matter degeneration.

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  • Pathomechanisms and Control of Epileptogenic Foci: Imaging Practices for Surgical Specimens

    Grant number:19H01061

    2019.4 - 2022.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (A)

    Awarding organization:Japan Society for the Promotion of Science

    Kakita Akiyoshi

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    Grant amount:\45500000 ( Direct Cost: \35000000 、 Indirect Cost:\10500000 )

    How is abnormal neural excitation elicited and propagated in epileptogenic brain lesions? In this study, we performed physiological analysis using fresh brain slices and three-dimensional pathological analysis of epileptic focal brain tissue that had been surgically removed. The physiological analysis was performed using an originally developed flavin fluorescence imaging method, and the morphological analysis was performed using a newly developed tissue clearing technique for human brain slices. From this analysis, we characterized the spatiotemporal excitation dynamics, verified the pharmacological effects, and clarified the network basis of neurons and glial cells.

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  • Mechanism of inactivation of neuropathogenic protein toxicity by aggresomes

    Grant number:19H03432

    2019.4 - 2022.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

    FUJII MASAHIRO

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    Grant amount:\17550000 ( Direct Cost: \13500000 、 Indirect Cost:\4050000 )

    Parkinson's disease, amyotrophic lateral sclerosis, and Alzheimer's disease are neurodegenerative diseases. In these diseases, the respective pathogenic proteins, α-synuclein, tau, and TDP-43, form aggregates in neurons, and these aggregates are believed to be neurotoxic and cause neurodegenerative diseases. It has been suggested that stress granules and aggresomes are involved in the formation of these pathogenic aggregates. Stress granules and aggresomes are intracytoplasmic aggregates induced by various stresses. In this study, we show that USP10 and G3BP1 induce the formation of stress granules and aggresomes and regulate the formation of α-synuclein, tau, and TDP-43 aggregates.

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  • Ex vivo optical imaging of human brain tissues for visualization of epileptogenic networks.

    Grant number:19H03542

    2019.4 - 2022.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

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    Grant amount:\17160000 ( Direct Cost: \13200000 、 Indirect Cost:\3960000 )

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  • Mechanisms of lesion formation in Parkinson's disease: an analysis using tissue clearing and 3D observation

    Grant number:19K07841

    2019.4 - 2022.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    Shimizu Hiroshi

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    Grant amount:\4290000 ( Direct Cost: \3300000 、 Indirect Cost:\990000 )

    In the early and incidental cases of Parkinson's disease, alpha-synuclein accumulation was observed in various areas of the nervous system, including the brain and peripheral autonomic nervous system, suggesting that these may have occurred multicentrally. In progressive supranuclear palsy, the distribution/density of tau-positive structures were consistent with the manifesting clinical features. Furthermore, the distribution/laterality of tau-positive structures suggested the possibility of lesion extension along fiber connections. Tissue clearing and three-dimensional analysis enabled high-resolution imaging of tau-positive structures in progressive supranuclear palsy and provided important insights into the pathomechanism of lesion formation in this disease.

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  • Visualization of epileptogenic foci of MRI non-lesional neocortical epilepsy patients by 7T-MRI

    Grant number:17K10888

    2017.4 - 2022.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    Fujii Yukihiko

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    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

    This three-year prospective study was intended to visualize epileptogenic foci, as organic lesions, of non-lesional neocortical epilepsy patients by means of our imaging protocol including 7T-MRI and to understand the present status of these patients. However, the study was suspended for a long period because of mechanical failure of the 7T-MRI system, followed by the pandemic of coronavirus disease 2019 (COVID-19) pandemic. Therefore, the study period was finally extended to 5 years to catch up with our study schedule. Unfortunately, although 7T-MRI studies did not restart until the end of the study due to the protracted COVID-19 situation, we could obtain the following results: our imaging protocol could potentially visualize the epileptogenic foci of non-lesional neocortical epilepsy patients and provide insights into the present status of these patients.

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  • Microglial involvement in the pathomechanisms of white matter degeneration

    Grant number:16K07041

    2016.4 - 2019.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    Tada Mari, Ikeuchi Takeshi, Takebayashi Hirohide, Hashimoto Koichi

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    Grant amount:\5070000 ( Direct Cost: \3900000 、 Indirect Cost:\1170000 )

    Hereditary diffuse leukoencephalopathy with spheroids (HDLS) is caused by the mutation of a gene encoding the colony stimulating factor-1 receptor (CSF-1R). In the CNS, the receptor is expressed predominantly in microglia, and therefore HDLS has recently been considered one of the primary microglial disorders known as microgliopathies. However, there has been little direct evidence to characterize HDLS as a microglial disorder. In this study, we analyzed histologicaly and biochemicaly brains of patients with HDLS and also microglia specific CSF-1R knock out mice. In HDLS brains, microglia showed reduction in number in less affected areas, maldistribution, and abnormality of ultra fine structures. These features implied the focal deficiency of microglial functions in the brain of HDLS. While microglial features similar to those were not observed in the brains of model mice used in this study.

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  • Stages of glial inclusion pathology in multiple system pathology

    Grant number:16H04665

    2016.4 - 2019.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

    Yamada Mitsunori, Tada Mari, Toyoshima Yasuko

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    Grant amount:\10530000 ( Direct Cost: \8100000 、 Indirect Cost:\2430000 )

    Multiple system atrophy (MSA) is a sporadic neurodegenerative disease of unknown etiology. There are two major clinical phenotypes: MSA-P with predominant parkinsonian features and MSA-C with predominant cerebellar ataxia. The former is correspond to the previous striatonigral degeneration (SND) and the latter is olivopontocerebellar atrophy (OPCA). Shy-Drager syndrome (SDS) is another subtype of MSA and characterized by the presence of prominent autonomic dysfunctions, but has been discouraged in the recent MSA criteria (Gilman, 1999) because of the commonality of the feature in all forms of MSA. Analyses of 99 MSA brains revealed that GCI was an excellent biomarker representing the degree of disease progress of MSA. GCI profiles in this study revealed the presence of some subtypes in each clinical phenotype. The combination of four GCI curves in restricted brain regions enabled us to classify the MSA progression into four stages.

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  • A feasibility study for 3D neuropathology

    Grant number:16K14571

    2016.4 - 2018.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Challenging Exploratory Research

    Awarding organization:Japan Society for the Promotion of Science

    Kakita Akiyoshi

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    Grant amount:\3770000 ( Direct Cost: \2900000 、 Indirect Cost:\870000 )

    To investigate the 3-dimensional cytoarchitecture of the cerebral cortex taken from patients with epilepsy, we developed new chemical protocols for clearing human brain tissue and driving methodology of the sheet-scanning fluorescence microscopy. By the methods, we were able to observe fine features of neurons and glia distributed widely within extremely thick brain blocks. The methods created by this feasibility study would open an innovative era for the neuropathology field.

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  • On the transneuronal propagation in neurodegenerative diseases

    Grant number:15K06754

    2015.4 - 2019.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    Oyanagi Kiyomitsu

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    Grant amount:\5070000 ( Direct Cost: \3900000 、 Indirect Cost:\1170000 )

    Phosphorylated (p-) TDP-43 inclusions were frequently observed in the axons of the lower motoneurons of 19 autopsy cases with amyotrophic lateral sclerosis (ALS). The forms of the inclusions were granuloreticular and massive aggregate types. Presynaptic p-TDP-43 inclusions were observed around the neurons of the red nucleus, however, postsynaptic p-TDP-43 aggregates were not seen. The finding showed transsynaptic p-TDP-43 propagation was not examined in the ALS patients. Stages of brain lesions by phosphorylated tau-immunohistochemistry in the Guam PDC, Guam ALS and Guam controls were identified five (0 - IV). Differences from those of Alzheimer’s disease were massive progression into brainstem and rare neuropile threads.

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  • Epileptogenesis in Mesial Temporal Lobe Epilepsy

    Grant number:15K06751

    2015.4 - 2018.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    Kitaura Hiroki

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    Grant amount:\5070000 ( Direct Cost: \3900000 、 Indirect Cost:\1170000 )

    The majority of seizures originate primarily from the hippocampus in patient of Mesial temporal lobe epilepsy (MTLE). The resected hippocampal tissue often shows severe neuronal loss, a condition referred to as hippocampal sclerosis. Here we investigated epileptiform activities ex vivo using living hippocampal tissue taken from patients with MTLE. Flavoprotein fluorescence imaging and local field potential recordings revealed that epileptiform activities developed from the subiculum. Moreover, physiological and morphological experiments revealed possible impairment of K+ clearance in the subiculum affected by HS. Stimulation of mossy fibers induced recurrent trans-synaptic activity in the granule cell layer of the dentate gyrus, suggesting that mossy fiber sprouting in HS also contributes to the epileptogenic mechanism. These results indicate that pathophysiological alterations involving the subiculum and dentate gyrus could be responsible for epileptogenesis in patients with MTLE.

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  • Development of a preoperative highly accurate evaluation method to detect epileptic foci -Analyzing high frequency oscillations with dense array EEG-

    Grant number:15K19955

    2015.4 - 2018.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Young Scientists (B)

    Awarding organization:Japan Society for the Promotion of Science

    HIRAISHI TETSUYA, FUKUDA MASAFUMI, OISHI MAKOTO, TAKAO TETSUROU, KAKITA AKIYOSHI

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    Grant amount:\4030000 ( Direct Cost: \3100000 、 Indirect Cost:\930000 )

    Epileptic focus identification based on new approach is necessary to the spread of epilepsy surgery. Dense array EEG, which is constructed to include electrode coverage over the face and neck, the purpose of which is to feasibly electrographically sample basal brain regions, is a method of recording electroencephalography (EEG) with many more electrodes (up to 256) . High frequency oscillations (HFO) near epileptic discharges from patients with intractable epilepsy were detected by the dense array EEG. Dense array EEG is helpful to understanding epileptic focus with analyzing HFO.

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  • Amyotrophic Lateral Sclerosis and TDP-43: Elucidation of molecular neuropathology in terms of spread from its beginning

    Grant number:26250017

    2014.4 - 2017.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (A)

    Awarding organization:Japan Society for the Promotion of Science

    Takahashi Hitoshi, KAKITA Akiyoshi, SAKIMURA Kenji, IKEUCHI Takeshi

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    Grant amount:\39780000 ( Direct Cost: \30600000 、 Indirect Cost:\9180000 )

    We found that TDP-43 regulates the level of-its-own protein by alternative splicing within exon 6. Surprisingly, we found that the proportion of TDP-43 mRNA associated with this autoregulation increases in the spinal cord of ALS patients. It was confirmed that this mutant co-localized with TDP-43 immuno-positive inclusion body in anterior horn cells of ALS patients. This suggested that this abnormal protein may be the beginning of ALS lesion.
    We reevaluated the cortical TDP-43 pathology in cases of sporadic ALS, using semi-quantitative estimation of pTDP-43-positive dystrophic neurite in the temporal neocortex,the case were divided into three groups, types 1, 2a and 2b. Type 2b has characteristic clinicopathological features. Considering the patient survaival time and severity of motor neuron loss, each group was regarded as independent subtype, indicating that transition from type 1 to type 2a, or from type 2a to type 2b during the disease course appeared unlikely.

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  • Pathomechanisms underlying human temporal lobe epilepsy

    Grant number:25250008

    2013.4 - 2017.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (A)

    Awarding organization:Japan Society for the Promotion of Science

    KAKITA Akiyoshi

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    Grant amount:\47710000 ( Direct Cost: \36700000 、 Indirect Cost:\11010000 )

    Mesial temporal lobe epilepsy (MTLE) is the most frequent focal epileptic syndrome in adults, and the majority of seizures originate primarily from the hippocampus. The resected hippocampus shows several degrees of neuronal loss (hippocampal sclerosis: HS), accordingly there would arise a paradox between clinical and pathological findings; how these atrophic tissues cause epilepsy? Here we investigated epileptiform activities using hippocampal specimens taken from MTLE patients ex vivo. Flavoprotein fluorescence imaging and local field potential recordings (LFPs) revealed that epileptiform activities were arise from subiculum of MTLE groups. Moreover, loss of inwardly rectifying K+ channel 4.1 (Kir 4.1) was evident in the astrocytes of the subiculum of HS. These results suggest that epileptogenic mechanisms would correlate to the distinct pathologies, and Kir 4.1 may play a pivotal role in epileptogensis of the HS.

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  • Regulation of neuronal cell size control in normal and disease condition

    Grant number:25430064

    2013.4 - 2016.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    Takei Nobuyuki, KAKITA Akiyoshi

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    Grant amount:\5330000 ( Direct Cost: \4100000 、 Indirect Cost:\1230000 )

    We have analyzed the signaling transduction pathways of mammalian target of rapamycin (mTOR), that is a key enzyme of cell size control. We identified several molecules that regulate the activity of mTOR in neurons. We revealed that activation of mTOR leads to the upregulation of protein and lipid synthesis and its link to the cell size in CNS neurons. In disease study, we found novel somatic mutations of MTOR in Forcal Cortical Dysplasia IIb (FCDIIb) brain and confirm that these mutations make mTOR hyperactive.

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  • Autoreguation of TDP-43 in ALS

    Grant number:25253065

    2013.4 - 2016.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (A)

    Awarding organization:Japan Society for the Promotion of Science

    Nishizawa Masatoyo, ONODERA Osamu, ISHIHARA Tomohiko, KAKITA Akiyoshi, SATO Toshiya

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    Grant amount:\45890000 ( Direct Cost: \35300000 、 Indirect Cost:\10590000 )

    Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disorder. In motor neurons of ALS, TAR DNA binding protein-43 (TDP-43), a nuclear protein encoded by TARDBP, is absent from the nucleus and forms cytoplasmic inclusions. TDP-43 auto-regulates the amount by regulating the TARDBP mRNA, which has three polyadenylation signals (PASs) and three additional alternative introns within the last exon. We show that TDP-43 inhibits the selection of the most proximal PAS and induces splicing of multiple alternative introns in TARDBP mRNA to decrease the amount of cytoplasmic TARDBP mRNA by nonsense-mediated mRNA decay. When TDP-43 is depleted, the TARDBP mRNA uses the most proximal PAS and is increased in the cytoplasm. Finally, we have demonstrated that in ALS motor neurons; especially neurons with mislocalized TDP-43; the amount of TARDBP mRNA is increased in the cytoplasm. Our observations suggests that that the absence of nuclear TDP-43 induces an abnormal autoregulation.

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  • Pathogenesis of focal cortical dysplasia: possible mechanistic implification of somatic mutations

    Grant number:25640027

    2013.4 - 2015.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Challenging Exploratory Research

    Awarding organization:Japan Society for the Promotion of Science

    KAKITA Akiyoshi, TAKEI Nobuyuki

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    Grant amount:\4030000 ( Direct Cost: \3100000 、 Indirect Cost:\930000 )

    We explore the possible involvement of somatic mutations in focal cortical dysplasia (FCD) Type IIb. We performed whole exome sequencing using brain and blood samples from nine of the FCD Type IIb subjects. Somatic MTOR mutations were identified. The effect of MTOR mutations on mTOR kinase signaling was evaluated. We identified four lesion-specific somatic MTOR mutations in six of 13 (46%) individuals with FCD Type IIb showing mutant allele rates of 1.11 - 9.31%. Functional analyses showed that phosphorylation of ribosomal protein S6 in FCD Type IIb brain tissues with MTOR mutations was clearly elevated compared with control samples. Transfection of any of the four MTOR mutants into HEK293T cells led to elevated phosphorylation of 4EBP, the direct target of mTOR kinase. We found low-prevalence somatic mutations in MTOR in FCD Type IIb, indicating that activating somatic mutations in MTOR cause FCD Type IIb.

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  • Cytokine-Induced Neuropathologic Endophenotypes of Psychiatric Diseases

    Grant number:24116010

    2012.6 - 2017.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)

    Awarding organization:Japan Society for the Promotion of Science

    Nawa Hiroyuki, NAMBA Hisaaki, KAKITA Akiyoshi, TAKEI Nobuyuki, KIDA Satoshi

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    Grant amount:\95940000 ( Direct Cost: \73800000 、 Indirect Cost:\22140000 )

    The animals that had been exposed to cytokines as neonates later develop the abnormal behaviors relevant to schizophrenia. In the present investigation, we explored the cytokine animal model for schizophrenia, focusing on the monoaminergic pathways. Among various cytokines, epidermal growth factor (EGF) produced the most remarkable impact on animal behaviors. In the EGF model, dopaminergic neurons exhibited abnormal pallidal innervations and a postpubertal firing increase as well as their antipsychotic sensitivity. There were no significant influences on the other monoaminergic neurons in the EGF model. In addition, the EGF model in rats displayed the remarkable deficits particularly in the auditory system. These observations suggest that prenatal or perinatal cytokine exposure results in dopaminergic mal-development and deficits in auditory cognition.

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  • A study on the molecular mechanisms of neurodegeneration induced by high-mass amyloid-beta assembly, amylospheroids (ASPD)

    Grant number:23390079

    2011.4 - 2014.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

    HOSHI Minako, OHNISHI Takayuki, INOUE Masafumi, KAKITA Akiyoshi

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    Grant amount:\19630000 ( Direct Cost: \15100000 、 Indirect Cost:\4530000 )

    Amyloid beta protein (Abeta) plays a central role in Alzheimer's disease (AD). To elucidate the molecular identities of pathogenic Abeta oligomers and their neuronal targets responsible for neurodegeneration, we have previously isolated highly toxic Abeta assemblies termed amylospheroids (ASPD) from AD patient brains. Patient-derived ASPD were toxic to human mature neurons and their amount in AD susceptible regions well correlated with pathological severity of AD. In this study, we found that ASPD neurotoxicity requires Ca2+ influx. We also found that voltage gated calcium channels (VGCC) are involved in ASPD neurotoxicity. Interestingly, the abnormal Ca2+ overload induced by ASPD activated two tau protein kinases, and increased the phosphorylation of tau. Importantly, we found that ASPD-binding to the ASPD target protein on mature neuronal surface impairs its activity, responsible for the above abnormal Ca2+ homeostasis and to the severe neurodegeneration.

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  • ALS and TDP-43: Dose the splicing failure underlie the pathogenesis of ALS?

    Grant number:23240049

    2011.4 - 2014.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (A)

    Awarding organization:Japan Society for the Promotion of Science

    HITOSHI Takahashi, TOYOSHIMA Yasuko, ONODERA Osamu, KUWANO Ryozo, SAKIMURA Kenji, KAKITA Akiyoshi, YOKOYAMA Minesuke

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    Grant amount:\45890000 ( Direct Cost: \35300000 、 Indirect Cost:\10590000 )

    Amyotrophic lateral sclerosis (ALS) is fatal neurodegenerative disease. For a development of therapeutic methods for this disease, we investigated the splicing variants of TDP-43, and its own function associated with splicing for other genes. We found that THP-43 has menu splicing variants, and investigate the mechanism how splicing factors influence this splicing. In addition, we found some of the mutation with ALS10, which is caused by a mutation in TDP-43, affects the efficiency of its own splicing. These findings may open new avenue for the investigation of the pathogenesis of ALS.

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  • Personal genome analysis on Alzheimer's disease

    Grant number:22129004

    2010.4 - 2015.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)

    Awarding organization:Japan Society for the Promotion of Science

    KUWANO Ryozo, KAKITA Akiyoshi, MIYASHITA Akinori

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    Grant amount:\125840000 ( Direct Cost: \96800000 、 Indirect Cost:\29040000 )

    Twin studies and λs (=5.0) of Alzheimer’s disease indicate that genetic risk factors are thought to contribute the development and progression. SNP-based genome-wide association studies have been intensively done. As the most of risk SNPs identified are only small effect on the disease, the family-based genome analysis has been re-evaluated. The next generation sequencing proved to be a new powerful tool to determine rare variants in patents with family history. In addition to genome sequencing, we performed gene expression analysis of human brains diagnosed as to senile plaques and neurofibrillary tangles by the exon-array and next generation sequencing. It should be innovated the possible mechanism that gene expression is regulated by a gene-gene cluster between distal regions on the same chromosome or on a different chromosome, and alternatively by non-coding RNA including microRNA.

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  • Molecular pathogenesis of ALS: approach from TDP-43 function.

    Grant number:22249036

    2010 - 2012

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (A)

    Awarding organization:Japan Society for the Promotion of Science

    NISHIZAWA Masatoyo, ABE Manabu, KUWANO Ryozo, ONODERA Osamu, KAKITA Akiyoshi, SATOU Toshiya

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    Grant amount:\48880000 ( Direct Cost: \37600000 、 Indirect Cost:\11280000 )

    Disappearance of TAR-DNA binding protein 43 kDa (TDP-43) from the nucleuscontributes to the pathogenesis of amyotrophic lateral sclerosis (ALS), but the nuclearfunction of TDP-43 is not yet fully understood. TDP-43 associates with nuclear bodiesincluding Gemini of coiled bodies (GEMs). GEMs contribute to the biogenesis ofuridine-rich small nuclear RNA (U snRNA), a component of splicing machinery. Thenumber of GEMs and a subset of U snRNAs decrease in spinal muscular atrophy, alower motor neuron disease, suggesting that alteration of U snRNAs may also underliethe molecular pathogenesis of ALS. We investigated the number of GEMs andU11/12-type small nuclear ribonucleoproteins (snRNP) by immunohistochemistry andthe level of U snRNAs using real-time quantitative RT-PCR in ALS tissues. GEMsdecreased in both TDP-43-depleted HeLa cells and spinal motor neurons in ALSpatients. Levels of several U snRNAs decreased in TDP-43-depleted SH-SY5Y andU87MG cells. The level of U12 snRNA was decreased in tissues affected by ALS butnot in tissues unaffected by ALS. These findings suggest that loss of TDP-43 functiondecreases the number of GEMs, which is followed by a disturbance of pre-mRNAsplicing by the U11/U12 spliceosome in tissues affected by ALS.

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  • Clarification of epileptogenicity using human brain slices in vitro

    Grant number:22700376

    2010 - 2011

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Young Scientists (B)

    Awarding organization:Japan Society for the Promotion of Science

    KITAURA Hiroki, KAKITA Akiyoshi, FUKUDA Masafumi, KAMEYAMA Shigeki

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    Grant amount:\4030000 ( Direct Cost: \3100000 、 Indirect Cost:\930000 )

    Epilepsy is one of the major neurological disorders in Japan. It is believed that hyper-excitability of the pyramidal neurons in the cerebral cortex contributes to epileptogenicity. However, the precise mechanism of the alteration was not still clarified. We struggled to observe spatiotemporal dynamics of epileptic activities using human brain slices taken from epileptic patients. As a result, we found unique epileptiform propagation of the activities in epileptogenic tissues but not in control tissues.

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  • Magnetic Resonance Molecular Microimaging

    Grant number:21220007

    2009.5 - 2014.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (S)

    Awarding organization:Japan Society for the Promotion of Science

    NAKADA Tsutomu, NISHIZAWA Masatoyo, FUJII Yukihiko, IGARASHI Hironaka, HUBER Vincent, TSUJITA Mika, SUZUKI Kiyotaka, KAKITA Akiyoshi

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    Grant amount:\213720000 ( Direct Cost: \164400000 、 Indirect Cost:\49320000 )

    The research project was one of the most ambitious proposals aiming to develop ligand based MRI molecular imaging, a goal that has eluded world scientists for more than 30 years. Our research team successfully developed such a "dream" imaging method as we promised. The technique utilized O17, a stable isotope of oxygen, labeled specific ligand and its JJ vicinal coupling to its covalent proton. The method was termed JJ Vicinal Coupling Proton Exchange (JJVCPE) imaging by the project director. We applied this method to study water molecule dynamics utilizing H2O17, and beta-amyloid imaging utilizing O17-PiB in vivo. The studies showed that aquaporin-4 (AQP-4), abundant in glia in brain, plays a major role in the interstitional flow through the Virchow-Robin space. The disturbance in this system, which is critical for beta-amyloid clearance, plays a major role in the pathogentesis of Alzheimer disease.

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  • Spatiotemopral dynamics of epiletiform propagations in surgical specimens taken from patients with intractable epilepsy

    Grant number:21300134

    2009 - 2011

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

    KAKITA Akiyoshi, KITAURA Hiroki, FUKUDA Masafumi

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    Grant amount:\19370000 ( Direct Cost: \14900000 、 Indirect Cost:\4470000 )

    Seizure activities often originate from a localized region of the cerebral cortex and spread across large areas of the brain. The properties of these spreading abnormal discharges may account for clinical phenotypes in epilepsy patients, although the manner of their propagation and the underlying mechanisms are not well understood. In the present study we performed flavoprotein fluorescence imaging of cortical brain slices surgically resected from patients with partial epilepsy caused by various symptomatic lesions. Elicited neural activities in the epileptogenic tissue spread horizontally over the cortex momentarily, but those in control tissue taken from patients with brain tumors who had no history of epilepsy demonstrated only localized responses. Characteristically, the epileptiform propagation comprised early and late phases. When the stimulus intensity was changed gradually, the early phase showed an all-or-none behavior, whereas the late phase showed a gradual increase in the response. Moreover, the two phases were propagated through different cortical layers, suggesting that they are derived from distinct neural circuits. Morphological investigation revealed the presence of hypertrophic neurons and loss of dendritic spines, which imaging. These findings indicate that synchronized activities of the early phase may play a key role in spreading abnormal discharges in human cortical epilepsies.

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  • Amyotrophic lateral sclerosis and TDP-43 : elucidation of the entire neuropathological picture and molecular pathomechanism

    Grant number:20240037

    2008 - 2010

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (A)

    Awarding organization:Japan Society for the Promotion of Science

    TAKAHASHI Hitoshi, TAN ChenーFeng, TOYOSHIMA Yasuko, ONODERA Osamu, KAKITA Akiyoshi, SAKIMURA Kenji, KUWANO Ryozo, YOKOYAMA Minesuke

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    Grant amount:\37440000 ( Direct Cost: \28800000 、 Indirect Cost:\8640000 )

    We examined clinicopathologically and immunohistochemically a large series of sporadic amyotrophic lateral sclerosis (SALS) cases, including those having long disease durations with artificial respiratory support. In each case, various brain regions were immunostained with an antibody against TDP-43, showing occurrence of TDP-43-positive neuronal (NCIs) and glial cytoplasmic inclusions in many regions, including the lower motor neuron nuclei. The results obtained indicate that SALS is a multisystem neuro-glial proteinopathy of TDP-43 and can show two pathological phenotypes (types 1 and 2 ; type 2 can be distinguished from type 1 by the presence of TDP-43-positive NCIs in the frontotemoral cortex, hippocampal formation, neostriatum and substantia nigra). We also generated a transgenic TDP-43 KO mouse model for further biochemical and molecular analyses on the pathomechanisms underlying SALS. The several data obtained strongly suggest that our next target is "splicing abnormalities of TDP-43".

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  • Epileptogenic mechanisms underlying cortical lesions in patients with intractable seizures

    Grant number:19300124

    2007 - 2008

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

    KAKITA Akiyoshi, KITAURA Hiroki

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    Grant amount:\8970000 ( Direct Cost: \6900000 、 Indirect Cost:\2070000 )

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  • Comparative Transcriptome Study of Brain

    Grant number:17018015

    2005 - 2009

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research on Priority Areas

    Awarding organization:Japan Society for the Promotion of Science

    NAWA Hiroyuki, KAKITA Akiyoshi

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    Grant amount:\44800000 ( Direct Cost: \44800000 )

    Using the DNA microarray technique, we performed comparative expression profiling of brain transcriptomes among primates. The profiling revealed the marked strain variation in mRNA signal intensity or homology of the zinc finger genes located at human chromosome 19q13.43. DNA sequence analysis suggests that this genomic region has evolved rapidly in primates.

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  • Tracing of regenerating nerve along its length using adenovirus vector

    Grant number:16390509

    2004 - 2006

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

    SHIBATA Minoru, KAKITA Akiyoshi

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    Grant amount:\14000000 ( Direct Cost: \14000000 )

    Experiment I.
    Adenoviral vectors containing LacZ gene were administrated to the cut proximal stumps of median nerves (median nerve group) and tibial nerves (tibial nerve group) using Wister rats. At different time points post transfection, the sections of spinal cord of C5 to Th1 or L2 to L6 and the corresponding DRGs and brachial or sacral plexuses nerves were processed for X-gal staining. The results show that LacZ gene specially targeted to the motor and sensory neurons of the transected nerves and that B-gal anterogradely labeled the axons of the neurons as far as to the distal of the nerve repairing sites. The initial time, peak time, persisting period and the number of B-gal labeling of DRG neurons, motor neurons and peripheral nerve axons in the two groups were also detected.
    Experiment II
    HYPOTHESIS : Crossing of the ulnar or median nerve funiculi to the distal cut end of musculocutaneous motor components provides independent good flexion of the elbow. We hypothesized that some neurotropism or plasticity may work not only in brain but also in spinal cord for nerve crossing which should invite misdirectional nerve regeneration.
    METHODS : We used upper limb of 41 male Wistar rats. RESULTS/STATISTICS: Group I: Stained roots for musculocutaneous located in C5-C7, median in C6-Th1 and ulna in C8-Th1. These root level innervations are same with those human. There was no innervating root level overlap between musculocutaneous and ulnar nerves. Group II : Infection through the distal ulnar nerve demonstrated staining of C5-Th 1 roots and proximal ulna nerve coapted to the distal musculocutaneous nerve(7/7). Infection through distal musculocutaneous nerve labeled C8 and Th1 roots(7/7).
    SUMMARY POINT : Result of the infection from crossed distal ulnar nerve shows new fact that C5-C7 neurons may send sprouting axons to proximal ulnar nerve through C8-Th1 roots probably through inside of spinal cord.

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  • 内在性相補鎖RNAによる遺伝子発現調節機構に注目したシヌクレイン関連蛋白の解析

    Grant number:16659229

    2004 - 2005

    System name:科学研究費助成事業

    Research category:萌芽研究

    Awarding organization:日本学術振興会

    小野寺 理, 柿田 明美

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    Grant amount:\2800000 ( Direct Cost: \2800000 )

    多系統萎縮症(MSA)は本邦に一万人程の罹患患者がいると考えられるが,その原因および有効な治療戦略は提案されていない。本症はGlial Cytoplasmic Inclusion(GCI)というα-synucleinからなる神経細胞内封入体を特徴とする。α-synucleinが主成分である神経細胞内封入体にはパーキンソン病で認められるLewy小体があるがGCIではsynphilin-1の存在が特徴的である。このことからsynphilin-1とシヌクレイン関連蛋白の関与が疑われている(Acta Neuropathol 2002 103)。我々はこれらの遺伝子の特定のハプロタイプが疾患感受性を規定すると考え,synphilin-1を含むシヌクレイン関連遺伝子のMSA患者群におけるSNPsとEM法を用いたハプロタイプ解析を行った。しかし,これら遺伝子の翻訳領域のハプロタイプ解析では疾患群と対照群で差を見いだすことはできなかった。今年度はsynphilin-1近傍のマーカーにて,有意差を認める領域を同定し,本領域の一塩基置換が,疾患の発症との関与を示した.

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  • Molecular mechanisms underlying progenitor migration following methylmercury exposure in the developing brain

    Grant number:16500214

    2004 - 2005

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    KAKITA Akiyoshi, SAKAMOTO Mineshi, TAKAHASHI Hitoshi

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    Grant amount:\3700000 ( Direct Cost: \3700000 )

    To understand the effects of methylmercury (MeHg) on neuronal and glial progenitor migration in the developing cerebral cortex, we examined profile alterations in gene expression in the telencephalic mantle following fetal or neonatal administration of MeHg, wher an apparent disrupition of the progenitor migration had been elucidated histopathologically. We applied extracted mRNA samples to two kinds of DNA microarrays, which had been made under different biotechnological concepts. Then, we performed analysis of the plenty of data according to the bioinformatics methodologies. We selected 11 molecules, which could be regarded as candidates of specific molecular cues closely associated with the migration disturbance underlying MeHg neurotoxicity.

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  • 難治てんかん原性病巣としての「皮質形成異常」の分子病理学的診断基準の確立

    Grant number:15650062

    2003 - 2004

    System name:科学研究費助成事業

    Research category:萌芽研究

    Awarding organization:日本学術振興会

    高橋 均, 柿田 明美, 佐藤 俊哉

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    Grant amount:\3100000 ( Direct Cost: \3100000 )

    1.研究目的
    てんかんは人口の約1%もの人を苦しめている精神神経疾患であり、その病態と病因の解明は医学的にも社会的にも重要な問題である。近年、難治性てんかん患者における外科的脳切除が広く行われるようになり、その切除組織についての病理組織学的知見が蓄積されるにつれ、大脳皮質の発生異常、特に神経細胞の移動障害を含む局所病変が、てんかん原性病巣となり得ることが指摘されてきた。そのようなことから、これらてんかん原性切除組織の組織病理学的背景を明らかにし、その病態を形成する分子・細胞病理学的実態を明らかにするべく研究を行った。
    2.研究結果
    当該研究期間を含め、これまで経験した計173例の外科切除例について、詳細な組織病理学的解析を行った(研究発表:参照)。そこでは、皮質異形成(cortical dysplasia)に代表される発生異常が表現されており、これらが病態形成基盤をなすことは間違いないと考えるに至った。しかしながら、それだけではphenotype発現には充分ではなく、実はグリア細胞、特にアストロサイトが担う役割が重要である可能性に思い至った。つまり、これまで神経細胞の機能ばかりが注目されがちではあるが、ニューロン-グリア連関、glial signal transmissionが重要ではないかとの仮説を思考するに至った。
    これと平行して、方法論的には、DNAチップを含めた分子病理学的方法論に加え、蛋白発現解析手技を確立した(研究発表:参照)。
    3.まとめ
    当萌芽研究期間に蓄積した切除脳凍結組織は、充分な数と症例のvarietyを得るに至った。上記、組織検索とそこから思考された仮説は、てんかん原生病変の分子病態機序を解明する上で、極めて重要なものである。当萌芽研究によって、今後、大規模・多角的研究を展開する上で、不可欠かつ重要な成果を得ることができた。

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  • Migration pathways and fate determination of progenitors in the subventricular zone

    Grant number:14580767

    2002 - 2003

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    KAKITA Akiyoshi, TAKAHASHI Hitoshi, KAKITA Akiyoshi

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    Grant amount:\3100000 ( Direct Cost: \3100000 )

    The great majority of glial cells of the mammalian forebrain are generated in the perinatal period from progenitors in the subventricular zone(SVZ). We investigated the migration of progenitors from the neonatal(postnatal day O,PO) rat forebrain SVZ by labeling them in vivo with a GFP-retrovirus, and monitoring their movements by time-lapse video microscopy in P3 slices. We identified a small number of progenitors that migrated tangentially within the corpus callosum(CC) and crossed the midline. These retained a relatively uniform morphology : the leading process was extended toward the contralateral side, but showed no process branching or turning away from the migratory direction. Net migration requires the elongation of the leading process and nuclear translocation, and the migrating cells in the CC showed both modes. We confirmed the presence of unmyelihated axon bundles within the P3 CC, but failed to detect any radially directed glial processes(vimentin-or GLAST-immunolabeled fibers) spanning through the CC Confocal images showed a close proximity between neurofilament-immunolabeled axons and the leading process of the GFP-expressing progenitors in the CC. The destination of the callosal fibers was examined by applying Dil to the right cingulum ; the labeled fibers ran throughout the CC and reached the left cingulate and motor areas. The distribution and final fates of the retrovirus-labeled cells were examined in P28 brains. A small proportion of the labeled cells, were found in the contralateral hemisphere, where, as oligodendrocytes and astrocytes, they colonized predominantly the cortex and the underlying white matter of the cingulate and secondary motor areas. The distribution pattern appears to coincide well with the projection direction of the callosal fibers. Thus, glial progenitors migrate across the CC, presumably in conjunction with unmyelinated axons, to colonize the contralateral hemisphere.

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  • 脳内サイトカインによる中枢神経機能の制御メカニズム:分子から精神活動へ

    Grant number:13GS0014

    2001 - 2005

    System name:科学研究費助成事業

    Research category:学術創成研究費

    Awarding organization:日本学術振興会

    那波 宏之, 武井 延之, 柿田 明美, 水野 誠, 難波 寿明, 高橋 誠, 豊岡 和彦

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    Grant amount:\312000000 ( Direct Cost: \258000000 、 Indirect Cost:\54000000 )

    本研究では、5年間にわたりサイトカインの脳内標的とそのシグナル路、生理作用、認知行動作用を解析してきた。最終年度においては脳内サイトカインの作用部位、機序の分析、とりまとめを中心に以下のような研究を実施した。
    1)遺伝子改変動物やサイトカイン投与動物の神経興奮性薬物に対する反応を分析する。
    サイトカインの過剰発現はメタアンフェタミンなどの神経刺激薬の反応性を亢進させる。なかでもドパミン感受性、特にD2受容体反応性がEGFの乳幼仔期投与によって変動することが判明した。
    2)遺伝子改変動物やサイトカイン投与動物のストレス耐久能を行動テストで評価、分析する。
    IL-1投与動物を中心に拘束ストレスに対する反応性を対照群と比較した。拘束後の驚愕反応がIL-1投与で上昇しており、、炎症性サイトカインとストレス反応には相互作用があることが判明した。
    3)DNAチップ解析等で得られた精神疾患における脳内遺伝子発現パターンと遺伝子改変動物やサイトカイン投与動物における脳内遺伝子発現パターンを比較、分析する。
    サイトカインモデルの脳よりRNAを抽出して、GENEチップを用いて遺伝子発現プロファイルを実施した。,EGF投与群線条体では145遺伝子が2倍以上の変化を、IL-1投与群では77遺伝子がその変化を示したが、大半は未同定の未知遺伝子であり、統合失調症患者のデータとは一致を見なかった。
    4)得られた各種サイトカインによる動物脳機能画像についてヒト精神疾患での報告と比較対比する。
    免疫組織化学的手法によりリン酸化ERK蛋白やリン酸化CREBの脳内分布を検討したところ、背側部線条体においてD2アゴニストへの反応性が亢進していることが確認できた。
    5)遺伝子改変動物やサイトカイン投与動物の脳活動異常部位に対して、電気生理学的に脳内活動のレコーディングを行ない、脳機能画像解析結果の裏づけを取る。
    乳仔期EGF投与ラットは、中脳ドパミン神経のグルタミン酸感受性が亢進していることがパッチクランプ法により証明された。このことはドパミン神経路の標的部位、線条体でその感受性が変化していることと合致した。
    6)これまでのデータ整理を行うと共に、研究の取りまとめを実施する。
    上記の結果は、炎症性サイトカインは脳内ドパミン系を改変することで、ストレス反応を持続的に修飾することが示唆された。

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  • A study on the molecular pathomechanisms underflying intractable epilepsy

    Grant number:12470287

    2000 - 2002

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

    TAKAHASHI Hitoshi, TANAKA Ryuichi, NAWA Hiroyuki, KAKITA Akiyoshi

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    Grant amount:\11900000 ( Direct Cost: \11900000 )

    1. We carried out the histopathological observations in 125 patients with pharmacoresistant intractable epilepsy. Cortical dysplasia (Grade I) in the medial temporal lobe was found to be the most frequent abnormality (66 cases). The mean ages at onset of seizure and at surgery were 12.2 years and 31.4 years, respectively. In all the cases, glial fibrillary acidic protein-positive reactive astrocytes were present in the affected cortex as well as in the subcortical white matter. The hippocampus was examined in a total of 32 cases : there were no correlation between histological severity of hippocampal sclerosis and that of cortical dysplasia.
    2. We reported the histopathological features of an autopsy case of bilateral periventricular nodular heterotopia with widespread glomeruloid microvascular anomaly and dysplastic cytoarchitecture in the cerebral cortex, in whom we found a novel exon 11 (Val528Met) filamin 1 mutation.
    3. We employed the DNA array technique to compare the mRNA expression profiles of three neocortical subregions of the human brain : prefrontal cortex (Area 46), motor cortex (Area 4) and visual cortex (Area 17). The macroarray analysis on high quality mRNA from postmortem brains revealed that the expression profiles of the different cortical areas are almost similar : only six out of 1088 known genes exhibited significant differences (>2-fold) in their expression. RT-PCR studies with an increased number of samples confirmed that expression of only two genes, annexin II and early growth response protein 1, varied by 2-fold among the regions, whereas exoression of the others showed large inter-individual difference. These results suggest that the whole neocortex of humans is more homogeneous than we expected at the level of gross gene expression profiles.

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  • Investigation on migration mechanisms of glial progenitors: observations of living cells labeled by dual fluorescent molecules

    Grant number:12680770

    2000 - 2001

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    KAKITA Akiyoshi, YAMADA Mitsunori, TAKAHASHI Hitoshi

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    Grant amount:\3600000 ( Direct Cost: \3600000 )

    The great majority of glial cells of the mammalian forebrain are generated in the perinatal period from progenitors in the subventricular zone (SVZ). We investigated the migration of progenitors from the neonatal (postnatal day 0, PO) rat forebrain SVZ by labeling them in vivo with a GFP-retrovirus, and monitoring their movements by time-lapse video microscopy in P3 slices. We identified a small number of progenitors that migrated tangentially within the corpus callosum (CC) and crossed the midline. These retained a relatively uniform morphology: the leading process was extended toward the contralateral side, but showed no process branching or turning away from the migratory direction. Net migration requires the elongation of the leading process and nuclear translocation, and the migrating cells in the CC showed both modes. We confirmed the presence of unmyelinated axon bundles within the P3 CC, but failed to detect any radially directed glial processes (vimentin- or GLAST-immunolabeled fibers) spanning through the CC. The destination of the callosal fibers was examined by applying DiI to the right cingulum; the labeled fibers ran throughout the CC and reached the left cingulate and motor areas. The distribution and final fates of the retrovirus-labeled cells were examined in P28 brains. A small proportion of the labeled cells, less than 1%, were found in the contralateral hemisphere, where, as oligodendrocytes and astrocytes, they colonized predominantly the cortex and the underlying white matter of the cingulate and secondary motor areas. The distribution pattern appears to coincide well with the projection direction of the callosal fibers. Thus, glial progenitors migrate across the CC, presumably in conjunction with unmyelinated axons, to colonize the contralateral hemisphere.

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  • ニューロブラストの産生および移動の障害に基づく脳奇形の形成機序に関する研究

    Grant number:08780722

    1996

    System name:科学研究費助成事業

    Research category:奨励研究(A)

    Awarding organization:日本学術振興会

    柿田 明美

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    Grant amount:\1000000 ( Direct Cost: \1000000 )

    異所性neuroglial cell nest(NGN)は、多脳回症などの奇形脳でしばしば観察される脳表の形成異常である。採択者は、この奇形の形成機序を知る目的から、妊娠ラットにメチル水銀を投与し新生児または幼若ラットの脳を経時的に採取し病理組織学的に観察した。
    1.妊娠ラットを用い、胎児終脳が未分化なneuroepithelial cellのみからなる妊娠第11日(E11)、神経芽細胞産生期にあるE13またはE16に20mg/kgのメチル水銀を1回経口投与した。
    2.いずれも妊娠は順調に継続し、分娩予定日に全匹出産した。出生第2日(P2)、P7またはP14で児ラット脳を採取し光顕観察した。E11投与群では14%、E13では36%、E16では6%の児大脳側頭部(supplementary somatosensory area,visceral area,gustatory area)のくも膜下腔に、異所性NGNが形成された。NGNの大きさは個体により様々であったが、いずれのNGN内にも神経細胞およびグリア細胞が特別な配列を示すことなく認められた。
    3.NGNと大脳皮質とは単一あるいは複数の部位で連続し、そこでは柔膜が断裂していた。またNGNと連続する皮質では、分子層にも神経細胞が散見され皮質深層におよぶ層構造の乱れ(focal cortical dysplasia)が全例で認められた。
    4.NGNの電顕では、少数のシナプス結合およびcollagen fiberが観察された。
    5.母体に投与されたメチル水銀は、経胎盤的に胎児に移行し、その毒性は投与後数日間に亘り持続・漸減するものと考えられる。脳室近傍のneuroepithelium層で産生された神経芽細胞はラジアルファイバーに沿って移動し皮質層構造を形成すると考えられている。今回の観察から、大脳くも膜下腔の異所性NGNは、胎児終脳が神経芽細胞産生初期に障害を受けた場合に形成される奇形であり、皮質形成異常(cortical dysplasia)を伴うものであることが示された。

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Teaching Experience

  • 生体防御と感染(総合)

    2024
    Institution name:新潟大学

  • 病理総論

    2020
    Institution name:新潟大学

  • 臓器別講義・演習Ⅰ

    2020
    Institution name:新潟大学