Updated on 2025/09/03

写真a

 
HAMASAKI Hideomi
 
Organization
Brain Research Institute Specially Appointed Assistant Professor
Title
Specially Appointed Assistant Professor
External link

Degree

  • Doctor of Philosophy ( 2019.4   Kyushu University )

Research Areas

  • Life Science / Anatomy  / Alzheimer病、神経病理学

Research History

  • Niigata University   Brain Research Institute   Specially Appointed Assistant Professor

    2023.4

  • Kyushu University   Assistant Professor

    2019.4 - 2022.4

 

Papers

  • Alzheimer's Disease With Cardiac Transthyretin Amyloidosis: A Clinicopathological Study of Autopsy Cases

    Yasuo Sugita, Takuya Furuta, Kenji Takahashi, Koichi Higaki, Yoshiro Koda, Shin‐ichiro Mori, Shoko Hongo, Hideomi Hamasaki, Akiyoshi Kakita, Mitsuharu Ueda, Keisuke Kitagawa

    Neuropathology   2025.8

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

    <jats:title>ABSTRACT</jats:title><jats:p>The relationship between Alzheimer's disease and cardiac transthyretin amyloidosis (ATTR) has been reported epidemiologically. However, the details of its clinicopathological characteristics are unclear. To clarify the pathogenesis of Alzheimer's disease combined with cardiac ATTR, 50 autopsy cases of Alzheimer's disease with cardiac hypertrophy were examined. Transthyretin amyloid deposition was studied by immunostaining in cases where amyloid deposition was suspected in various organs by HE staining. ATTR in systemic organs was also examined. The pathological diagnosis of Alzheimer's disease was done based on the National Institute on Aging and Alzheimer's Association (NIA‐AA) guidelines. Cerebral amyloid angiopathy (CAA) was rated on a 3‐point scale according to the Vonsattel scale. The pathological diagnosis of cardiac ATTR was done using a 3‐point scale based on previously published findings on amyloid amounts. Six out of 50 patients were found to have cardiac ATTR by immunostaining and protein mass analysis of myocardial tissue. The sex distribution of the six patients was two males (Cases 3 and 6) and four females (Cases 1, 2, 4, and 5), and their ages were 97, 89, 91, 104, 86, and 77 years in Cases 1–6, respectively. In Cases 1–6, the NIAA score/CAA assessment/ATTR stages were intermediate/severe/G3, intermediate/moderate/G3, high/severe/G3, high/severe/G2, high/severe/G2, and intermediate/moderate/G2, respectively. Cases 1–5 also had cerebral infarction. In all cases, Transthyretin amyloid deposition was seen mainly in the vessel walls of various organs throughout the body. In the heart, transthyretin amyloid deposition was observed in the myocardial vessel walls and between myocardial fibers. On autopsy, cardiogenic cerebral infarction or heart failure was considered to be the main cause of death in Cases 1–5. These results indicate that Alzheimer's disease could be regarded as a systemic disease rather than just a localized disease presenting with dementia.</jats:p>

    DOI： 10.1111/neup.70011

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  • Mutations in the human CSF1R gene impact microglia’s maintenance of brain white matter integrity

    Siling Du, Yingyue Zhou, Dian Li, Julia Lier, Marina Cella, Mari Tada, Hideomi Hamasaki, Junjie Wu, Zhangying Cai, Jennifer L. Orthmann-Murphy, Akiyoshi Kakita, Jonathan Kipnis, Caroline G. Bergner, Marco Colonna

    Nature Immunology   2025.7

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

    DOI： 10.1038/s41590-025-02195-7

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  • Novel method for classification of prion diseases by detecting PrPres signal patterns from formalin-fixed paraffin-embedded samples. International journal

    Sachiko Koyama, Kaoru Yagita, Hideomi Hamasaki, Hideko Noguchi, Masahiro Shijo, Kosuke Matsuzono, Kei-Ichiro Takase, Keita Kai, Shin-Ichi Aishima, Kyoko Itoh, Toshiharu Ninomiya, Naokazu Sasagasako, Hiroyuki Honda

    Prion   18 ( 1 )   40 - 53   2024.12

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

    Prion disease is an infectious and fatal neurodegenerative disease. Western blotting (WB)-based identification of proteinase K (PK)-resistant prion protein (PrPres) is considered a definitive diagnosis of prion diseases. In this study, we aimed to detect PrPres using formalin-fixed paraffin-embedded (FFPE) specimens from cases of sporadic Creutzfeldt-Jakob disease (sCJD), Gerstmann-Sträussler-Scheinker disease (GSS), glycosylphosphatidylinositol-anchorless prion disease (GPIALP), and V180I CJD. FFPE samples were prepared after formic acid treatment to inactivate infectivity. After deparaffinization, PK digestion was performed, and the protein was extracted. In sCJD, a pronounced PrPres signal was observed, with antibodies specific for type 1 and type 2 PrPres exhibited a strong or weak signals depending on the case. Histological examination of serial sections revealed that the histological changes were compatible with the biochemical characteristics. In GSS and GPIALP, prion protein core-specific antibodies presented as PrPres bands at 8-9 kDa and smear bands, respectively. However, an antibody specific for the C-terminus presented as smears in GSS, with no PrPres detected in GPIALP. It was difficult to detect PrPres in V180I CJD. Collectively, our findings demonstrate the possibility of detecting PrPres in FFPE and classifying the prion disease types. This approach facilitates histopathological and biochemical evaluation in the same sample and is safe owing to the inactivation of infectivity. Therefore, it may be valuable for the diagnosis and research of prion diseases.

    DOI： 10.1080/19336896.2024.2337981

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  • Altered expression of human myxovirus resistance protein A in amyotrophic lateral sclerosis.

    Honda H, Sadashima S, Yoshimura M, Sakurada N, Koyama S, Yagita K, Hamasaki H, Noguchi H, Arahata H, Sasagasako N

    Journal of neuropathology and experimental neurology   2024.9

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    DOI： 10.1093/jnen/nlae052

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  • Increased expression of human antiviral protein MxA in FUS proteinopathy in amyotrophic lateral sclerosis.

    Honda H, Yagita K, Arahata H, Hamasaki H, Noguchi H, Koyama S, Sasagasako N

    Brain pathology (Zurich, Switzerland)   2023.8

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    DOI： 10.1111/bpa.13191

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  • Ribosomal protein SA is a common component of neuronal intranuclear inclusions in polyglutamine diseases and Marinesco bodies.

    Yagita K, Sadashima S, Koyama S, Noguchi H, Hamasaki H, Sasagasako N, Honda H

    Neuropathology : official journal of the Japanese Society of Neuropathology   2023.6

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    DOI： 10.1111/neup.12927

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  • Mutated FUS in familial amyotrophic lateral sclerosis involves multiple hnRNPs in the formation of neuronal cytoplasmic inclusions

    Hiroyuki Honda, Motoi Yoshimura, Hajime Arahata, Kaoru Yagita, Shoko Sadashima, Hideomi Hamasaki, Masahiro Shijo, Sachiko Koyama, Hideko Noguchi, Naokazu Sasagasako

    Journal of Neuropathology &amp; Experimental Neurology   82 ( 3 )   231 - 241   2023.1

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    Publishing type：Research paper (scientific journal)   Publisher：Oxford University Press (OUP)  

    DOI： 10.1093/jnen/nlac124

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    Other Link： https://journals.lww.com/10.1093/jnen/nlac124

  • Silence of resident microglia in GPI anchorless prion disease and activation of microglia in Gerstmann-Sträussler-Scheinker disease and sporadic Creutzfeldt-Jakob disease International journal

    Hideko Noguchi, Sachiko Koyama, Kaoru Yagita, Masahiro Shijo, Kosuke Matsuzono, Hideomi Hamasaki, Takaaki Kanemaru, Tsuyoshi Okamoto, Keita Kai, Shinichi Aishima, Koji Abe, Naokazu Sasagasako, Hiroyuki Honda

    Journal of Neuropathology &amp; Experimental Neurology   82 ( 1 )   38 - 48   2022.11

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Oxford University Press ({OUP})  

    <jats:title>Abstract</jats:title>
    <jats:p>GPI anchorless prion diseases (GPIALPs) show numerous coarse prion protein (PrP) deposits in the CNS but neuropil spongiform changes are mild and the incidence of dementia is low. Here, we examined differences in resident microglial phenotypes between GPIALP (D178fs25) and the other prion diseases Gerstmann-Sträussler-Scheinker (GSS) disease and sporadic Creutzfeldt-Jakob disease (sCJD) with respect to homeostasis and activation. Immunohistochemistry was performed on 2 GPIALP (D178fs25), 4 GSS (P102L), and 4 sCJD cases. Homeostatic microglia expressing TMEM119 and P2RY12 were preserved in GPIALP compared to GSS and sCJD. Microglia/macrophage activation in GSS and sCJD was associated with the extent of spongiform change. Immunoelectron microscopy revealed TMEM119 and P2RY12 in PrP plaque cores. Activated microglia/macrophages expressing HLA-DR and CD68 were predominant in GSS and sCJD whereas in GPIALP, homeostatic microglia were retained and activated microglia/macrophages were rarely observed. These data suggest that PrP deposition in GPIALP is less toxic and that microglia may be immune-tolerant to PrP deposition. This may be associated with milder tissue damage and a low incidence of dementia. Whereas microglia/macrophage activation is considered to be a reaction to tissue injury, this study shows that the degree of microglia/macrophage activity might influence the extent of tissue damage.</jats:p>

    DOI： 10.1093/jnen/nlac098

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  • Neuropathology of classic myotonic dystrophy type 1 is characterized by both early initiation of primary age-related tauopathy of the hippocampus and unique 3-repeat tauopathy of the brainstem.

    Hamasaki H, Maeda N, Sasagasako N, Honda H, Shijo M, Mori SI, Yagita K, Arahata H, Iwaki T

    Journal of neuropathology and experimental neurology   2022.11

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Oxford University Press ({OUP})  

    <jats:title>Abstract</jats:title>
    <jats:p>Myotonic dystrophy type 1 (DM1) is an inherited autosomal-dominant condition that induces altered splicing of transcripts, including MAPT, leading to a distinctive abnormal deposition of tau protein in the CNS. We characterized the tau isoforms of abnormal depositions in the brains of 4 patients with classic DM1 by immunohistochemistry using isoform-specific antibodies. All patients, including those of presenile age, showed numerous neurofibrillary tangles (NFTs) of both 3-repeat and 4-repeat tau in the limbic area and mild involvement in the cerebral cortex. Amyloid-β deposition was only seen in 1 senile case while cortical tauopathy in all other cases was consistent with primary age-related tauopathy (PART). In the putamen and globus pallidus, only a few tau deposits were observed. Tau deposits in the brainstem frequently showed a DM1-specific pattern with 3-repeat tau dominant NFTs. Additionally, tau-positive astrocytes morphologically similar to tufted astrocytes and astrocytic plaques were occasionally observed in the brainstem; however, they were predominantly composed of 3-repeat tau. Thus, the classic DM1 showed both early onset of PART-like pathology in the limbic areas as a progeroid syndrome of DM1 and an abnormal splicing event in the brainstem leading to 3-repeat tau dominant accumulation with both neuronal and astrocytic involvement.</jats:p>

    DOI： 10.1093/jnen/nlac097

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  • Chronological Changes in the Expression Pattern of Hippocampal Prion Proteins During Disease Progression in Sporadic Creutzfeldt-Jakob Disease MM1 Subtype. International journal

    Kaoru Yagita, Hideko Noguchi, Sachiko Koyama, Hideomi Hamasaki, Takashi Komori, Shinichi Aishima, Takayuki Kosaka, Mitsuharu Ueda, Yoshihiro Komohara, Akihiro Watanabe, Naokazu Sasagasako, Toshiharu Ninomiya, Yoshinao Oda, Hiroyuki Honda

    Journal of neuropathology and experimental neurology   81 ( 11 )   900 - 909   2022.10

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

    The differential effects of sporadic Creutzfeldt-Jakob disease (sCJD) on the hippocampus and other neocortical areas are poorly understood. We aimed to reveal the histological patterns of cellular prion protein (PrPC) and abnormal prion protein (PrPSc) in hippocampi of sCJD patients and normal controls (NCs). Our study examined 18 postmortem sCJD patients (MM1, 14 cases; MM1 + 2c, 3 cases; MM1 + 2t, 1 case) and 12 NCs. Immunohistochemistry was conducted using 4 primary antibodies, of which 3 targeted the N-terminus of the prion protein (PrP), and 1 (EP1802Y) targeted the C-terminal domain. PrPC expression was abundant in the hippocampus of NCs, and the distribution of PrPC at CA3/4 was reminiscent of synaptic complexes. In sCJD cases with a disease history of <2 years, antibodies against the N-terminus could not detect synapse-like PrP expression at CA4; however, EP1802Y could characterize the synapse-like expression. PrPSc accumulation and spongiform changes became evident after 2 years of illness, when PrPSc deposits were more noticeably detected by N-terminal-specific antibodies. Our findings highlighted the chronology of histopathological alterations in the CA4 region in sCJD patients.

    DOI： 10.1093/jnen/nlac078

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  • Characteristic distribution and molecular properties of normal cellular prion protein in human endocrine and exocrine tissues. International journal

    Sachiko Koyama, Hideko Noguchi, Kaoru Yagita, Hideomi Hamasaki, Masahiro Shijo, Motoi Yoshimura, Kohei Inoshita, Naokazu Sasagasako, Hiroyuki Honda

    Scientific reports   12 ( 1 )   15289 - 15289   2022.9

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

    Prion disease is an infectious and fatal neurodegenerative disease. Human prion disease autopsy studies have revealed abnormal prion protein (PrPSc) deposits in the central nervous system and systemic organs. In deer, chronic wasting disease has also become a global problem, with PrPSc in saliva and feces. Therefore, understanding normal cellular prion proteins (PrPc) characteristics in human systemic organs is important since they could be a PrPSc source. This study used western blotting and immunohistochemistry to investigate endocrine and exocrine tissues, such as the human pituitary, adrenal, submandibular glands and the pancreas. All tissues had 30-40 kDa PrP signals, which is a slightly higher molecular weight than normal brain tissue. Most cytoplasmic PrP-positive adenohypophyseal cells were immunopositive for nuclear pituitary-specific positive transcription factor 1. The adrenal medulla and islet cells of the pancreas were PrP-positive and colocalized with chromogranin A. The duct epithelium in the submandibular gland and pancreas were immunopositive for PrP. This study reports the characteristic molecular properties and detailed tissue localization of PrPc in endocrine and exocrine tissues, which is important for infection control and diagnosis.

    DOI： 10.1038/s41598-022-19632-4

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  • A Comparative Study of Site-Specific Distribution of Aging-Related Tau Astrogliopathy and Its Risk Factors Between Alzheimer Disease and Cognitive Healthy Brains: The Hisayama Study. International journal

    Kaoru Yagita, Hiroyuki Honda, Tomoyuki Ohara, Hideomi Hamasaki, Sachiko Koyama, Hideko Noguchi, Akane Mihara, Taro Nakazawa, Jun Hata, Toshiharu Ninomiya, Toru Iwaki

    Journal of neuropathology and experimental neurology   81 ( 2 )   106 - 116   2022.1

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    Knowledge of aging-related tau astrogliopathy (ARTAG) in healthy elderly individuals remains incomplete and studies to date have not focused on the olfactory nerve, which is a vulnerable site of various neurodegenerative disease pathologies. We performed a semiquantitative evaluation of ARTAG in 110 autopsies in the Japanese general population (Hisayama study). Our analysis focused on Alzheimer disease (AD) and cognitive healthy cases (HC), including primary age-related tauopathy. Among the various diseased and nondiseased brains, ARTAG was frequently observed in the amygdala. The ARTAG of HC was exclusively limited to the amygdala whereas gray matter ARTAG in AD cases was prominent in the putamen and middle frontal gyrus following the amygdala. ARTAG of the olfactory nerve mainly consists of subpial pathology that was milder in the amygdala. A logistic regression analysis revealed that age at death and neurofibrillary tangle Braak stage significantly affected the ARTAG of HC. In AD, age at death and male gender had significant effects on ARTAG. In addition, the Thal phase significantly affected the presence of white matter ARTAG. In conclusion, our research revealed differences in the distribution of ARTAG and affected variables across AD and HC individuals.

    DOI： 10.1093/jnen/nlab126

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  • PCBP2 Is Downregulated in Degenerating Neurons and Rarely Observed in TDP-43-Positive Inclusions in Sporadic Amyotrophic Lateral Sclerosis International journal

    Yoshimura, M., Honda, H., Sasagasako, N., Mori, S., Hamasaki, H., Suzuki, S.O., Ishii, T., Ninomiya, T., Kira, J.-I., Iwaki, T.

    Journal of neuropathology and experimental neurology   80 ( 3 )   220 - 228   2021

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    DOI： 10.1093/jnen/nlaa148

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  • Transactivation response DNA-binding protein of 43 kDa proteinopathy and lysosomal abnormalities in spastic paraplegia type 11 International journal

    Mori, S., Honda, H., Hamasaki, H., Sasagasako, N., Suzuki, S.O., Furuya, H., Taniwaki, T., Iwaki, T.

    Neuropathology   41 ( 4 )   253 - 265   2021

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    DOI： 10.1111/neup.12733

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  • CD206 Expression in Induced Microglia-Like Cells From Peripheral Blood as a Surrogate Biomarker for the Specific Immune Microenvironment of Neurosurgical Diseases Including Glioma

    Tanaka, S., Ohgidani, M., Hata, N., Inamine, S., Sagata, N., Shirouzu, N., Mukae, N., Suzuki, S.O., Hamasaki, H., Hatae, R., Sangatsuda, Y., Fujioka, Y., Takigawa, K., Funakoshi, Y., Iwaki, T., Hosoi, M., Iihara, K., Mizoguchi, M., Kato, T.A.

    Frontiers in Immunology   12   2021

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    Publishing type：Research paper (scientific journal)   Publisher：Frontiers Media SA  

    DOI： 10.3389/fimmu.2021.670131

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  • Symmetrical glial hyperplasia in the brainstem of fibrodysplasia ossificans progressiva International journal

    Mori, S., Suzuki, S.O., Honda, H., Hamasaki, H., Sakae, N., Sasagasako, N., Furuya, H., Iwaki, T.

    Neuropathology   41 ( 2 )   146 - 151   2021

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

    DOI： 10.1111/neup.12715

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  • Concurrent cardiac transthyretin and brain β amyloid accumulation among the older adults: The Hisayama study International journal

    Hamasaki, H., Shijo, M., Nakamura, A., Honda, H., Yamada, Y., Oda, M., Ohara, T., Ninomiya, T., Iwaki, T.

    Brain Pathology   32 ( 1 )   e13014   2021

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

    DOI： 10.1111/bpa.13014

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  • Tauopathy in basal ganglia involvement is exacerbated in a subset of patients with Alzheimer's disease: The Hisayama study International journal

    Hamasaki, H., Honda, H., Suzuki, S.O., Shijo, M., Ohara, T., Hatabe, Y., Okamoto, T., Ninomiya, T., Iwaki, T.

    Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring   11   415 - 423   2019.12

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    DOI： 10.1016/j.dadm.2019.04.008

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  • Upregulation of annexin A1 in reactive astrocytes and its subtle induction in microglia at the boundaries of human brain infarcts International journal

    Shijo, M., Hamasaki, H., Honda, H., Suzuki, S.O., Tachibana, M., Ago, T., Kitazono, T., Iihara, K., Iwaki, T.

    Journal of Neuropathology and Experimental Neurology   78 ( 10 )   961 - 970   2019.10

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    DOI： 10.1093/jnen/nlz079

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  • Frequent detection of pituitary-derived PRP<sup>REs</sup> in human prion diseases International journal

    Honda, H., Matsumoto, M., Shijo, M., Hamasaki, H., Sadashima, S., Suzuki, S.O., Aishima, S., Kai, K., Nakayama, K.I., Sasagasako, N., Iwaki, T.

    Journal of Neuropathology and Experimental Neurology   78 ( 10 )   922 - 929   2019.10

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

    DOI： 10.1093/jnen/nlz075

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  • Dynactin is involved in Lewy body pathology International journal

    Shen, C., Honda, H., Suzuki, S.O., Maeda, N., Shijo, M., Hamasaki, H., Sasagasako, N., Fujii, N., Iwaki, T.

    Neuropathology   38 ( 6 )   583 - 590   2018.12

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

    DOI： 10.1111/neup.12512

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  • Four-repeat tau dominant pathology in a congenital myotonic dystrophy type 1 patient with mental retardation International journal

    Mizuno, Y., Maeda, N., Hamasaki, H., Arahata, H., Sasagasako, N., Honda, H., Fujii, N., Iwaki, T.

    Brain Pathology   28 ( 3 )   431 - 433   2018.5

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

    DOI： 10.1111/bpa.12603

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  • Expression of CRYM in different rat organs during development and its decreased expression in degenerating pyramidal tracts in amyotrophic lateral sclerosis International journal

    Hommyo, R., Suzuki, S.O., Abolhassani, N., Hamasaki, H., Shijo, M., Maeda, N., Honda, H., Nakabeppu, Y., Iwaki, T.

    Neuropathology   38 ( 3 )   247 - 259   2018.3

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

    DOI： 10.1111/neup.12466

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  • DCTN1 F52L mutation case of Perry syndrome with progressive supranuclear palsy-like tauopathy International journal

    Honda, H., Sasagasako, N., Shen, C., Shijo, M., Hamasaki, H., Suzuki, S.O., Tsuboi, Y., Fujii, N., Iwaki, T.

    Parkinsonism and Related Disorders   51   105 - 110   2018.2

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

    DOI： 10.1016/j.parkreldis.2018.02.038

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  • Association of adipocyte enhancer-binding protein 1 with Alzheimer's disease pathology in human hippocampi. Reviewed International journal

    Masahiro Shijo, Hiroyuki Honda, Satoshi O Suzuki, Hideomi Hamasaki, Masaaki Hokama, Nona Abolhassani, Yusaku Nakabeppu, Toshiharu Ninomiya, Takanari Kitazono, Toru Iwaki

    Brain pathology (Zurich, Switzerland)   28 ( 1 )   58 - 71   2018.1

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

    DOI： 10.1111/bpa.12475

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  • Molecular pathophysiology of impaired glucose metabolism, mitochondrial dysfunction, and oxidative DNA damage in Alzheimer's disease brain. Reviewed International journal

    Nona Abolhassani, Julio Leon, Zijing Sheng, Sugako Oka, Hideomi Hamasaki, Toru Iwaki, Yusaku Nakabeppu

    Mechanisms of ageing and development   161 ( Pt A )   95 - 104   2017.1

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  • Recent Increases in Hippocampal Tau Pathology in the Aging Japanese Population: The Hisayama Study Reviewed

    Hamasaki, H., Honda, H., Okamoto, T., Koyama, S., Suzuki, S.O., Ohara, T., Ninomiya, T., Kiyohara, Y., Iwaki, T.

    Journal of Alzheimer's Disease   55 ( 2 )   613 - 624   2017

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

    DOI： 10.3233/JAD-160521

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  • Trends in autopsy-verified dementia prevalence over 29 years of the Hisayama study Reviewed

    Hiroyuki Honda, Kensuke Sasaki, Hideomi Hamasaki, Masahiro Shijo, Sachiko Koyama, Tomoyuki Ohara, Toshiharu Ninomiya, Yutaka Kiyohara, Satoshi O. Suzuki, Toru Iwaki

    NEUROPATHOLOGY   36 ( 4 )   383 - 387   2016.8

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

    DOI： 10.1111/neup.12298

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  • Trends in autopsy-verified dementia prevalence over 29 years of the Hisayama study Reviewed

    Honda, H., Sasaki, K., Hamasaki, H., Shijo, M., Koyama, S., Ohara, T., Ninomiya, T., Kiyohara, Y., Suzuki, S.O., Iwaki, T.

    Neuropathology   36 ( 4 )   383 - 387   2016.8

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

    DOI： 10.1111/neup.12298

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  • Loss of hnRNPA1 in ALS spinal cord motor neurons with TDP-43-positive inclusions Reviewed

    Hiroyuki Honda, Hideomi Hamasaki, Tomihiro Wakamiya, Sachiko Koyama, Satoshi O. Suzuki, Naoki Fujii, Toru Iwaki

    NEUROPATHOLOGY   35 ( 1 )   37 - 43   2015.2

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

    DOI： 10.1111/neup.12153

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  • Elevated expression of fatty acid synthase and nuclear localization of carnitine palmitoyltransferase 1C are common among human gliomas Reviewed

    Tomihiro Wakamiya, Satoshi O. Suzuki, Hideomi Hamasaki, Hiroyuki Honda, Masahiro Mizoguchi, Koji Yoshimoto, Toru Iwaki

    NEUROPATHOLOGY   34 ( 5 )   465 - 474   2014.10

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

    DOI： 10.1111/neup.12132

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  • Down-regulation of MET in hippocampal neurons of Alzheimer's disease brains. Reviewed International journal

    Hideomi Hamasaki, Hiroyuki Honda, Satoshi O Suzuki, Masaaki Hokama, Yutaka Kiyohara, Yusaku Nakabeppu, Toru Iwaki

    Neuropathology : official journal of the Japanese Society of Neuropathology   34 ( 3 )   284 - 90   2014.6

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Research Projects

  • Wide-area, high-resolution digital image analysis for neurodegenerative diseases

    Grant number：22K15214

    2022.4 - 2025.3

    System name：Grants-in-Aid for Scientific Research

    Research category：Grant-in-Aid for Early-Career Scientists

    Awarding organization：Japan Society for the Promotion of Science

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    Grant amount：\3770000 （ Direct Cost: \2900000 、 Indirect Cost：\870000 ）

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