Updated on 2022/12/05

写真a

 
SHIMIZU Hiroshi
 
Organization
Brain Research Institute Associate Professor
Title
Associate Professor
External link

Degree

  • 博士(医学) ( 2010.3   新潟大学 )

Research Interests

  • 認知症

  • 脳腫瘍病理

  • 筋疾患

  • 神経変性疾患

  • 神経病理学

Research Areas

  • Life Science / Anatomy and histopathology of nervous system

  • Life Science / Neurology

  • Life Science / Tumor diagnostics and therapeutics

  • Life Science / Pathophysiologic neuroscience

Research History (researchmap)

  • Brain Research Institute, Niigata University   Department of Pathology   Associate Professor

    2019.4

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  • Brain Research Institute, Niigata University   Department of Pathology   Assistant Professor

    2011.4 - 2019.3

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    Country:Japan

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Research History

  • Niigata University   Brain Research Institute   Associate Professor

    2019.4

  • Niigata University   Brain Research Institute Pathological Neuroscience Branch   Assistant Professor

    2011.4 - 2019.3

Education

  • Niigata University   医歯学総合研究科   生体機能調節医学専攻

    2006.4 - 2010.3

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    Country: Japan

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  • Hokkaido University   School of Medicine

    1994 - 2000

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Professional Memberships

  • The Japanese Society of Neuropathology

    2005.4

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  • Japanese Society of Neurology

    2002.6

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  • The Japanese Society of Internal Medicine

    2000.12

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Papers

  • A Case of Giant Cell Arteritis that Presented with Buccal Skin Ulceration along the Facial Artery

    Eriko Hasegawa, Yoichi Kurosawa, Ayako Wakamatsu, Hiroe Sato, Daisuke Kobayashi, Takeshi Nakatsue, Takeshi Kuroda, Hiroshi Shimizu, Ichiei Narita

    Internal Medicine   2023

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    Publishing type:Research paper (scientific journal)   Publisher:Japanese Society of Internal Medicine  

    DOI: 10.2169/internalmedicine.0395-22

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

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

    DOI: 10.1002/mds.29186

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    Other Link: https://onlinelibrary.wiley.com/doi/full-xml/10.1002/mds.29186

  • 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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    Publishing type:Research paper (scientific journal)   Publisher:MDPI AG  

    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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  • Patients with biallelic GGC repeat expansions in NOTCH2NLC exhibiting a typical neuronal intranuclear inclusion disease phenotype

    Shinichi Kameyama, Takeshi Mizuguchi, Hiroshi Doi, Shigeru Koyano, Masaki Okubo, Mikiko Tada, Hiroshi Shimizu, Hiromi Fukuda, Naomi Tsuchida, Yuri Uchiyama, Eriko Koshimizu, Kohei Hamanaka, Atsushi Fujita, Kazuharu Misawa, Satoko Miyatake, Kazuaki Kanai, Fumiaki Tanaka, Naomichi Matsumoto

    Genomics   114 ( 5 )   110469 - 110469   2022.9

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    Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.ygeno.2022.110469

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  • A Machine Learning-Based Approach to Discrimination of Tauopathies Using [18 F]PM-PBB3 PET Images.

    Hironobu Endo, Kenji Tagai, Maiko Ono, Yoko Ikoma, Asaka Oyama, Kiwamu Matsuoka, Naomi Kokubo, Kosei Hirata, Yasunori Sano, Masaki Oya, Hideki Matsumoto, Shin Kurose, Chie Seki, Hiroshi Shimizu, Akiyoshi Kakita, Keisuke Takahata, Hitoshi Shinotoh, Hitoshi Shimada, Takahiko Tokuda, Kazunori Kawamura, Ming‐Rong Zhang, Kenichi Oishi, Susumu Mori, Yuhei Takado, Makoto Higuchi

    Movement Disorders   2022.8

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

    DOI: 10.1002/mds.29173

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    Other Link: https://onlinelibrary.wiley.com/doi/full-xml/10.1002/mds.29173

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

    Kiyomitsu Oyanagi, Hiroshi Shimizu, Mitsunori Yamada, Akiyoshi Kakita

    Neuropathology   2022.5

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

    DOI: 10.1111/neup.12811

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    Other Link: https://onlinelibrary.wiley.com/doi/full-xml/10.1111/neup.12811

  • Cell type-specific abnormalities of central nervous system in myotonic dystrophy type 1

    Masayuki Nakamori, Hiroshi Shimizu, Kotaro Ogawa, Yuhei Hasuike, Takashi Nakajima, Hidetoshi Sakurai, Toshiyuki Araki, Yukinori Okada, Akiyoshi Kakita, Hideki Mochizuki

    Brain Communications   4 ( 3 )   fcac154   2022.5

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

    Abstract

    Myotonic dystrophy type 1 is a multisystem genetic disorder involving the muscle, heart and CNS. It is caused by toxic RNA transcription from expanded CTG repeats in the 3′-untranslated region of DMPK, leading to dysregulated splicing of various genes and multisystemic symptoms. Although aberrant splicing of several genes has been identified as the cause of some muscular symptoms, the pathogenesis of CNS symptoms prevalent in patients with myotonic dystrophy type 1 remains unelucidated, possibly due to a limitation in studying a diverse mixture of different cell types, including neuronal cells and glial cells. Previous studies revealed neuronal loss in the cortex, myelin loss in the white matter and the presence of axonal neuropathy in patients with myotonic dystrophy type 1. To elucidate the CNS pathogenesis, we investigated cell type-specific abnormalities in cortical neurons, white matter glial cells and spinal motor neurons via laser-capture microdissection. We observed that the CTG repeat instability and cytosine–phosphate–guanine (CpG) methylation status varied among the CNS cell lineages; cortical neurons had more unstable and longer repeats with higher CpG methylation than white matter glial cells, and spinal motor neurons had more stable repeats with lower methylation status. We also identified splicing abnormalities in each CNS cell lineage, such as DLGAP1 in white matter glial cells and CAMKK2 in spinal motor neurons. Furthermore, we demonstrated that aberrant splicing of CAMKK2 is associated with abnormal neurite morphology in myotonic dystrophy type 1 motor neurons. Our laser-capture microdissection-based study revealed cell type-dependent genetic, epigenetic and splicing abnormalities in myotonic dystrophy type 1 CNS, indicating the significant potential of cell type-specific analysis in elucidating the CNS pathogenesis.

    DOI: 10.1093/braincomms/fcac154

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    Other Link: https://academic.oup.com/braincomms/article-pdf/4/3/fcac154/44180640/fcac154.pdf

  • Fibrodysplasia ossificans progressiva: histopathological implications of aberrant bone morphogenic protein signalling for CNS dysgenesis International journal

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

    Neuropathology and Applied Neurobiology   48 ( 4 )   e12805   2022.3

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

    DOI: 10.1111/nan.12805

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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.

    DOI: 10.1016/j.jneuroim.2021.577748

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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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    Authorship:Corresponding author   Language:English  

    DOI: 10.1136/jnnp-2021-326257

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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

    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   2020.12

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

    DOI: 10.1186/s40478-020-00945-2

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    Other Link: https://link.springer.com/article/10.1186/s40478-020-00945-2/fulltext.html

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

    Progressive supranuclear palsy (PSP) presents with a wide variety of signs/symptoms, making early initial diagnosis difficult. We investigated the clinical and neuropathological features of five patients with autopsy-proven PSP of short duration, ranging from 11 to 41 months (average, 26.2 months) due to unexpected death, focusing particularly on the distribution and severity of neuronal loss as well as neuronal and glial tau pathology in the affected brain. Clinical features were studied retrospectively through careful review of the medical records, and neuropathological examinations were carried out, along with tau immunohistochemistry using a monoclonal antibody AT8. These patients were diagnosed as having probable PSP (n = 4) and suggestive PSP (n = 1), respectively. In all cases, neuronal loss was evident in the substantia nigra, subthalamic nucleus, globus pallidus, and locus ceruleus. AT8-identified tau lesions, that is, pretangles/neurofibrillary tangles (PTs/NFTs), tufted astrocytes (TAs), and coiled bodies/neuropil threads (CBs/NTs), were distributed widely in the brain regions, especially in patients with longer disease duration. All cases showed variation in the regional tau burden among PTs/NFTs, TAs, and CBs/NTs. There was also a tendency for tau deposition to be more predominant in neuronal cells in the brainstem and cerebellum and in glial cells in the cerebral cortex and subcortical gray matter. These findings suggest that in PSP, the initial signs/symptoms are associated with degeneration and subsequent death of neurons with pathological tau deposition, and that the tau deposition in neuronal cells is independent of that in glial cells.

    DOI: 10.1111/neup.12707

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  • Amyotrophic Lateral Sclerosis with Pallidonigroluysian Degeneration: A Clinicopathological Study

    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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    Authorship:Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:Wiley  

    DOI: 10.1002/ana.25652

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    Other Link: https://onlinelibrary.wiley.com/doi/full-xml/10.1002/ana.25652

  • 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.

    DOI: 10.3389/fped.2020.00579

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  • Shrinkage of the myenteric neurons of the small intestine in patients with multiple system atrophy

    Tetsutaro Ozawa, Hiroshi Shimizu, Hideaki Matsui, Osamu Onodera, Akiyoshi Kakita

    Autonomic Neuroscience   221   102583 - 102583   2019.11

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    Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.autneu.2019.102583

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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

    Yumi Yamada, Takao Fukushima, Satoshi Kodama, Hiroshi Shimizu, Akiyoshi Kakita, Kunihiko Makino, Yoshiki Sekijima

    Amyloid   26 ( 4 )   251 - 252   2019.10

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    Publishing type:Research paper (scientific journal)   Publisher:Informa UK Limited  

    DOI: 10.1080/13506129.2019.1632829

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  • An autopsy case of peliosis hepatis with X-linked myotubular myopathy

    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   38   77 - 82   2019.5

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    Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.legalmed.2019.04.005

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  • Two distinct prions in fatal familial insomnia and its sporadic form

    Atsuko Takeuchi, Shirou Mohri, Hideaki Kai, Akira Tamaoka, Atsushi Kobayashi, Hidehiro Mizusawa, Yasushi Iwasaki, Mari Yoshida, Hiroshi Shimizu, Shigeo Murayama, Shigetoshi Kuroda, Masanori Morita, Piero Parchi, Tetsuyuki Kitamoto

    Brain Communications   1 ( 1 )   fcz045   2019.1

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

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    Fatal familial insomnia is a genetic prion disease, which is associated with the aspartic acid to asparagine substitution at codon 178 of the prion protein gene. Although the hallmark pathological feature is thalamic and olivary degeneration, there is a patient with an atypical fatal familial insomnia without the hallmark feature. The cause of the pathological variability is unclear. We analysed a Japanese fatal familial insomnia kindred and compared one atypical clinicopathological fatal familial insomnia phenotype case and typical fatal familial insomnia phenotype cases with transmission studies using multiple lines of knock-in mice and with protein misfolding cyclic amplification. We also analysed the transmissibility and the amplification properties of sporadic fatal insomnia. Transmission studies revealed that the typical fatal familial insomnia with thalamic and olivary degeneration showed successful transmission only using knock-in mice expressing human–mouse chimeric prion protein gene. The atypical fatal familial insomnia with spongiform changes showed successful transmission only using knock-in mice expressing bank vole prion protein gene. Two sporadic fatal insomnia cases with thalamic and olivary degeneration showed the same transmissibility as the typical fatal familial insomnia phenotype. Interestingly, one sporadic fatal insomnia case with thalamic/olivary degeneration and spongiform changes showed transmissibility of both the typical and atypical fatal familial insomnia phenotypes. Protein misfolding cyclic amplification could amplify both typical fatal familial insomnia cases and sporadic fatal insomnia cases but not the atypical fatal familial insomnia phenotype or other sporadic Creutzfeldt–Jakob disease subtypes. In addition to clinical findings and neuropathological features, the transmission properties and the amplification properties were different between the typical and atypical fatal familial insomnia phenotypes. It is suggested that two distinct prions were associated with the diversity in the fatal familial insomnia phenotype, and these two prions could also be detected in sporadic fatal insomnia.

    DOI: 10.1093/braincomms/fcz045

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    Other Link: http://academic.oup.com/braincomms/article-pdf/1/1/fcz045/33639239/fcz045.pdf

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

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

    Journal of Neuropathology & Experimental Neurology   77 ( 11 )   981 - 986   2018.11

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    DOI: 10.1093/jnen/nly082

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  • Ca<sup>2+</sup>-permeable AMPA receptors associated with epileptogenesis of hypothalamic hamartoma

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

    DOI: 10.1111/epi.13700

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

    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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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:WILEY  

    We previously reported familial amyotrophic lateral sclerosis (FALS) of 11years duration in a 57-year-old woman, who received artificial ventilation for 5years prior to death and exhibited widespread multisystem degeneration and neurofilamentous aggregates, so-called conglomerate inclusions (CIs). In the present study, we re-evaluated this autopsied patient (proband) with further immunohistochemical observation as well as mutational analysis of the superoxide dismutase 1 (SOD1) gene. A review of the clinical features of the proband's family revealed five affected members (including the proband) over two successive generations who showed marked variability in clinical presentation, such as the age at onset. The proband was found to harbor a heterozygous missense mutation in exon 4 (I104F) of the SOD1 gene. In the brain and spinal cord, SOD1-positive neuronal cytoplasmic inclusions (NCIs) were found to be more widely distributed than CIs, the latter being weakly positive for SOD1. No Lewy body-like hyaline inclusions were found. This is considered to be the first description of an autopsy case of FALS with an I104F SOD1 gene mutation, suggesting that combination of marked intra-familial clinical variability and multisystem degeneration with occurrence of CIs and SOD1-positive NCIs is a characteristic feature of FALS with this SOD1 gene mutation.

    DOI: 10.1111/neup.12324

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  • Heterogeneity of cerebral TDP-43 pathology in sporadic amyotrophic lateral sclerosis: Evidence for clinico-pathologic subtypes

    Ryoko Takeuchi, Mari Tada, Atsushi Shiga, Yasuko Toyoshima, Takuya Konno, Tomoe Sato, Hiroaki Nozaki, Taisuke Kato, Masao Horie, Hiroshi Shimizu, Hirohide Takebayashi, Osamu Onodera, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    Acta Neuropathologica Communications   4 ( 1 )   61   2016.12

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

    DOI: 10.1186/s40478-016-0335-2

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  • Biallelic TBCD Mutations Cause Early-Onset Neurodegenerative Encephalopathy

    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

    The American Journal of Human Genetics   99 ( 4 )   950 - 961   2016.10

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    Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.ajhg.2016.08.005

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  • Significant association of cadaveric dura mater grafting with subpial Aβ deposition and meningeal amyloid angiopathy

    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

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

    DOI: 10.1007/s00401-016-1588-3

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    Other Link: http://link.springer.com/article/10.1007/s00401-016-1588-3/fulltext.html

  • Globular Glial Mixed Four Repeat Tau and TDP-43 Proteinopathy with Motor Neuron Disease and Frontotemporal Dementia

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

    DOI: 10.1111/bpa.12262

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  • Sporadic ALS with compound heterozygous mutations in the SQSTM1 gene

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

    DOI: 10.1007/s00401-013-1150-5

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    Other Link: http://link.springer.com/article/10.1007/s00401-013-1150-5/fulltext.html

  • Epstein‐Barr virus‐associated primary central nervous system cytotoxic T‐cell lymphoma

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

    DOI: 10.1111/neup.12005

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    Other Link: https://onlinelibrary.wiley.com/doi/full-xml/10.1111/neup.12005

  • Early adult-onset orbital apex Langerhans cell histiocytosis histologically confirmed during “truly spontaneous” regression

    Keisuke Satoh, Masayoshi Tada, Hiroshi Shimizu, Yuichiro Yoneoka

    Acta Neurochirurgica   154 ( 2 )   301 - 302   2012.2

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

    DOI: 10.1007/s00701-011-1250-8

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    Other Link: http://link.springer.com/article/10.1007/s00701-011-1250-8/fulltext.html

  • Involvement of Onuf’s nucleus in Machado–Joseph disease: a morphometric and immunohistochemical study

    Hiroshi Shimizu, Mitsunori Yamada, Yasuko Toyoshima, Takeshi Ikeuchi, Osamu Onodera, Hitoshi Takahashi

    Acta Neuropathologica   120 ( 4 )   439 - 448   2010.10

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

    DOI: 10.1007/s00401-010-0699-5

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    Other Link: http://link.springer.com/article/10.1007/s00401-010-0699-5/fulltext.html

  • Creutzfeldt-Jakob disease with an M232R substitution: report of a patient showing slowly progressive disease with abundant plaque-like PrP deposits in the cerebellum

    Hiroshi Shimizu, Mitsunori Yamada, Nae Matsubara, Hiroki Takano, Yoshitaka Umeda, Yasuhiro Kawase, Tetsuyuki Kitamoto, Masatoyo Nishizawa, Hitoshi Takahashi

    Neuropathology   29 ( 6 )   735 - 743   2009.12

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Wiley  

    DOI: 10.1111/j.1440-1789.2009.01019.x

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  • Spinal cord tau pathology in cervical spondylotic myelopathy

    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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    Other Link: http://link.springer.com/article/10.1007/s00401-007-0321-7/fulltext.html

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Books

  • Neurodegeneration with brain iron accumulationの一剖検例

    村松一洋, 清水宏( Role: Joint author ,  小児神経学の進歩 第48集 p74-86)

    日本小児神経学会教育委員会(編集)  2019.5 

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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: Joint author ,  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:300-307   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: Joint author ,  プリオン病とは何ですか?)

    中外医学社  2017.1  ( ISBN:9784498129863

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    Total pages:435   Responsible for pages:374-378   Language:Japanese Book type:Textbook, survey, introduction

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MISC

  • 剖検・ブレインカッティング Invited

    清水 宏

    第17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   1 - 10   2022.6

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  • リピート病 Reviewed

    清水 宏

    第16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   21 - 30   2021.6

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  • トリプレットリピート病(1)脊髄小脳失調症.連載‐変性疾患のみかた- Invited

    38 ( 1 )   67 - 71   2020.1

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    Authorship:Lead author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (other)  

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  • ポリグルタミン病 Invited

    清水 宏

    第13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   66 - 73   2017.6

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    Authorship:Lead author   Language:Japanese   Publishing type:Lecture material (seminar, tutorial, course, lecture, etc.)  

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  • 頭蓋咽頭腫 Craniopharyngioma Invited

    33   332 - 332   2015.4

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    Authorship:Lead author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (other)  

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  • 胚芽異形成性神経上皮腫瘍 Dysembryoplastic neuroepithelial tumor. Invited

    33   334 - 334   2015.4

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Presentations

  • パーキンソン症候群の病態:臨床と病理の相関から考える Invited

    清水 宏

    第24回兵庫臨床神経病理カンファレンス  2022.7 

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    Presentation type:Oral presentation (invited, special)  

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  • 剖検・ブレインカッティング Invited

    清水 宏

    第17回神経病理コアカリキュラム教育セミナー  2022.6 

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  • 運動ニューロン疾患―臨床への還元のための病理確定診断の重要性 Invited

    清水 宏

    2021.5 

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    Presentation type:Symposium, workshop panel (public)  

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  • リピート病 Invited

    清水 宏

    第16回神経病理コアカリキュラム教育セミナー (第62回日本神経病理学会総会学術研究会).  2021.5 

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  • ポリグルタミン病 Invited

    清水 宏

    第13回神経病理コアカリキュラム教育セミナー (第58回日本神経病理学会総会学術研究会).  2017.6 

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Research Projects

  • パーキンソン病の多中心性病巣形成と伝播:剖検組織の透明化と三次元観察による検証

    Grant number:19K07841  2019.4 - 2022.3

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    清水 宏, 柿田 明美, 吉田 眞理, 宮原 弘明

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    Authorship:Principal investigator 

    Grant amount:\4290000 ( Direct Cost: \3300000 、 Indirect Cost:\990000 )

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  • 多系統萎縮症:乏突起膠細胞の鉄代謝異常と酸化ストレス亢進の病的意義の解明

    2015.4 - 2018.3

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    清水 宏

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    Authorship:Principal investigator  Grant type:Competitive

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  • ブニナ小体を欠く筋萎縮性側索硬化症についての臨床病理学的研究

    2013.4 - 2015.3

    日本学術振興会  科学研究費助成事業  若手研究(B)

    清水宏

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    Authorship:Principal investigator  Grant type:Competitive

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