Updated on 2026/03/07

写真a

 
ANDO Shoichiro
 
Organization
University Medical and Dental Hospital Neurology Assistant Professor
Title
Assistant Professor
External link

Degree

  • 学士（医学） ( 2013.3   新潟大学 )

Research Interests

  • Cerebral small vessel disease

Research Areas

  • Life Science / Neurology  / Cerebral small vessel disease

Research History (researchmap)

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

    2022.4

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    Country：Japan

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Research History

  • Niigata University   University Medical and Dental Hospital   Assistant Professor

    2022.4

  • Niigata University   Brain Research Institute   Specially Appointed Assistant Professor

    2021.4 - 2021.9

Education

  • Niigata University   Graduate School of Medical and Dental Sciences

    2018.4 - 2022.3

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    Country： Japan

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  • Niigata University   Faculty of Medicine   School of Medicine

    2007.4 - 2013.3

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    Country： Japan

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Professional Memberships

 

Papers

  • “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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  • The analysis of schizophrenia-like psychosis in dentatorubral-pallidoluysian atrophy. International journal

    Ichiko Ikegami, Yuka Mitsuhashi Koike, Hideki Hayashi, Sachiko Hirokawa, Shoichiro Ando, Tomohiko Ishihara, Osamu Onodera

    Frontiers in neurology   16   1564856 - 1564856   2025

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

    BACKGROUND: Dentatorubral-pallidoluysian atrophy (DRPLA) is a progressive neurodegenerative disorder caused by expanded CAG repeats in the ATN1 gene, characterized by cerebellar ataxia, seizures, tremors, and myoclonus. Although approximately 10% of patients with DRPLA reportedly develop schizophrenia-like psychosis (SLP), the distinct association between the clinical course of DRPLA and SLP remains unclear. This study aimed to elucidate the clinical features of SLP in patients with DRPLA. METHODS: We reviewed 22 cases of pathologically or genetically confirmed DRPLA with SLP, including 21 from the literature and one from our institution. Patient data, including clinical features, treatment information, and disease course, were extracted and analyzed. RESULTS: The age of onset was categorized as juvenile (n = 6), early adult (n = 8), and late adult (n = 8). Initially, 10 patients presented with motor symptoms, with six exhibiting psychiatric symptoms and six with both motor and psychiatric symptoms simultaneously. Furthermore, three patients were initially diagnosed with schizophrenia, while four experienced progressive worsening of psychiatric symptoms. The number of CAG repeats ranged from 57 to 76 (mean, 66.0) in the 10 patients with a genetic diagnosis. Summarily, 12 patients received psychotropic medications, with nine showing improvement in delusions and hallucinations. CONCLUSION: SLP can manifest across all DRPLA forms (juvenile-, early adult-, and late adult-onset) and may precede or follow motor symptoms. The clinical course and efficacy of psychotropic medications in patients with DRPLA and SLP suggest a shared pathogenesis between DRPLA and schizophrenia.

    DOI： 10.3389/fneur.2025.1564856

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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

  • Distal CIDPと鑑別を要したが、M蛋白やVEGFの再検が診断に有用であったPOEMS症候群の一例

    鈴木 大介, 鈴木 佑弥, 菊池 謙次, 鈴木 義広, 小出 伸, 安藤 昭一朗, 石黒 敬信, 金澤 雅人, 小野寺 理, 諏訪部 達也, 瀧澤 淳

    臨床神経学   64 ( 5 )   365 - 365   2024.5

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    Language：Japanese   Publisher：(一社)日本神経学会  

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  • Missense Variants in COL4A1/2 Are Associated with Cerebral Aneurysms: A Case Report and <span aria-describedby="tippy-31">Literature Review

    Masahiro Uemura, Natsuki Tanaka, Shoichiro Ando, Takehiko Yanagihara, Osamu Onodera

    Neurology International   2023.12

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.20944/preprints202312.1336.v1

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  • Inappropriate interpretation of non-pathogenic HTRA1 variant as pathogenic. International journal

    Masahiro Uemura, Sho Kitahara, Taisuke Kato, Hiroaki Nozaki, Shoichiro Ando, Tomohiko Ishihara, Osamu Onodera

    Annals of clinical and translational neurology   10 ( 7 )   1261 - 1262   2023.7

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  • Heterogenous Genetic, Clinical, and Imaging Features in Patients with Neuronal Intranuclear Inclusion Disease Carrying NOTCH2NLC Repeat Expansion

    Yusran Ady Fitrah, Yo Higuchi, Norikazu Hara, Takayoshi Tokutake, Masato Kanazawa, Kazuhiro Sanpei, Tomone Taneda, Akihiko Nakajima, Shin Koide, Shintaro Tsuboguchi, Midori Watanabe, Junki Fukumoto, Shoichiro Ando, Tomoe Sato, Yohei Iwafuchi, Aki Sato, Hideki Hayashi, Takanobu Ishiguro, Hayato Takeda, Toshiaki Takahashi, Nobuyoshi Fukuhara, Kensaku Kasuga, Akinori Miyashita, Osamu Onodera, Takeshi Ikeuchi

    Brain Sciences   13 ( 6 )   955 - 955   2023.6

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

    Neuronal intranuclear inclusion disease (NIID) is a neurodegenerative disorder that is caused by the abnormal expansion of non-coding trinucleotide GGC repeats in NOTCH2NLC. NIID is clinically characterized by a broad spectrum of clinical presentations. To date, the relationship between expanded repeat lengths and clinical phenotype in patients with NIID remains unclear. Thus, we aimed to clarify the genetic and clinical spectrum and their association in patients with NIID. For this purpose, we genetically analyzed Japanese patients with adult-onset NIID with characteristic clinical and neuroimaging findings. Trinucleotide repeat expansions of NOTCH2NLC were examined by repeat-primed and amplicon-length PCR. In addition, long-read sequencing was performed to determine repeat size and sequence. The expanded GGC repeats ranging from 94 to 361 in NOTCH2NLC were found in all 15 patients. Two patients carried biallelic repeat expansions. There were marked heterogenous clinical and imaging features in NIID patients. Patients presenting with cerebellar ataxia or urinary dysfunction had a significantly larger GGC repeat size than those without. This significant association disappeared when these parameters were compared with the total trinucleotide repeat number. ARWMC score was significantly higher in patients who had a non-glycine-type trinucleotide interruption within expanded poly-glycine motifs than in those with a pure poly-glycine expansion. These results suggested that the repeat length and sequence in NOTCH2NLC may partly modify some clinical and imaging features of NIID.

    DOI： 10.3390/brainsci13060955

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  • High frequency of<i>HTRA1</i>AND<i>ABCC6</i>mutations in Japanese patients with adult-onset cerebral small vessel disease

    Masahiro Uemura, Yuya Hatano, Hiroaki Nozaki, Shoichiro Ando, Hajime Kondo, Akira Hanazono, Akira Iwanaga, Hiroyuki Murota, Yosuke Osakada, Masato Osaki, Masato Kanazawa, Mitsuyasu Kanai, Yoko Shibata, Reiko Saika, Tadashi Miyatake, Hitoshi Aizawa, Takeshi Ikeuchi, Hidekazu Tomimoto, Ikuko Mizuta, Toshiki Mizuno, Tomohiko Ishihara, Osamu Onodera

    Journal of Neurology, Neurosurgery &amp; Psychiatry   jnnp - 2022   2022.10

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

    Background

    This study aimed to clarify the frequency and clinical features of monogenic cerebral small vessel disease (mgCSVD) among patients with adult-onset severe CSVD in Japan.

    Methods

    This study included patients with adult-onset severe CSVD with an age of onset ≤55 years (group 1) or &gt;55 years and with a positive family history (group 2). After conducting conventional genetic tests forNOTCH3andHTRA1, whole-exome sequencing was performed on undiagnosed patients. Patients were divided into two groups according to the results of the genetic tests: monogenic and undetermined. The clinical and imaging features were compared between the two groups.

    Results

    Group 1 and group 2 included 75 and 31 patients, respectively. In total, 30 patients hadNOTCH3mutations, 11 patients hadHTRA1mutations, 6 patients hadABCC6mutations, 1 patient had aTREX1mutation, 1 patient had aCOL4A1mutation and 1 patient had aCOL4A2mutation. The total frequency of mutations inNOTCH3,HTRA1andABCC6was 94.0% in patients with mgCSVD. In group 1, the frequency of a family history of first relatives, hypertension and multiple lacunar infarctions (LIs) differed significantly between the two groups (monogenic vs undetermined; family history of first relatives, 61.0% vs 25.0%, p=0.0015; hypertension, 34.1% vs 63.9%, p=0.0092; multiple LIs, 87.8% vs 63.9%, p=0.0134).

    Conclusions

    More than 90% of mgCSVDs were diagnosed by screening forNOTCH3,HTRA1andABCC6. The target sequences for these three genes may efficiently diagnose mgCSVD in Japanese patients.

    DOI： 10.1136/jnnp-2022-329917

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

    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.

    DOI： 10.1172/JCI140555

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  • Corrigendum: HTRA1 Mutations Identified in Symptomatic Carriers Have the Property of Interfering the Trimer-Dependent Activation Cascade (Front. Neurol., (2019), 10, (693), 10.3389/fneur.2019.00693)

    Masahiro Uemura, Hiroaki Nozaki, Akihide Koyama, Naoko Sakai, Shoichiro Ando, Masato Kanazawa, Taisuke Kato, Osamu Onodera

    Frontiers in Neurology   12   2021.9

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Frontiers Media S.A.  

    DOI： 10.3389/fneur.2021.756038

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  • [Rethinking Lacunar Stroke: Beyond Fisher's Curse].

    Osamu Onodera, Masahiro Uemura, Shoichiro Ando, Hideki Hayashi, Masato Kanazawa

    Brain and nerve = Shinkei kenkyu no shinpo   73 ( 9 )   991 - 998   2021.9

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

    Lipohyalinosis is an important concept in the independence of lacunar stroke; however, its role has been overemphasized and has led to much confusion in the understanding of lacunar stroke. Classical lipohyalinosis has declined following the widespread availability of antihypertensive therapy, and lacunar stroke secondary to age-related hyaline atherosclerosis is more commonly observed in clinical practice. Clinically diagnosed lacunar stroke is associated with several etiopathogenetic contributors. Excluding cardiogenic embolism, lacunar stroke can be categorized based on the detection of an atheroma. Atheroma imaging is possible in recent years, and strokes that are not associated with an atheroma are shown to present with deep white matter hyperintensity on MRI. Additionally, risk gene analysis has confirmed a group of risk genes associated with the extracellular matrix in lacunar stroke with white matter hyperintensity on MRI. These findings suggest the role of a variety of etiopathogenetic mechanisms underlying lacunar stroke and that lacunar stroke with deep white matter hyperintensity on MRI may be attributable to unique pathogenetic contributors. This group is known to be strongly associated with genetic contributors. Hopefully, lacunar stroke will be diagnosed from this perspective with the development of interventional strategies tailored to the pathogenesis of this condition.

    DOI： 10.11477/mf.1416201876

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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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  • 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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  • ゲノム編集による遺伝子サイレンシングを用いたDRPLA治療戦略

    安藤 昭一朗, 加藤 泰介, 小池 佑佳, 廣川 祥子, 小林 憲太, 辻 省次, 小野寺 理

    Dementia Japan   34 ( 4 )   531 - 531   2020.10

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    Language：Japanese   Publisher：(一社)日本認知症学会  

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  • ゲノム編集による遺伝子サイレンシングを用いたDRPLA治療戦略

    安藤 昭一朗, 加藤 泰介, 小池 佑佳, 廣川 祥子, 小林 憲太, 辻 省次, 小野寺 理

    Dementia Japan   34 ( 4 )   531 - 531   2020.10

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    Language：Japanese   Publisher：(一社)日本認知症学会  

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  • 【RAN翻訳と相分離で紐解くリピート病 くり返し配列の"長さ"が発症の原因となる謎に挑む】DNA、RNAを標的としたポリグルタミン病の新規治療戦略

    安藤 昭一朗, 加藤 泰介, 小野寺 理

    実験医学   38 ( 13 )   2191 - 2196   2020.8

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    Language：Japanese   Publisher：(株)羊土社  

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  • Excessive Production of Transforming Growth Factor β1 Causes Mural Cell Depletion From Cerebral Small Vessels

    Taisuke Kato, Yumi Sekine, Hiroaki Nozaki, Masahiro Uemura, Shoichiro Ando, Sachiko Hirokawa, Osamu Onodera

    Frontiers in Aging Neuroscience   12   2020.6

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.3389/fnagi.2020.00151

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  • Progressive Supranuclear Palsy with Predominant Cerebellar Ataxia Reviewed

    Shoichiro Ando, Masato Kanazawa, Osamu Onodera

    Journal of Movement Disorders   13 ( 1 )   20 - 26   2020.1

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    Publishing type：Research paper (scientific journal)   Publisher：The Korean Movement Disorder Society  

    DOI： 10.14802/jmd.19061

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    Other Link： http://e-jmd.org/journal/view.php?doi=10.14802/jmd.19061

  • Type IV collagen α1の3'UTRの新規変異による脳小血管病

    酒井 直子, 上村 昌寛, 加藤 泰介, 安藤 昭一朗, 野崎 洋明, 亀井 博之, 加藤 元博, 小野寺 理

    臨床神経学   59 ( Suppl. )   S327 - S327   2019.11

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    Language：Japanese   Publisher：(一社)日本神経学会  

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  • 【脳の自浄システムとしてのアストロサイトとglymphaticシステム】神経脳小血管単位による排泄機構と疾病との関係

    安藤 昭一朗, 上村 昌寛, 小野寺 理

    Dementia Japan   33 ( 3 )   257 - 262   2019.9

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    Language：Japanese   Publisher：(一社)日本認知症学会  

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  • 【嚥下障害と誤嚥性肺炎】主な神経疾患の嚥下障害の臨床 多系統萎縮症

    安藤 昭一朗, 金澤 雅人, 小野寺 理

    Clinical Neuroscience   37 ( 5 )   555 - 557   2019.5

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    Language：Japanese   Publisher：(株)中外医学社  

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  • A case of chordoma presenting as recurrent bacterial meningitis with cerebrospinal fluid leakage Reviewed

    Shoichiro Ando, Hiroyuki Usuda, Yoshitaka Umeda, Maiko Umeda, Mutsuo Oyake, Nobuya Fujita

    Rinsho Shinkeigaku   59 ( 5 )   264 - 267   2019

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    Publishing type：Research paper (scientific journal)   Publisher：Societas Neurologica Japonica  

    DOI： 10.5692/clinicalneurol.cn-001272

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  • A patient clinically diagnosed as multiple system atrophy harboring LRRK2 p.G2019S

    Shoichiro Ando, Takuya Konno, Tomohiko Ishihara, Hideki Hayashi, Natsumi Saito, Kenya Nishioka, Nobutaka Hattori, Zbigniew K. Wszolek, Osamu Onodera

    Clinical Parkinsonism & Related Disorders   1   100 - 101   2019

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

    DOI： 10.1016/j.prdoa.2019.11.002

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  • HTRA1 mutations identified in symptomatic carriers have the property of interfering the trimer-dependent activation cascade

    Masahiro Uemura, Hiroaki Nozaki, Akihide Koyama, Naoko Sakai, Shoichiro Ando, Masato Kanazawa, Taisuke Kato, Osamu Onodera

    Frontiers in Neurology   10 ( JUN )   2019

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.3389/fneur.2019.00693

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  • MSA-Pと鑑別を要したPARK8の75歳女性例

    林 秀樹, 石原 智彦, 斎藤 奈つみ, 安藤 昭一朗, 小野寺 理

    臨床神経学   58 ( 12 )   779 - 779   2018.12

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    Language：Japanese   Publisher：(一社)日本神経学会  

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  • 臨床経過および画像所見よりMSA-Pとの鑑別を要したPARK8の一例

    石原 智彦, 林 秀樹, 齋藤 奈つみ, 安藤 昭一朗, 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   12回   100 - 100   2018.7

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    Language：Japanese   Publisher：Movement Disorder Society of Japan (MDSJ)  

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  • A case of multiple cerebral hemorrhage caused by sudden increase of eosinophil in a patient with eosinophilic granulomatosis with polyangiitis

    Yumi Yamada, Shoichiro Ando, Yoshitaka Umeda, Maiko Umeda, Mutsuo Oyake, Nobuya Fujita

    Clinical Neurology   58 ( 9 )   565 - 569   2018

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    Language：Japanese   Publishing type：Research paper (scientific journal)   Publisher：Societas Neurologica Japonica  

    DOI： 10.5692/clinicalneurol.cn-001188

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MISC

  • TREX1遺伝子変異による相同組換え修復阻害を介した全身小血管病の発症機序解明

    安藤昭一朗, 杉江淳, 加藤怜, 畠野雄也, MINER Jonathan, 小野寺理, 加藤泰介

    日本内科学会雑誌   114   2025

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  • 本邦におけるABCC6関連脳小血管病の臨床的・画像的特徴

    北原匠, 安藤昭一朗, 安藤昭一朗, 上村昌寛, 畠野雄也, 野崎洋明, 板橋亮, 廣澤太輔, 野村恵美, 大久保浩平, 宗兼麻美, 田代匠, 浅井可奈子, 山岡美奈子, 種田朝音, 相澤仁志, 相澤仁志, 本間温, 近藤初, 岩永聰, 室田浩之, 小野寺理

    日本神経学会学術大会プログラム・抄録集   65th   2024

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  • Venous abnormality is a useful diagnostic marker for HTRA1-related cerebral small vessel disease

    ANDO Shoichiro, SAITO Rie, UEMURA Masahiro, KITAHARA Sho, HATANO Yuya, WATANABE Masaki, KATO Taisuke, ITO Yosuke, NALINI Atchayaram, MURAYAMA Shigeo, MURAYAMA Shigeo, IGARASHI Hironaka, KAKITA Akiyoshi, ONODERA Osamu

    日本神経学会学術大会プログラム・抄録集   65th   2024

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  • Matrisomeの擾乱から見た脳小血管病の分子病態と治療法への展望

    加藤泰介, 眞鍋理一郎, 五十嵐博中, 亀谷富由樹, 齊藤聡, 畠野雄也, 安藤昭一朗, 福永雅喜, 佐藤俊哉, 齋藤理恵, 豊島靖子, 河田浩敏, 村山繁雄, 柿田明美, 長谷川成人, 猪原匡史, 西澤正豊, 辻省次, 小野寺理

    Dementia Japan   36 ( 4 )   2022

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  • 遺伝性脳小血管病モデルから見えてきたmatrisomeの破綻と治療法の展望

    加藤泰介, 眞鍋理一郎, 五十嵐博中, 亀谷富由樹, 齊藤聡, 畠野雄也, 安藤昭一朗, 福永雅喜, 佐藤俊哉, 齋藤理恵, 豊島靖子, 河田浩敏, 村山繁雄, 柿田明美, 長谷川成人, 猪原匡史, 西澤正豊, 辻省次, 小野寺理

    Dementia Japan   36 ( 4 )   2022

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  • HTRA1-Related Cerebral Small Vessel Disease: A Review of the Literature

    Masahiro Uemura, Hiroaki Nozaki, Taisuke Kato, Akihide Koyama, Naoko Sakai, Shoichiro Ando, Masato Kanazawa, Nozomi Hishikawa, Yoshinori Nishimoto, Kiran Polavarapu, Atchayaram Nalini, Akira Hanazono, Daisuke Kuzume, Akihiro Shindo, Mohammad El-Ghanem, Arata Abe, Aki Sato, Mari Yoshida, Takeshi Ikeuchi, Ikuko Mizuta, Toshiki Mizuno, Osamu Onodera

    Frontiers in Neurology   11   2020.7

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    Publishing type：Book review, literature introduction, etc.  

    DOI： 10.3389/fneur.2020.00545

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  • Type IV collagen α1の3'UTRの新規変異による脳小血管病

    酒井 直子, 上村 昌寛, 加藤 泰介, 安藤 昭一朗, 野崎 洋明, 亀井 博之, 加藤 元博, 小野寺 理

    臨床神経学   59 ( Suppl. )   S327 - S327   2019.11

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    Language：Japanese   Publisher：(一社)日本神経学会  

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  • 臨床経過および画像所見よりMSA-Pとの鑑別を要したPARK8の一例

    石原 智彦, 林 秀樹, 齋藤 奈つみ, 安藤 昭一朗, 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   12回   100 - 100   2018.7

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    Language：Japanese   Publisher：Movement Disorder Society of Japan (MDSJ)  

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  • 臨床ケース 再発性胸腺腫術後に腹壁の難治性疼痛を呈した重症筋無力症の44歳男性例

    山岸 拓磨, 佐治 越爾, 荻根沢 真也, 安藤 昭一郎, 茂木 崇秀, 他田 正義, 河内 泉, 小野寺 理

    神経免疫学   22 ( 1 )   106 - 106   2017.10

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    Language：Japanese   Publisher：日本神経免疫学会  

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  • 臨床ケース 再発性胸腺腫術後に腹壁の難治性疼痛を呈した重症筋無力症の44歳男性例

    山岸 拓磨, 佐治 越爾, 荻根沢 真也, 安藤 昭一郎, 茂木 崇秀, 他田 正義, 河内 泉, 小野寺 理

    神経免疫学   22 ( 1 )   106 - 106   2017.10

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    Language：Japanese   Publisher：日本神経免疫学会  

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Awards

  • 第65回日本神経学会学術集会. 一般演題 最優秀ポスター賞（臨床部門）.

    2024.5   日本神経学会  

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  • Best Poster Award

    2023.12   Asia Pacific Stroke Conference  

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Research Projects

  • 白質脳症をきたす変異型TREX1によるDNA損傷毒性誘導機序とその抑制分子の解明

    Grant number：22K20882

    2022.8 - 2024.3

    System name：科学研究費助成事業

    Research category：研究活動スタート支援

    Awarding organization：日本学術振興会

    安藤 昭一朗

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    Grant amount：\2860000 （ Direct Cost: \2200000 、 Indirect Cost：\660000 ）

    本研究の目的は、Retinal vasculopathy with cerebral leukoencephalopathy（RVCL）疾患変異TREX1による細胞毒性を低減するヒト遺伝子種を同定することである。この背景には、RVCL疾患変異TREX1が、DNA切断損傷を誘導し、細胞毒性を引き起こすことがある。
    RVCLショウジョウバエモデルを用いた、RNAiスクリーニングで見出した、表現型抑制遺伝子4種のヒトホモログ遺伝子が、RVCLヒト細胞モデルにおいて細胞毒性を抑制し得るかを検討した。
    まず、HEK293細胞株を対象に、Flp-in systemを用いて、RVCL疾患変異であるp.Val235GlyfsTer6（V235fs）ヒトTREX1遺伝子を挿入し、RVCLヒト細胞モデルを作製した。このモデル細胞はドキシサイクリン誘導性に変異TREX1を発現する。
    次に、このモデル細胞に、表現型抑制候補遺伝子のshort hairpin RNA（shRNA）をレンチウイルスベクターを用いて導入した。shRNAによる遺伝子発現抑制効果は、droplet digital PCR（ddPCR）によって発現量解析を行った。いずれの遺伝子も発現抑制できていることを確認した。
    そして、このshRNAを導入したRVCLヒト細胞モデルを対象に、ToxiLight bioassayを用いて、表現型抑制候補遺伝子の抑制により、RVCL疾患変異TREX1による細胞毒性が低減するか検証した。結果、候補遺伝子4種のうち、2種の遺伝子において、ネガティブコントロールと比較して、shRNA導入群での細胞死率が低下した。従って、これらの2遺伝子が、ヒト細胞においてもRVCL疾患変異TREX1の細胞毒性を低減させる可能性が示唆された。

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Teaching Experience (researchmap)

  • 臓器別講義「脳・神経系」

    2022.4
    Institution name：新潟大学医学部医学科

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