西本 祥仁 (ニシモト ヨシノリ)

Nishimoto, Yoshinori



医学部 内科学教室(神経) (信濃町)



総合紹介 【 表示 / 非表示

  • (臨床研究)
    慶應義塾大学医学部・病院 倫理委員会 承認番号:20221155

経歴 【 表示 / 非表示

  • 2022年04月

    慶應義塾大学 医学部, 神経内科, 専任講師

  • 2020年04月

    慶應義塾大学医学部, 神経内科, 助教

  • 2018年04月

    慶應義塾大学医学部, 百寿総合研究センター, 特任助教

  • 2016年10月

    東京都済生会中央病院, 神経内科, 医員

  • 2016年08月

    慶應義塾大学 医学部, 生理学教室, 助教

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学歴 【 表示 / 非表示

  • 2003年04月

    慶應義塾大学医学部 大学院 (内科学 / 神経内科), 内科学/神経内科学

    大学院, 卒業, 博士

  • 1997年04月

    慶應義塾大学 医学部

    大学, 卒業

学位 【 表示 / 非表示

  • MD, 慶應義塾大学, 課程, 2003年03月

  • PhD, 慶應義塾大学, 課程, 2008年10月

    Determination of editors at the novel A-to-I editing positions.

免許・資格 【 表示 / 非表示

  • 日本国 医師免許

  • 日本内科学会認定 総合内科専門医

  • 日本内科学会認定 認定内科医

  • 日本内科学会認定 指導医

  • 日本神経学会認定 神経内科専門医

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職務上の実績に関する事項 【 表示 / 非表示

  • 2023年01月

    臨床研究 承認番号:20221155 「筋萎縮性側索硬化症(ALS)の病態に関連する分子メカニズムの解明と効果的薬剤標的を同定するための臨床研究」


    慶應義塾大学医学部・病院 倫理委員会 承認番号:20221155


研究分野 【 表示 / 非表示

  • ライフサイエンス / 神経内科学

研究キーワード 【 表示 / 非表示

  • 筋萎縮性側索硬化症 (ALS)

  • 神経変性疾患

  • 神経分子生物学

  • 神経再生医学

  • RNA/ノンコーディングRNA

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研究テーマ 【 表示 / 非表示

  • 筋萎縮性側索硬化症(ALS)の早期診断および包括的治療体制の確立, 


  • 筋萎縮性側索硬化症(ALS)の核酸医薬による分子標的療法の開発, 


  • 次世代シークエンス技術を活用した認知症の遺伝的リスク算出法の確立, 


  • 認知症のオンライン診療データを活用した自動病態評価技術の開発, 



著書 【 表示 / 非表示

  • 脳神経内科ゴールデンハンドブック (ALSほか運動ニューロン疾患 分担執筆)

    西本 祥仁, 南江堂, 2020年06月

    担当範囲: 運動ニューロン疾患及び類縁疾患

  • 図とイラストだからわかるサルコペニア・フレイル

    西本祥仁, 新井康通, クリニコ出版, 2019年11月

  • Drosophila Oogenesis: Methods and Protocols

    Shibata S, Murota Y, Nishimoto Y, Yoshimura M, Nagai T, Okano H, Siomi MC., 2015年

    担当範囲: Immuno-Electron Microscopy and Electron Microscopic In Situ Hybridization for Visualizing piRNA Biogenesis Bodies in Drosophila Ovaries.

論文 【 表示 / 非表示

  • Association between multimorbidity, self-rated health and life satisfaction among independent, community-dwelling very old persons in Japan: longitudinal cohort analysis from the Kawasaki Ageing and Well-being Project

    Ando T., Nishimoto Y., Hirata T., Abe Y., Takayama M., Maeno T., Fujishima S., Takebayashi T., Arai Y.

    BMJ Open (BMJ Open)  12 ( 2 )  2022年


    Objective This study aimed to identify associations between multimorbidity and subjective health outcomes among the very old persons, after adjusting for coexisting conditions such as frailty and depression. Study setting and participants This was an observational cross-sectional study involving 1012 independent, community-dwelling very old persons (507 men, 505 women; aged 85-89 years) in Kawasaki city, Japan. Outcome measures The primary outcome was the cross-sectional associations between multimorbidity and poor self-rated health (SRH) and life satisfaction using binary logistic regression. The secondary outcome was the association of subjective health with each chronic condition. Results The prevalence of multimorbidity (≥2 conditions) was 94.7%, and the average number of chronic conditions was 4.47±1.9. Multimorbidity was significantly associated with poor SRH in the adjusted model only when six or more chronic conditions were present (OR 4.80; 95% CI 1.34 to 17.11; p=0.016). Cerebrovascular disease, heart disease, respiratory disease, connective tissue disease and arthritis showed significant associations with poor SRH after multivariate adjustment. Sex-specific analysis replicated associations between multimorbidity with six or more conditions and SRH in both men and women, while the diseases with the greatest impact on SRH differed between men and women. Most conditions were not associated with low satisfaction with life scale, with the exception of arthritis (OR 1.92, 95% CI 1.32 to 2.78, p=0.001). Conclusions Multimorbidity is prevalent in the independent, community-dwelling very old persons and is associated with poor SRH when six or more conditions are present; conditions causing mobility limitations, such as cerebrovascular disease, connective tissue disease and arthritis, have a negative impact on SRH. Trial registration number UMIN000026053.

  • Impact of Amyloid and Tau PET on Changes in Diagnosis and Patient Management

    Sho Shimohama, Toshiki Tezuka, Takahata Keisuke, Shogyoku Bun, Hajime Tabuchi, Morinobu Seki, Yuki Momota, Natsumi Suzuki, Ayaka Morimoto, Yu Iwabuchi, Masahito Kubota, Yasuharu Yamamoto, Yasunori Sano, Ryo Shikimoto, Kei Funaki, Yu Mimura, Yoshinori Nishimoto, Ryo Ueda, Masahiro Jinzaki, Jin Nakahara, Masaru Mimura, Daisuke Ito

    Neurology 10   1212 2022年


  • ALDH2 p.E504K Variation and Sex Are Major Factors Associated with Current and Quitting Alcohol Drinking in Japanese Oldest Old

    Takashi Sasaki, Yoshinori Nishimoto, Takumi Hirata, Yukiko Abe, Toru Takebayashi, Yasumichi Arai

    Genes (Genes)  12 ( 6 )  2021年



    This study identified the factors associated with current and quitting alcohol drinking in the Oldest Old to better understand the associated factors and mechanisms underlying drinking behaviors in this age group. Results of a questionnaire for drinking behavior in 1015 Japanese Oldest Old citizens aged 85 to 89 years revealed that 56.0% of men and 24.0% of women were current drinkers. A genome-wide association study revealed that the rs671 G > A variation, which corresponds to the aldehyde dehydrogenase 2 (ALDH2) p.E504K missense variant, was significantly associated with current drinking (odds ratio: 3.8, p = 3.33 × 10−31 ). Variable selection with 41 factors and multivariate regression logistic analysis for current drinking indicated that the rs671 genotype and sex were the most significant factors in the Oldest Old. Further analysis revealed that the rs671 genotype, alcohol-associated biomarkers, a history of heart or kidney disease, and frailty score are factors associated with quitting drinking in the Oldest Old men, whereas smoking history, walking time, and depression score were factors associated with quitting drinking in the Oldest Old women. These results indicate that the ALDH2 p.E504K variation is a major factor associated with current and quitting drinking in the Japanese Oldest Old.

  • LncRNA NEAT1 and amyotrophic lateral sclerosis

    Yoshinori Nishimoto, Shinichi Nakagawa, Hideyuki Okano

    Neurochemistry International (Neurochemistry International)  150   105175 2021年

    研究論文(学術雑誌), 査読有り,  ISSN  01970186


    Amyotrophic lateral sclerosis (ALS) is a representative neurological disease that is known to devastate entire motor neurons within a period of just a few years. Discoveries of the specific pathologies of relevant RNA-binding proteins, including TAR DNA-binding protein-43 (TDP-43) and fused in sarcoma/translocated in liposarcoma (FUS/TLS), and the causative genes of both familial and sporadic ALS have provided crucial information that could lead to a cure. In recent ALS research the GGGGCC-repeat expansion in the C9orf72 gene was identified as one of the most important pathological findings, suggesting the significance of both nuclear dysfunction due to dipeptide repeat proteins (DPRs) and RNA toxicity (such as pathological alterations of non-coding RNAs). In research on model animals carrying ALS-related molecules, the determination of whether a factor is protective or toxic has been controversial. Herein, we review the findings regarding NEAT1 RNA and C9orf72 GGGGCC repeats associated with ALS, from the viewpoint of conversion from the protective stage in the nucleus in early-phase ALS to late-phase induction of cell death. This review will provide insights for the development of RNA effectors as novel ALS treatments.

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

    Masahiro Uemura, Hiroaki Nozaki, Taisuke Kato, Akihide Koyama, Naoko Sakai, Shouichirou 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 (Frontiers in Neurology)  11 2020年

    研究論文(学術雑誌), 査読有り


    Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) is clinically characterized by early-onset dementia, stroke, spondylosis deformans, and alopecia. In CARASIL cases, brain magnetic resonance imaging reveals severe white matter hyperintensities (WMHs), lacunar infarctions, and microbleeds. CARASIL is caused by a homozygous mutation in high-temperature requirement A serine peptidase 1 (HTRA1). Recently, it was reported that several heterozygous mutations in HTRA1 also cause cerebral small vessel disease (CSVD). Although patients with heterozygous HTRA1-related CSVD (symptomatic carriers) are reported to have a milder form of CARASIL, little is known about the clinical and genetic differences between the two diseases. Given this gap in the literature, we collected clinical information on HTRA1-related CSVD from a review of the literature to help clarify the differences between symptomatic carriers and CARASIL and the features of both diseases. Forty-six symptomatic carriers and 28 patients with CARASIL were investigated. Twenty-eight mutations in symptomatic carriers and 22 mutations in CARASIL were identified. Missense mutations in symptomatic carriers are more frequently identified in the linker or loop 3 (L3)/loop D (LD) domains, which are critical sites in activating protease activity. The ages at onset of neurological symptoms/signs were significantly higher in symptomatic carriers than in CARASIL, and the frequency of characteristic extraneurological findings and confluent WMHs were significantly higher in CARASIL than in symptomatic carriers. As previously reported, heterozygous HTRA1-related CSVD has a milder clinical presentation of CARASIL. It seems that haploinsufficiency can cause CSVD among symptomatic carriers according to the several patients with heterozygous nonsense/frameshift mutations. However, the differing locations of mutations found in the two diseases indicate that distinct molecular mechanisms influence the development of CSVD in patients with HTRA1-related CSVD. These findings further support continued careful examination of the pathogenicity of mutations located outside the linker or LD/L3 domain in symptomatic carriers.

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KOARA(リポジトリ)収録論文等 【 表示 / 非表示

競争的研究費の研究課題 【 表示 / 非表示

  • 武田科学振興財団 医学系研究助成 (精神・神経・脳領域) 「核内非翻訳RNA制御によるALS患者由来運動ニューロン変性抑制の試み」



  • 文部科学省 科学研究費補助金 基盤研究(C) 「ALSゲノム編集マウスを用いたGC/UGリッチRNA配列での病態考察と治療法開発」


    補助金,  研究代表者

  • KGRI (Keio University Global Research Institute)スタートアップ研究補助 (KGRI startup award) 「オンライン診療を用いた認知症診療の有効性、安全性評価」


    補助金,  研究代表者

  • 日本学術振興会 海外特別研究員 「Investigating the regulatory function of the exosome complex in RNA metabolism a nd motor neuron disease」



  • 日本ワックスマン財団 留学研究助成


    補助金,  未設定

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Works 【 表示 / 非表示

  • 朝日学生新聞連載コラム「からだの教室 -知識の玉手箱-」

    西本 祥仁

    朝日学生新聞 毎週金曜日 全26回, 



受賞 【 表示 / 非表示

  • Neurogenetics Editor’s Pick 2021 (Frontiers in Neurology)


    受賞区分: 学会誌・学術雑誌による顕彰

  • KGRI (Keio University Global Research Institute) Startup Award

    2020年06月, Keio University Global Research Institute, 「オンライン診療を用いた認知症診療の有効性、安全性評価」

    受賞区分: 塾内表彰等

  • Selected key poster (Harvard Stem Cell Institute Retreat)

    2016年05月, 11th Annual Harvard Stem Cell Institute Malkin Retreat 2016, 「Altered tRNA metabolism links RNA Exosome deficiency with motor neuron disease」

  • Physician's Recognition Award

    2015年08月, American Medical Association, 「Pediatric Advanced Care Team Rounds」

  • 日本学術振興会 海外特別研究員


    受賞区分: その他

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担当授業科目 【 表示 / 非表示

  • 内科学(神経)講義


  • 内科学(神経)講義