2022/09/29 更新

写真a

アンドウ シヨウイチロウ
安藤 昭一朗
ANDO Shoichiro
所属
医歯学総合病院 脳神経内科 助教
職名
助教
外部リンク

学位

  • 学士(医学) ( 2013年3月   新潟大学 )

研究キーワード

  • 脳小血管病

経歴

  • 新潟大学   医歯学総合病院 脳神経内科   助教

    2022年4月 - 現在

  • 新潟大学   脳研究所   特任助教

    2021年4月 - 2021年9月

学歴

  • 新潟大学   医学部   医学科

    2007年4月 - 2013年3月

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    国名: 日本国

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所属学協会

 

論文

  • Candesartan prevents arteriopathy progression in cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy model. 査読 国際誌

    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年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    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

    PubMed

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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年9月

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

    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

    PubMed

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

    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年6月

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

    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年6月

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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年10月

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    記述言語:日本語   出版者・発行元:(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年10月

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    記述言語:日本語   出版者・発行元:(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年8月

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    記述言語:日本語   出版者・発行元:(株)羊土社  

    ポリグルタミン病(polyQ病)は、原因遺伝子のエキソン内に存在するCAGリピートの異常伸長により、伸長polyQ鎖を含む変異タンパク質が神経細胞内で凝集する疾患群である。これまで、polyQ病への治療は対症療法によるところが大きかった。しかし、近年の精力的な遺伝子治療研究への取り組みにより、polyQ病に対しても、進行抑制や発症予防につながるような治療アプローチが試みられ、すでにヒトでの臨床試験が行われているものもある。ここでは、アンチセンスオリゴヌクレオチドとCRISPR/Cas9システムを中心に、最近のpolyQ病に対する遺伝子治療研究の動向を概説する。(著者抄録)

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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年6月

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    掲載種別:研究論文(学術雑誌)  

    It is increasingly becoming apparent that cerebrovascular dysfunction contributes to the pathogenic processes involved in vascular dementia, Alzheimer’s disease, and other neurodegenerative disorders. Under these pathologic conditions, the degeneration of cerebral blood vessels is frequently accompanied by a loss of mural cells from the vascular walls. Vascular mural cells play pivotal roles in cerebrovascular functions, such as regulation of cerebral blood flow and maintenance of the blood-brain barrier (BBB). Therefore, cerebrovascular mural cell impairment is involved in the pathophysiology of vascular-related encephalopathies, and protecting these cells is essential for maintaining brain health. However, our understanding of the molecular mechanism underlying mural cell abnormalities is incomplete. Several reports have indicated that dysregulated transforming growth factor β (TGFβ) signaling is involved in the development of cerebral arteriopathies. These studies have specifically suggested the involvement of TGFβ overproduction. Although cerebrovascular toxicity via vascular fibrosis by extracellular matrix accumulation or amyloid deposition is known to occur with enhanced TGFβ production, whether increased TGFβ results in the degeneration of vascular mural cells in vivo remains unknown. Here, we demonstrated that chronic TGFβ1 overproduction causes a dropout of mural cells and reduces their coverage on cerebral vessels in both smooth muscle cells and pericytes. Mural cell degeneration was also accompanied by vascular luminal dilation. TGFβ1 overproduction in astrocytes significantly increased TGFβ1 content in the cerebrospinal fluid (CSF) and increased TGFβ signaling-regulated gene expression in both pial arteries and brain capillaries. These results indicate that TGFβ is an important effector that mediates mural cell abnormalities under pathological conditions related to cerebral arteriopathies.

    DOI: 10.3389/fnagi.2020.00151

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  • Progressive Supranuclear Palsy with Predominant Cerebellar Ataxia 査読

    Shoichiro Ando, Masato Kanazawa, Osamu Onodera

    Journal of Movement Disorders   13 ( 1 )   20 - 26   2020年1月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:The Korean Movement Disorder Society  

    DOI: 10.14802/jmd.19061

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    その他リンク: 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年11月

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    記述言語:日本語   出版者・発行元:(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年9月

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    記述言語:日本語   出版者・発行元:(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年5月

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    記述言語:日本語   出版者・発行元:(株)中外医学社  

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

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

    Rinsho Shinkeigaku   59 ( 5 )   264 - 267   2019年

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    掲載種別:研究論文(学術雑誌)   出版者・発行元: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年

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    掲載種別:研究論文(学術雑誌)   出版者・発行元: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年

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    掲載種別:研究論文(学術雑誌)  

    Background: Mutations in the high-temperature requirement A serine peptidase 1 (HTRA1) cause cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL). Most carriers for HTRA1 mutations are asymptomatic, but more than 10 mutations have been reported in symptomatic carriers. The molecular differences between the mutations identified in symptomatic carriers and mutations identified only in CARASIL patients are unclear. HTRA1 is a serine protease that forms homotrimers, with each HTRA1 subunit activating the adjacent HTRA1 via the sensor domain of loop 3 (L3) and the activation domain of loop D (LD). Previously, we analyzed four HTRA1 mutant proteins identified in symptomatic carriers and found that they were unable to form trimers or had mutations in the LD or L3 domain. The mutant HTRA1s with these properties are presumed to inhibit trimer-dependent activation cascade. Indeed, these mutant HTRA1s inhibited wild-type (WT) protease activity. In this study, we further analyzed 15 missense HTRA1s to clarify the molecular character of mutant HTRA1s identified in symptomatic carriers. Methods: We analyzed 12 missense HTRA1s identified in symptomatic carriers (hetero-HTRA1) and three missense HTRA1s found only in CARASIL (CARASIL-HTRA1). The protease activity of the purified recombinant mutant HTRA1s was measured using fluorescein isothiocyanate-labeled casein as substrate. Oligomeric structure was evaluated by size-exclusion chromatography. The protease activities of mixtures of WT with each mutant HTRA1 were also measured. Results: Five hetero-HTRA1s had normal protease activity and were excluded from further analysis. Four of the seven hetero-HTRA1s and one of the three CARASIL-HTRA1s were unable to form trimers. The other three hetero-HTRA1s had mutations in the LD domain. Together with our previous work, 10 of 11 hetero-HTRA1s and two of six CARASIL-HTRA1s were either defective in trimerization or had mutations in the LD or L3 domain (P = 0.006). By contrast, eight of 11 hetero-HTRA1s and two of six CARASIL-HTRA1 inhibited WT protease activity (P = 0.162). Conclusions: HTRA1 mutations identified in symptomatic carriers have the property of interfering the trimer-dependent activation cascade of HTRA1.

    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年12月

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    記述言語:日本語   出版者・発行元:(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年7月

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    記述言語:日本語   出版者・発行元:Movement Disorder Society of Japan (MDSJ)  

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▶ 全件表示

MISC

  • 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年7月

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    掲載種別:書評論文,書評,文献紹介等  

    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.

    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年11月

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    記述言語:日本語   出版者・発行元:(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年7月

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    記述言語:日本語   出版者・発行元: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年10月

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    記述言語:日本語   出版者・発行元: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年10月

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    記述言語:日本語   出版者・発行元:日本神経免疫学会  

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