M
Masashi Aoki
Researcher at Tohoku University
Publications - 418
Citations - 14303
Masashi Aoki is an academic researcher from Tohoku University. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Neuromyelitis optica. The author has an hindex of 55, co-authored 374 publications receiving 11702 citations. Previous affiliations of Masashi Aoki include Kyowa Hakko Kirin Co., Ltd. & Kumamoto University.
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Journal ArticleDOI
Mutations of optineurin in amyotrophic lateral sclerosis
Hirofumi Maruyama,Hiroyuki Morino,Hidefumi Ito,Hidefumi Ito,Yuishin Izumi,Hidemasa Kato,Yasuhito Watanabe,Yoshimi Kinoshita,Masaki Kamada,Masaki Kamada,Hiroyuki Nodera,Hidenori Suzuki,Osamu Komure,Shinya Matsuura,Keitaro Kobatake,Nobutoshi Morimoto,Koji Abe,Naoki Suzuki,Masashi Aoki,Akihiro Kawata,Takeshi Hirai,Takeo Kato,Kazumasa Ogasawara,Asao Hirano,Toru Takumi,Hirofumi Kusaka,Koichi Hagiwara,Ryuji Kaji,Hideshi Kawakami +28 more
TL;DR: It is shown that there are mutations in the gene encoding optineurin (OPTN), earlier reported to be a causative gene of primary open-angle glaucoma (POAG), in patients with ALS and these findings strongly suggest that OPTN is involved in the pathogenesis of ALS.
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Distinction between MOG antibody-positive and AQP4 antibody-positive NMO spectrum disorders
Douglas Kazutoshi Sato,Dagoberto Callegaro,Marco Aurélio Lana-Peixoto,Patrick Waters,Frederico Jorge,Toshiyuki Takahashi,Ichiro Nakashima,Samira Luisa Apostolos-Pereira,Natalia Talim,Renata Simm,Angelina Maria Martins Lino,Tatsuro Misu,Maria Isabel Leite,Masashi Aoki,Kazuo Fujihara +14 more
TL;DR: Patients with NMOSD with MOG antibodies have distinct clinical features, fewer attacks, and better recovery than patients with AQP4 antibodies or patients seronegative for both antibodies.
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Safety and efficacy of edaravone in well defined patients with amyotrophic lateral sclerosis: a randomised, double-blind, placebo-controlled trial
Koji Abe,Masashi Aoki,Shoji Tsuji,Yasuto Itoyama,Gen Sobue,Masanori Togo,Chikuma Hamada,Masahiko Tanaka,Makoto Akimoto,Kazue Nakamura,Fumihiro Takahashi,Kazuoki Kondo,Hiide Yoshino,Hidenao Sasaki,Ichiro Yabe,Shizuki Doi,Hitoshi Warita,Takashi Imai,Hiroaki Ito,Mitsumasa Fukuchi,Etsuko Osumi,Manabu Wada,Imaharu Nakano,Mitsuya Morita,Katsuhisa Ogata,Yuichi Maruki,Kimiko Ito,Osamu Kano,Mineo Yamazaki,Yuji Takahashi,Hiroyuki Ishiura,Mieko Ogino,Ryoko Koike,Chiho Ishida,Tsuyoshi Uchiyama,Kouichi Mizoguchi,Tomokazu Obi,Hirohisa Watanabe,Naoki Atsuta,Ikuko Aiba,Akira Taniguchi,Hideyuki Sawada,Takanori Hazama,Harutoshi Fujimura,Hirofumi Kusaka,Takenobu Kunieda,Hitoshi Kikuchi,Hidenori Matsuo,Hidetsugu Ueyama,Kazutoshi Uekawa,Masaki Ueda,Aiko Murakami,Rie Sumii,Takuya Kudou,Kazunori Morimoto,Takatomo Yoneoka,Manabu Hirai,Kouichi Sasaki,Hidetomo Terai,Tomoko Natori,Hiroshi Matsui,Kuniko Kotani,Kaori Yoshida,Tomohisa Iwasaki +63 more
TL;DR: The primary efficacy outcome was the change in ALSFRS-R score from the baseline to 24 weeks (or at discontinuation if this was after the third cycle) after randomisation and the least-squares mean difference between groups was 2·49 (SE 0·76, 95% CI 0·99-3·98) in favour of edaravone.
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The gene mutated in ataxia-ocular apraxia 1 encodes the new HIT/Zn-finger protein aprataxin
Maria-Ceu Moreira,Maria-Ceu Moreira,Clara Barbot,Nobutada Tachi,Naoki Kozuka,Eiji Uchida,Toby J. Gibson,P. Mendonça,Manuela Costa,José Barros,Takayuki Yanagisawa,Mitsunori Watanabe,Yoshio Ikeda,Masashi Aoki,Tetsuya Nagata,Paula Coutinho,Jorge Sequeiros,Michel Koenig +17 more
TL;DR: The results suggest that aprataxin is a nuclear protein with a role in DNA repair reminiscent of the function of the protein defective in ataxia-telangiectasia, but that would cause a phenotype restricted to neurological signs when mutant.
Journal ArticleDOI
Rats Expressing Human Cytosolic Copper–Zinc Superoxide Dismutase Transgenes with Amyotrophic Lateral Sclerosis: Associated Mutations Develop Motor Neuron Disease
Makiko Nagai,Masashi Aoki,Ichiro Miyoshi,Masaaki Kato,Piera Pasinelli,Noriyuki Kasai,Robert H. Brown,Yasuto Itoyama +7 more
TL;DR: Rats that express a human SOD1 transgene with two different ALS-associated mutations develop striking motor neuron degeneration and paralysis, providing additional support for the proposition that motor neuron death in S OD1-related ALS reflects one or more acquired, neurotoxic properties of the mutant SOD 1 protein.