M
Minako Hoshi
Researcher at Foundation for Biomedical Research
Publications - 34
Citations - 2644
Minako Hoshi is an academic researcher from Foundation for Biomedical Research. The author has contributed to research in topics: Amyloid & Neurodegeneration. The author has an hindex of 15, co-authored 33 publications receiving 2370 citations. Previous affiliations of Minako Hoshi include Kyoto University & Mitsubishi.
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Journal ArticleDOI
Aβ(1–42) fibril structure illuminates self-recognition and replication of amyloid in Alzheimer's disease
Yiling Xiao,Buyong Ma,Dan McElheny,Sudhakar Parthasarathy,Fei Long,Minako Hoshi,Ruth Nussinov,Yoshitaka Ishii +7 more
TL;DR: The atomic model of an Aβ(1–42) amyloid fibril, from solid-state NMR (ssNMR) data, is presented, providing insight into the A β(1-42)-selective self-replicating amyloids-propagation machinery in early-stage Alzheimer's disease.
Journal ArticleDOI
Spherical aggregates of β-amyloid (amylospheroid) show high neurotoxicity and activate tau protein kinase I/glycogen synthase kinase-3β
Minako Hoshi,Michio Sato,Shinichiro Matsumoto,Akihiko Noguchi,Kaori Yasutake,Natsuko Yoshida,Kazuki Sato,Kazuki Sato +7 more
TL;DR: The identification and characterization of ASPD is described and its possible role in the neurodegeneration in Alzheimer's disease is discussed and inhibition experiments with lithium suggest the involvement of tau protein kinase I/glycogen synthase kinase-3β in the early stages of ASD-induced neurodegenersation.
Journal ArticleDOI
Regulation of mitochondrial pyruvate dehydrogenase activity by tau protein kinase I/glycogen synthase kinase 3beta in brain
Minako Hoshi,Akihiko Takashima,Kaori Noguchi,Miyuki Murayama,Michio Sato,Shunzo Kondo,Yoshito Saitoh,Koichi Ishiguro,Toshimitsu Hoshino,Kazutomo Imahori +9 more
TL;DR: Results suggest that TPKI/GSK-3beta plays a key role in the pathogenesis of Alzheimer disease and regulates PDH and participates in energy metabolism and acetylcholine synthesis.
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Exposure of rat hippocampal neurons to amyloid β peptide (25–35) induces the inactivation of phosphatidyl inositol-3 kinase and the activation of tau protein kinase I/glycogen synthase kinase-3β
Akihiko Takashima,Kaori Noguchi,Gilles Michel,Marc Mercken,Minako Hoshi,Koichi Ishiguro,Kazutomo Imahori +6 more
TL;DR: Results suggest that A beta (25-35) inhibition of PI-3 kinase results in the activation of TPK I/GSK-3 beta, the phosphorylation of tau, and resultant neuronal death in rat hippocampal neurons.
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Isolation and Characterization of Patient-derived, Toxic, High Mass Amyloid β-Protein (Aβ) Assembly from Alzheimer Disease Brains
Akihiko Noguchi,Satoko Matsumura,Mari Dezawa,Mari Dezawa,Mari Tada,Masako Yanazawa,Akane Ito,Manami Akioka,Satoru Kikuchi,Michio Sato,Shouji Ideno,Munehiro Noda,Atsushi Fukunari,Shin-ichi Muramatsu,Yutaka Itokazu,Kazuki Sato,Hitoshi Takahashi,David B. Teplow,Yo-ichi Nabeshima,Akiyoshi Kakita,Kazutomo Imahori,Minako Hoshi,Minako Hoshi +22 more
TL;DR: The findings indicate that native ASPDs with a distinct toxic surface induce neuronal loss through a different mechanism from other Aβ assemblies, which is a central phenotype in neurodegenerative diseases such as AD.