A
Akiyoshi Kakita
Researcher at Niigata University
Publications - 444
Citations - 15675
Akiyoshi Kakita is an academic researcher from Niigata University. The author has contributed to research in topics: Medicine & Amyotrophic lateral sclerosis. The author has an hindex of 60, co-authored 395 publications receiving 13064 citations. Previous affiliations of Akiyoshi Kakita include Columbia University.
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Journal ArticleDOI
Loss of aquaporin 4 in lesions of neuromyelitis optica: distinction from multiple sclerosis.
Tatsuro Misu,Kazuo Fujihara,Akiyoshi Kakita,H. Konno,M. Nakamura,S. Watanabe,Tetsuya Takahashi,Ichiro Nakashima,Hitoshi Takahashi,Yasuto Itoyama +9 more
TL;DR: It is demonstrated that the immunoreactivities of AQP4 and GFAP were consistently lost from the early stage of the lesions in NMO, notably in the perivascular regions with complement and immunoglobulin deposition.
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Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer’s disease
Yingyue Zhou,Wilbur M. Song,Prabhakar S. Andhey,Amanda Swain,Tyler Levy,Kelly R. Miller,Pietro Luigi Poliani,Manuela Cominelli,Shikha Grover,Susan Gilfillan,Marina Cella,Tyler K. Ulland,Konstantin Zaitsev,Konstantin Zaitsev,Akinori Miyashita,Takeshi Ikeuchi,Makoto Sainouchi,Akiyoshi Kakita,David A. Bennett,Julie A. Schneider,Michael R. Nichols,Sean A. Beausoleil,Jason D. Ulrich,David M. Holtzman,Maxim N. Artyomov,Marco Colonna +25 more
TL;DR: Single-nucleus RNA sequencing in a mouse model of Aβ accumulation and postmortem brain tissue from people with Alzheimer’s disease reveals substantial species-specific differences in transcriptional signatures, but both point to the contribution of glia and the importance of TREM2.
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TDP-43 mutation in familial amyotrophic lateral sclerosis
Akio Yokoseki,Atsushi Shiga,Chun-Feng Tan,Asako Tagawa,Hiroyuki Kaneko,Akihide Koyama,Hiroto Eguchi,Akira Tsujino,Takeshi Ikeuchi,Akiyoshi Kakita,Koichi Okamoto,Masatoyo Nishizawa,Hitoshi Takahashi,Osamu Onodera +13 more
TL;DR: In three affected individuals in two generations of one family, a single base‐pair change from A to G at position 1028 in TDP‐43 resulted in a Gln‐to‐Arg substitution at position 343, which provides a new insight into the molecular pathogenesis of ALS.
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Accumulation of alpha-synuclein/NACP is a cytopathological feature common to Lewy body disease and multiple system atrophy.
Koichi Wakabayashi,Shintaro Hayashi,Akiyoshi Kakita,Mitsunori Yamada,Yasuko Toyoshima,Makoto Yoshimoto,Hitoshi Takahashi +6 more
TL;DR: Study of 83 autopsied cases with various neurological disorders, using anti-NACP antibodies, strongly suggest that the accumulation of NACP is a cytopathological feature common to LB disease and MSA.
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TDP-43 immunoreactivity in neuronal inclusions in familial amyotrophic lateral sclerosis with or without SOD1 gene mutation.
Chun-Feng Tan,Hiroto Eguchi,Asako Tagawa,Osamu Onodera,Takuya Iwasaki,Akira Tsujino,Masatoyo Nishizawa,Akiyoshi Kakita,Hitoshi Takahashi +8 more
TL;DR: The findings indicate that the histological and molecular pathology of SALS can occur as a phenotype of FALS without SOD1 mutation.