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2017 Fiscal Year Final Research Report

Analysis of propagation molecule mechanism via exosome in Parkinson's disease related gene SNCA

Research Project

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Project/Area Number 15K06710
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Neurophysiology / General neuroscience
Research InstitutionKanazawa University

Principal Investigator

Kawahara Hironori  金沢大学, 医学系, 助教 (00424177)

Co-Investigator(Renkei-kenkyūsha) HANAYAMA Rikinari  金沢大学, 医学系, 教授 (40403191)
Research Collaborator MOCHIDUKI Hideki  大阪大学, 医学(系)研究科(研究院), 教授 (90230044)
OKUNO Tatsusada  大阪大学, 医学系研究科, 助教 (00464248)
FUJIMURA Harutoshi  独立行政法人国立病院機構, 刀根山病院, 副病院長 (20263246)
KAWASAKI Hiroshi  金沢大学, 医学系, 教授 (50303904)
SHINMYO Yohei  金沢大学, 医学系, 准教授 (00418831)
SATO Makoto  金沢大学, 新学術創成研究機構, 教授 (30345235)
YASUGI Tetsuo  金沢大学, 新学術創成研究機構, 助教 (90508110)
Project Period (FY) 2015-04-01 – 2018-03-31
Keywordsexosome / α-synuclein
Outline of Final Research Achievements

Exosome is not only signal small vesicle which is utilized as cell-cell communication in various cells but also in neuronal cells. Even in neurodegenerative diseases, it is considered to be related to the pathological condition. In addition, multisystem atrophy, which is a disease related to Parkinson's disease, is the most doubtful as to elucidation of the propagation / aggregate formation to oligodendrocytes in which the main causative molecule α-synuclein (α-syn) is not originally expressed. Therefore, the propagation mechanism model of α-syn mediated by Exosome for multisystem atrophy was clarified. This was due to the fact that Rpn1 induces the exosome-mediated propagation of α-synuclein and the enhanced expression in glia cells at the transmission destination. Furthermore, functional promoting molecules of Rpn1 were also identified.

Free Research Field

神経科学一般

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Published: 2019-03-29  

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