| Project/Area Number |
15K06710
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurophysiology / General neuroscience
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
HANAYAMA Rikinari 金沢大学, 医学系, 教授 (40403191)
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| 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)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | exosome / α-synuclein / Exosome / 脳神経疾患 / α-synucelin |
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| 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.
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