Oligodendrocytic protein contribute to neuronal accumulation of alpha-synuclein in multiple system atrophy
| Project/Area Number |
25830045
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Institute for Developmental Research, Aichi Human Service Center (2014)
National Center for Geriatrics and Gerontology (2013) |
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Principal Investigator |
SUZUKI Yasuyo 愛知県心身障害者コロニー発達障害研究所, 遺伝学部, 研究員 (60416188)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | α-synuclein / 神経変性疾患 / 多系統萎縮症 / 神経科学 / 多系統委縮症 / シスタチンC |
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| Outline of Final Research Achievements |
Multiple system atrophy (MSA) is a neurodegenerative disease in which oligodendrocytes and neurons in the central nervous system are affected. To clarify how oligodendrocytic α-synuclein inclusions cause neuronal degeneration, we generated a transgenic mouse for an MSA model in which human wild-type α-synuclein was overexpressed selectively in oligodendrocytes. We established primary culture cells derived from the brain of transgenic mice, and revealed that insoluble mouse α-synuclein was progressively accumulated in neurons, leading to neuronal dysfunction and degeneration. In this study, we identified cystatin C as a neurodegeneration-inducing factor released from oligodendrocytes. Cystatin C triggers insoluble α-synuclein accumulation in neurons of the mouse central nervous system.
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Report
(3 results)
Research Products
(6 results)
