| Project/Area Number |
22700386
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | National Center for Geriatrics and Gerontology |
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Principal Investigator |
SUZUKI Yasuyo 独立行政法人国立長寿医療研究センター, バイオリソース研究室, 特任研究員 (60416188)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 神経変性疾患 / 多系統萎縮症 / α-synuclein / 多系統委縮症(MSA) / オリゴデンドロサイト / トランスジェニックマウス / タンパク質精製 / 多系統萎縮症(MSA) |
|---|
| Research Abstract |
Multiple system atrophy(MSA) is a neurodegenerative disease in which oligodendrocytes and neurons in the central nervous system are affected. To clarify how oligodendrocyticα-synuclein inclusions cause neuronal degeneration, we generated a transgenic mouse for an MSA model in which human wild-typeα-synuclein was overexpressed selectively in oligodendrocytes. We established primary culture cells derived from the brain of transgenic mice, and revealed that insoluble mouseα-synuclein was progressively accumulated in neurons, leading to neuronal dysfunction and degeneration. In this study, we identified neurodegeneration-inducing factor released from oligodendrocytes.
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