| Project/Area Number |
23700433
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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 | Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
MASUDA-SUZUKAKE Masami 公益財団法人東京都医学総合研究所, 認知症・高次脳機能研究分野, 研究員 (20583751)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 国際情報交流 / αシヌクレイン / 神経変性疾患 / プリオン / パーキンソン病 / レビー小体型認知症 / 国際情報交換 / レビー小体 / モデルマウス / タウ |
|---|
| Research Abstract |
Alpha-Synuclein (asyn) is the major component of filamentous inclusions that constitute the defining characteristic of Parkinson's disease and dementia with Lewy bodies. However, the molecular mechanisms underlying asyn accumulation and spread are unclear.
In this study, we show that intracerebral injections of fibrils of recombinant asyn efficiently induced asyn pathologies in wild-type mice, whereas mice injected with soluble asyn did not. Immunoblot analysis demonstrated that endogenous mouse asyn started to accumulate 3 months after inoculation, while injected human asyn fibrils disappeared in about a week. These results indicate that asyn fibrils have prion-like properties and inoculation into wild-type brain induces asyn pathology in vivo. This is a new mouse model of sporadic asynucleinopathy, and should be useful for elucidating progression mechanisms and evaluating disease-modifying therapy.
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