| Project/Area Number |
15590874
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | TOHOKU UNIVERSITY |
|---|
Principal Investigator |
TAKEDA Atsushi Tohoku University, Hospital, Lecturer, 病院, 講師 (70261534)
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|---|
| Project Period (FY) |
2003 – 2005
|
| Project Status |
Completed (Fiscal Year 2005)
|
| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
|
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| Keywords | alpha-synuclein / neuronal death / quinone / dopamine oxidation / Parkinson disease / Multiple system atrophy / synucleinopathy / 細胞モデル / カテコラミン |
|---|
| Research Abstract |
The α-synuclein is a key molecule in the pathogenesis of synucleinopathy including Parkinson's disease and multiple system atrophy. We mainly focused on recent data obtained by cellular models for synucleinopathy and discussed possible mechanisms of neurodegeneration. Recent progress suggests that aggregate formation of α-synuclein is cytoprotective and that its precursor oligomer (protofibril) may be cytotoxic. The catechol-derived quinones are candidate molecules to facilitate the oligomer formation of α-synuclein. Furthermore, the cellular membranes are shown to be primary targets injured by mutant α-synucleins and the mitochondrial dysfunction seems to be an initial step in the neuronal death.
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