| Project/Area Number |
21800064
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Waseda University |
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Principal Investigator |
MATSUDA Nanami Waseda University, 先端科学・健康医療融合研究機構, 講師 (70360641)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥2,652,000 (Direct Cost: ¥2,040,000、Indirect Cost: ¥612,000)
Fiscal Year 2010: ¥1,261,000 (Direct Cost: ¥970,000、Indirect Cost: ¥291,000)
Fiscal Year 2009: ¥1,391,000 (Direct Cost: ¥1,070,000、Indirect Cost: ¥321,000)
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| Keywords | 神経変性疾患 / パーキンソン病 / 筋萎縮性軸索硬化症(ALS) / ショウジョウバエ / エネルギー代謝 / 病態モデル / 神経細胞死 / 老化 |
|---|
| Research Abstract |
There is increasing evidence that neurodegenerative diseases are a symptom of a deficiency in the regulation of mitochondrial function and metabolism, however the mechanism has been unclear. Mitochondria, as the central organelles in metabolic regulation might have a role to play in the common etiology of neurodegeneration. To address the roles of metabolic defect in neurodegenerative diseases, we established RNA interference-mediated Drosophila parkin (dparkin) knockdown flies and Drosophila ALS2/alsin (dALS2) knockdown flies, for Parkinson's disease and juvenile onset recessive familial amyotrophic lateral sclerosis (ALS2) models, respectively. We demonstrate that nervous system-specific knockdown of dparkin or dALS2 caused shorter lifespan and lower locomotor activity. Currently we are exploring the relevance of abnormality of metabolism and mitochondrial dysfunction in neurodegenerative pathogenesis caused by deficiency of parkin or ALS2.
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