| Project/Area Number |
17590880
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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 | Hiroshima University |
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Principal Investigator |
TAKAHASHI Tetsuya (2006) Hiroshima University, Graduate School of Biomedical Sciences, Assistant professor (00435942)
山下 拓史 (2005) 広島大学, 大学院・医歯薬学総合研究科, 助手 (20311813)
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| Co-Investigator(Kenkyū-buntansha) |
HATTORI Nobutaka Juntendo, University, School of Medicine, Professor (80218510)
MATSUMOTO Masayasu Hiroshima University, Graduate School of Biomedical Sciences, Professor (20192346)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2005: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | neurological disorder / neuroscience / gene / protein |
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| Research Abstract |
Synphilin-1 is a protein reported as a component of Lewy bodies, which characterize Parkinson's disease pathologically. In this study, we established synphilin-1 transgenic mice to analyze as model animal of Parkinson's disease.
We generated transgenic mice expressing human synphilin-1 under the prion protein promoter.
Synphilin-1 was widely expressed in neurons in the brain including the substantia nigra, where massive loss of dopamine neurons was not observed.
In the transgenic mouse brain, synphilin-1 protein was polyubiquitinated, and partially insoluble.
Although modified-SHIRPA revealed no significant difference in behavior and morphology, the reduced rotarod performance and step length were observed in transgenic mice as compared with non-transgenic littermates. Synphilin-1 might be involved in motor function, and its accumulation in the central nervous system can cause motor impairments.
We are now analyzing the mechanisms, by which transgenic mice showed motor impairment through the measurement of dopamine-metabolies in brain by HPLC.
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