| Project/Area Number |
21300135
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | 財団法人東京都医学総合研究所 (2011)
Tokyo Metropolitan Organization for Medical Research (2009-2010) |
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Principal Investigator |
HASHIMOTO Makoto 財団法人東京都医学総合研究所, 運動・感覚システム研究分野, 副参事研究員 (50189502)
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| Co-Investigator(Kenkyū-buntansha) |
WAKABAYASHI Koichi 弘前大学, 医学部, 教授 (50240768)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥9,100,000 (Direct Cost: ¥7,000,000、Indirect Cost: ¥2,100,000)
Fiscal Year 2011: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2010: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2009: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | アミロイド / シヌクレイン / パーキンソン病 / レビー小体 / 神経変性疾患 / 蛋白凝集 / 遺伝子変異 / レビー小体型認知症 / トランスジェニックマウス / ルイ小体 |
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| Research Abstract |
We show that transgenic(tg) mice expressing DLB-linked P123Hβs develop progressive neurodegeneration, as characterized by axonal swelling, astrogliosis and behavioural abnormalities, such as memory disorder. Furthermore, cross-breeding of P123Hβs tg mice withαs tg mice, greatly enhanced neurodegeneration phenotypes, suggesting that P123Hβs is pathogenic and cooperates with s to stimulate neurodegeneration in mouse brain. Thus, it is expected that P123Hβs tg mice will be a invaluable tool for the elucidation of the mechanism and development of novel treatment forα-synucleinopathies.
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