Mechanism by which the pathogenesis of Parkinson's disease is stimulated by Gaucher's mutation.
Project/Area Number |
23659462
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Neurology
|
Research Institution | Tokyo Metropolitan Institute of Medical Science |
Principal Investigator |
HASHIMOTO Makoto 公益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)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | シヌクレイン / パーキンソン病 / ゴーシェ病 / リソソーム / オートファゴソーム |
Research Abstract |
We observed that axonal globules are formed in both αsynuclein (αS)- and P123H Βsynuclein (βS) transgenic mice. Lysosomal pathology was similarly observed for both αS- and P123H βS-globules, while oxidative stress was associated with the αS-globules, and to a lesser extent with the P123H βS-globules. Other pathologies, such as mitochondrial alteration and LRRK2 accumulation, were exclusively detected for αS-globules. Collectively, both αS- and P123H βS-globules were formed through similar but distinct pathogenic mechanisms.
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Report
(3 results)
Research Products
(14 results)