| Project/Area Number |
23790974
|
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurology
|
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
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| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 脳・神経 / タンパク質 / パーキンソン病 / グルコセレブロシダーゼ / αシヌクレイン / カテプシン |
|---|
| Research Abstract |
Recent report showed glucocerebrosidase (GBA) mutation is a risk of PD, however, precise function between GBA mutation and neuronal degeneration. In this study, we explored the function of GBA mutation in its pathological process. GBA mutation fibroblasts showed apoptotic cell death after addition of mitochondrial toxin or starvation. Moreover, lysosomal enzyme, cathepsin B (CTSB) activity was significantly reduced. But we could not clearly show thatlpha-synuclein is the substrate of CTSB.
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