A study of microglial function to cure Alzheimer disease
| Project/Area Number |
23791358
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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 |
Psychiatric science
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ミクログリア / アポトーシス / 細胞死 / プロスタグランジン / cyclic AMP / GSK-3 / PGE2 / EP2 / EP4 |
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| Research Abstract |
PGE2 reduced cell viability in cultured rat microglia. This reduction in cell viability was due to apoptosis. Microglial apoptosis was also induced by two PGE2 receptor agonists, an EP2 agonist butaprost and an EP4 agonist PGE1 alcohol. However, PGE2-reduced cell viability was not reversed by EP1 - EP4 antagonists. On the other hand, PGE2-reduced cell viability was reversed by GSK-3 inhibitor SB216763. In addition, phsophorylated GSK-3 level was reduced by PGE2. There data suggest that PGE2 induces apoptosis in microglia, and this apoptosis is involved in GSK-3.
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Report
(4 results)
Research Products
(3 results)
