A study of the effect of EP receptor inhibitors on Alzheimer's disease
| Project/Area Number |
15K19752
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Psychiatric science
|
|---|
| Research Institution | Hyogo Medical University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| Keywords | ミクログリア / プロスタグランジン / インターフェロン |
|---|
| Outline of Final Research Achievements |
Prostaglandin E2 (PGE2) potentiated interferon-γ (IFN-γ)-induced nitric oxide production in cultured rat microglia. Instead of PGE2, EP2 agonist, butaprost, enhanced IFN-γ-induced nitric oxide production, and EP2 antagonist, TG4-155, reversed the effect of PGE2 on IFN-γ-induced nitric oxide production. These results suggest that PGE2 activates EP2 receptor, which potentiates IFN-γ-induced nitric oxide production. PGE2 is also reported to reduce phagocytosis of amyloid-β in microglia, indicating that Alzheimer's disease is exacerbated by PGE2 signaling. It is, therefore, suggested that the inhibition of PGE2 signaling is a potential strategy for the treatment of Alzheimer's disease.
|
Report
(4 results)
Research Products
(2 results)
