| Project/Area Number |
21590298
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Fukuoka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MISHIMA Kenichi 福岡大学, 薬学部, 准教授 (00320309)
TAKASAKI Kotaro 福岡大学, 薬学部, 助教 (70461506)
KATSURABAYASHI Shutaro 福岡大学, 薬学部, 助教 (50435145)
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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 |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 脳循環障害 / アルツハイマー病 / PPARγ / 動物モデル / 炎症性サイトカイン / TNFα / HMGB1 / Telmisartan / 迷路学習 / アポトーシス / β-アミロイド / アルツハマー病 |
|---|
| Research Abstract |
We made Alzheimer's disease model animals to complicate cerebrovascular disorders, and we proved that defects of memory such as the maze learning disability aggravated. It was supposed that the temporal increase of inflammatory cytokines including TNFα and HMGB1 and apoptosis of neurons in the hippocampus CA1 leaded with the onset of dementia by the cerebrovascular disorders. Furthermore, We were able to improve a spatial memory disorder by activating PPARγwith anti-inflammatory effect and anti-apoptosis effect. It was proved that drugs with PPARγ agonist effect could become the dementia therapeutic drug than this study.
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