The study on microglial activation by beta amyloid, peptides of Alzheimer's disease.
| Project/Area Number |
15591230
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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 |
Psychiatric science
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
MONJI Akira Kyushu University, University Hospital, Research Associate, 大学病院, 助手 (00294942)
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| Co-Investigator(Kenkyū-buntansha) |
NAKANISHI Hiroshi Kyushu University, Graduate School of Dental Sciences, Professor, 大学院・歯学研究院, 教授 (20155774)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | beta amyloid / microglia / Alzheimer / cytokine / free radical / bota-amilaid / microglio / Alzheimer / inflammation / cytokine / free radical / 炎症 |
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| Research Abstract |
There is increasing evidence that inflammatory activation of microglia has pathogenic infuence on Alzheimer's disease(AD). According to in vitro studies, microglia activated by beta amyloid (Abeta) peptides have been reported to damage or kill neurons by the release of neirotoxic molecules such as tumor necrosis factor-alpha(TNF-alfa), nitric oxide, or reactive oxygen species. This study has demonstrated the two following results on microglial activation by the A beta peptides.
1.Abeta fbril formation is not necessarily required for microglial activation by the peptides.
2.PS(phosphatidylserine)-liposomes can inhibit microglial activation by the Abeta peptides and suppress the generation of TNF-alfa, nitric oxide, and reactive oxygen species from microglia.
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Report
(3 results)
Research Products
(4 results)
