2015 Fiscal Year Final Research Report
A novel pathological mechanism of Alzheimer's disease as a chronic inflammation through RAGE signal activity.
| Project/Area Number |
25460649
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Applied pharmacology
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| Research Institution | Okayama University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NISHIBORI MASAHIRO 岡山大学, 大学院医歯薬学総合研究科, 教授 (50135943)
TERADA SEISHI 岡山大学, 大学院医歯薬学総合研究科, 准教授 (20332794)
LIU KEYUE 岡山大学, 大学院医歯薬学総合研究科, 助教 (40432637)
WAKE HIDENORI 岡山大学, 大学院医歯薬学総合研究科, 助教 (60570520)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | アルツハイマー / アミロイドβ / RAGE / AGE / 慢性炎症 / 神経 / ミクログリア / アストロサイト |
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| Outline of Final Research Achievements |
Alzheimer's disease (AD), which is considered that the main pathology is caused by accumulation of amyloid β in the brain, may have an aspect as chronic inflammation disease. We validated a novel mechanism of AD pathology that an inflammatory reaction through the receptor of advanced glycation end products (RAGE) is synergistically enhanced by increased amyloid β and anti-RAGE autoantibody in AD patients. Increased antibody titer against RAGE was shown in plasma of the AD patients, while an enhancements of immunoreactivity and an amyloid β binding to leukocytes were not detected in the AD patients. In future, we will evaluate whether examine plasma levels of the inflammatory factors are up-regulated or not in AD patients.
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| Free Research Field |
薬理学
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