| Project/Area Number |
25460649
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Applied pharmacology
|
|---|
| Research Institution | Okayama University |
|---|
Principal Investigator |
|
|---|
| 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)
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
|---|
| 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 / 炎症 / 神経細胞 |
|---|
| 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.
|
