| Project/Area Number |
20591418
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Psychiatric science
|
|---|
| Research Institution | Kitasato University |
|---|
Principal Investigator |
HIRUMA Hiromi Kitasato University, 医学部, 准教授 (10238397)
|
|---|
| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2009: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2008: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
|
|---|
| Keywords | アンギオテンシンII / アミロイドβ蛋自 / 軸索障害 / 軸索輸送 / アミロイドベータ蛋白 / アクチン / アンギオテンシン受容体 / 培養海馬ニューロン / アルツハイマー病 / アミロイド蛋白β |
|---|
| Research Abstract |
Amyloid (3 protein (A(3), a causal agent of Alzheimer's disease,damages axons of neurons through actin polymerization. The present study investigated the modifying effects of angiotensin II (AngII), a vasoconstrictive hormone, on A(3 action and obtained the following results. 1) Similar to A(3, AngII decreased axonal transport and constricted axons. These effects are mediated by AngII AT1 receptors and actin polymerization. 2) AngIl enhanced the A1-induced inhibition of axonal transport and constriction of axons. Therefore, AngII is suggested to enhance A(3-induced impairment of axons via actin polymerization.
|
