| Project/Area Number |
18500279
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Nerve anatomy/Neuropathology
|
|---|
| Research Institution | Saitama Medical University |
|---|
Principal Investigator |
MORI Takashi Saitama Medical University, 医学部, 准教授 (60239605)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Haruyasu 群馬大学, 医学部, 教授 (00158114)
ASANO Takao 埼玉医科大学, 医学部, 客員教授 (70090496)
|
|---|
| Project Period (FY) |
2006 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥690,000)
Fiscal Year 2009: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2008: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2007: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2006: ¥1,300,000 (Direct Cost: ¥1,300,000)
|
|---|
| Keywords | 神経科学 / 脳神経変性疾患 / 神経病理学 / 細胞・組織 / 獣医学 / 脳神経疾患 / 病理学 |
|---|
| Research Abstract |
Here, we aimed to examine the possible role of astrocyte-derived S100B in the progression of Alzheimer's disease pathology. First, using Alzheimer's disease model mice, we showed that Alzheimer's disease-like pathology was significantly ameliorated by the treatment of arundic acid [(R)-(-)-2-propyloctanoic acid], which is known to negatively regulate astrocyte synthesis of S100B. Subsequently, to dissect the relationship between S100B and Alzheimer's disease-like pathology, we took a genetic approach by crossing transgenic mice expressing human S100B with Alzheimer's disease model mice. We demonstrated evidence that (over)-expression of S100B acts to accelerate Alzheimer's disease-like pathology. Taken together, these data suggest that inhibiting astrocytic activation by blocking S100B biosynthesis may be a promising therapeutic strategy to delay Alzheimer's disease progression.
|
