| Project/Area Number |
08838004
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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 |
老化(加齢)
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| Research Institution | Gunma University |
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Principal Investigator |
YAMAGUCHI Haruyasu School of Health Sciences, Gunma University Professor, 医学部, 教授 (00158114)
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| Co-Investigator(Kenkyū-buntansha) |
SUGIHARA Shiro Gunma Cancer Center, Head of Pathology, 病理部, 部長
SATO Kumiko School of Health Sciences, Gunma University Professor, 医学部, 教授 (80008268)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Alzheimer's disease / dementia / amyloid-beta / apolipoprotein E / brain bank / brain aging / dementia / aging |
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| Research Abstract |
We did the following research works to reveal the enhancing and suppressing factors of cerebral beta amyloid deposition.
We corrected more than 40 brains from non-demented middle-aged subjects, and formed the Gunma Brain Bank. The samples from these brains were sent to several research institutes and universities, and are used for the research works on brain aging.
We immunostained the tissue sections from these brains, and revealed that cerebral beta amyloid deposition started in the fifth decades. We analyzed the Abeta species using 2 different kinds of antibodies directed to C-terminal end of Abeta, and found that Abeta42 was a major from in the early stage of cerebral beta amyloid deposition. Furthermore, we found Abeta-positive granules in astrocytes, which were associated with diffuse plaques. We suggest the positively that senile plaquse are removed by astrocytes.
We also analyzed the genotype of apolipoprotein E gene, and found high frequency of _<epsilon>4 genotype in the subjects with cerebral beta amyloid deposition.
We made antibodies directed to presenilin-1, a causative gene of the early-onset familial Alzheimer's disease, but found no relation between presenilin-1 immunoreactivity and beta amyloid deposition.
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