1998 Fiscal Year Final Research Report Summary
Analysis of pathological phenotypes of familial Alzheimer's disease-associated gene mutations in presenilin.
| Project/Area Number |
09672271
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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 |
Biological pharmacy
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| Research Institution | RIKEN Brain Science Institute |
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Principal Investigator |
SAIDO Takaomi C. RIKEN Brain Scinece Institute, Laboratory for Proteolytic Neuroscience, Laboratory Head., 神経蛋白制御研究チーム, チームリーダー(研究職) (80205690)
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| Co-Investigator(Kenkyū-buntansha) |
MARUYAMA Kei National Institute for Physiological Sciences and Graduate University for Advanc, 生理学研究所, 助教授 (30211577)
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| Project Period (FY) |
1997 – 1998
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| Keywords | ALZHEIMER'S DISEASE / PRESENILIN / beta-AMYLOID / SECRETASE |
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| Research Abstract |
Familial Alzheimer's disease is caused by mutations in several independent genes, among which presenilin mutations account for the majority of cases. Identification of pathological phenotypes of presenilin mutations would contribute to understanding the mechanism of other forms of Alzheimer's disease including sporadic Alzheimer's disease. We have discovered that the pathogenic mutations cause an increase in cellular production of 42mer beta-amyloid peptide, strongly supporting the role of beta-amyloid in Alzheimer's disease development. Furthermore, we identified a calcium-binding protein that interacts with presenilin in cells. This indicates that presenilin may influence cellular functions through influencing calcium-associated signal transduction and/or homeostasis.
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