| Project/Area Number |
24659349
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
General internal medicine (including Psychosomatic medicine)
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| Research Institution | Osaka University |
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Principal Investigator |
SATO Naoyuki 大阪大学, 医学(系)研究科(研究院), 准教授 (70372612)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 糖尿病 / アルツハイマー病 / βアミロイド / 認知症 / 脳科学 / 分子生物学 / ベータ・アミロイド / 相互病態修飾 / 糖代謝 |
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| Research Abstract |
We previously showed that Alzheimer's disease (AD) aggravates the diabetic phenotype in mice. To explore this mechanism, we initiated to create APP Tet-off mice. Plasma Abeta may mediate peripheral insulin resistance. We found plasma Abeta level is increased after glucose loading in an AD model. In humans, although the magnitude of changes is much smaller than in AD transgenic mice, the changes in plasma Abeta levels after oral glucose loading are different between AD and non-AD patients. These data suggest that one of the possible mechanisms by which AD aggravates the diabetic phenotype might be attributable to plasma Abeta. We are now constructing APP Tet-off plasmid and will create APP tet-off mice to control the periods of APP expression and exposure to diabetes.
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