| Project/Area Number |
24800015
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2012-08-31 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 脳神経疾患 / 神経科学 / アルツハイマー病 / アミロイドβタンパク質 / アポリポプロテインE / アミロイドβ蛋白質 |
|---|
| Research Abstract |
To elucidate the mechanism of the metabolism of amyloid beta peptide (Abeta) oligomers in the brain, we have developed in vivo microdialysis technique using a 1,000 kDa cut-off microdialysis probe. Using this techqnique, we identified that the clearance rate of Abeta in the brain of plaque-bearing APP transgenic mice was significantly slower than that in the brain of plaque-free APP transgenic mice. We also identified that the level of ISF Abeta in the brain of APP / CLAC double transgenic mice was significantly lower than that of APP transgenic mice. These observations suggested that amyloid plaque affect the metabolism of Abeta monomer and oligomers in the brain. We have also developed an easy and high-sensitive method to evaluate the interaction between Abeta and apoE using a plit-luciferase complementation assay.
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