Does an activation of RAR improve Alzheimer disease by the expression of transthyretin?
| Project/Area Number |
21700409
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KITAOKA Kazuyoshi The University of Tokushima, 大学院・ヘルスバイオサイエンス研究部, 助教 (50432753)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 老化 / アルツハイマー病 / レチノイン酸 / Adam10 / トランスサイレチン / 神経科学 / 学習 / ビタミンA |
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| Research Abstract |
I investigate the mechanism of anti-Alzheimer effect of retinoic acid receptor activation focused on the transthyretin (TTR), by using senescence accelerated (SAMP8) mice. As the results, the activation of RAR improves the memory function of SAMP8. However, the protein expression of TTR was not shown. On the other hands, Adam10 protein, which has α-secretase activity and correlates with neurogenesis, is significantly recovered by the RAR activation. The effect of Adam10-derivedα-secretase activity for amyloid beta is not clear because SAMP8 mice did not show the deposit of amyloid beta in this study. However, the expression of Hes5, which associates with neurogenesis, showed the significant increase in RAR-activated SAMP8 mice. Besides that, the expression of Adam10 and Hes5 are significantly correlated. The results in this study suggest that the RAR activation is improved memory function of SAMP8 by the recovery of Adam10 expression.
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Report
(3 results)
Research Products
(12 results)
