| Project/Area Number |
24770064
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Animal physiology/Animal behavior
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 嗅覚障害 / 神経回路 / X11 / アミロイド / 嗅球 / ドネぺジル / 経鼻投与 / アルツハイマー病 / 加齢 / 嗅覚 / 嗅細胞 |
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| Outline of Final Research Achievements |
Alzheimer's disease (AD) is a neurodegenerative disorder associated with the progressive impairment of cognition. The olfactory dysfunction occurs early in AD. However, the mechanism behind the dysfunction remains largely unknown. In this study, we tried to understand how Amyloid-β peptide (Aβ) induces the olfactory dysfunction, using transgenic mice deleting amyloid precursor protein binding protein, X11, that regulates amyloidogenesis. The young KO mice, that showed normal olfaction, have the higher level of soluble Aβ in the olfactory bulb (OB) than the wild-type mice. The KO mice accumulated the insoluble Aβ abundantly by aging. The Aβ aggregation might reduce an activity in the neural circuit of the OB and induce the olfactory dysfunction. Additionally, donepezil, an acetylcholinesterase inhibitor, prevented the Aβ aggregation in the OB, and improved the impaired olfactory function.
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