2014 Fiscal Year Final Research Report
Olfactory dysfunction in early Alzheimer's disease
| 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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| 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 |
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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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| Free Research Field |
感覚生理学
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