2015 Fiscal Year Final Research Report
Strategy for overcoming Alzheimer's disease based on Zn2+-mediated cognitive decline
| Project/Area Number |
25293032
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Environmental and hygienic pharmacy
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| Research Institution | University of Shizuoka |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 亜鉛 / アミロイドβ / 海馬 / アルツハイマー病 / 記憶 |
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| Outline of Final Research Achievements |
The hippocampus plays important roles for spatial and declarative memory. Zn2+ is released from glutamatergic (zincergic) neuron terminals in the hippocampus and serves as a signal factor. Synaptic Zn2+ homeostasis is critical for cognitive activity in the hippocampus. Amyloid-β (Aβ) is a candidate for the pathogenesis of Alzheimer’s disease (AD) and interacts with Zn2+. Aβ1-42 interacted with extracellular Zn2+ and was taken up into dentate granule cells, followed by transiently cognitive decline via attenuated LTP. Zn-Aβ1-42-mediated cognitive decline was rescued by extracellular and intracellular Zn2+ chelators. The present study indicates that extracellular Zn2+ in the hippocampus is a therapeutic target for AD.
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| Free Research Field |
神経科学
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