| Project/Area Number |
26830042
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Gunma University |
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Principal Investigator |
Ishizuka Yuta 群馬大学, 医学(系)研究科(研究院), 助教 (50614179)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 神経細胞 / シナプス / 樹状突起スパイン / Drebrin / アルツハイマー病 / Aβオリゴマー / エピジェネティクス / ヒストン脱アセチル化酵素 / drebrin |
|---|
| Outline of Final Research Achievements |
We demonstrate that ADDLs induce drebrin loss from dendritic spines in cultured hippocampal neurons without reducing drebrin expression or dendritic protrusion density. In addition, the inhibition of HDAC by SAHA attenuated ADDL-induced drebrin loss from dendritic spines. These results strongly suggest that the regulation of histone acetylation/deacetylation plays an important role in modulating actin cytoskeletal dynamics by inducing gene expression under cellular stress. Our findings provide insight into the mechanisms of amyloid toxicity and suggest that HDAC inhibitors may hold therapeutic potential in neuropsychiatric disorders, such as Alzheimer's disease and depression.
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