| Project/Area Number |
26350982
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Basic / Social brain science
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| Research Institution | Toho University |
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Principal Investigator |
SONE Masaki 東邦大学, 理学部, 准教授 (00397548)
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| Co-Investigator(Kenkyū-buntansha) |
田村 拓也 東京医科歯科大学, 難治疾患研究所, 助教 (80396647)
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| Co-Investigator(Renkei-kenkyūsha) |
OKAZAWA Hitoshi 東京医科歯科大学, 難治疾患研究所, 教授 (50261996)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | ショウジョウバエ / 神経変性 / 神経変性疾患 / アルツハイマー病 / 認知症 / 細胞内タンパク質輸送 / シナプス / 小胞輸送 |
|---|
| Outline of Final Research Achievements |
We have clarified that abnormalities in the regulatory mechanisms of intracellular protein trafficking cause neurodegeneration. In this study, we focused on the Drosophila yata gene which regulates intracellular trafficking of APP that is a causative molecule of Alzheimer's disease. We revealed that specific inhibition of synaptic transport of APP significantly ameliorates the pathology of the Drosophila model of Alzheimer's disease. We also analyzed the causative molecule of frontotemporal dementia and found that impaired neural development causes neurodegeneration.
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