| Project/Area Number |
15K14956
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Biological pharmacy
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| Research Institution | Tokyo University of Agriculture and Technology |
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Principal Investigator |
Tsukakoshi Kaori 東京農工大学, 工学(系)研究科(研究院), 助教 (20708474)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | アミロイドβ / オリゴマー / 凝集 / アルツハイマー病 |
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| Outline of Final Research Achievements |
Amyloid β (Aβ) consists of senile plaques that are pathological hallmarks of Alzheimer’s disease (AD). Many studies suggest Aβ oligomers possess toxic effects on the neuronal cells. However, it is still unclear what kind of Aβ oligomers arise in vivo and exist in the brain. In this study, I investigated generation process of Aβ oligomers in vivo by investigation of AD-model mice. As AD-model mice are being aged, aggregated Aβ is gradually increased in the brain, so that Aβ oligomers also accumulate in brain of AD-model mice during fibrillization.
I found that low-molecular-weight of Aβ oligomers was generated in membrane-enriched fraction of AD-model mouse brain. I also showed Aβ oligomers was generated from Aβ fibrils by disaggregation. Thus, Aβ oligomers may be processed by aggregation and disaggregation in vivo.
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