| Project/Area Number |
26860052
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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 |
Biological pharmacy
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| Research Institution | National Institute for Minamata Disease (2018)
Gakushuin University (2016)
National Center for Geriatrics and Gerontology (2014-2015) |
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Principal Investigator |
Sumioka Akio 国立水俣病総合研究センター, その他部局等, 主任研究員 (00431320)
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| Project Period (FY) |
2014-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | アルツハイマー病 / タウ / 脂質 / 神経細胞 |
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| Outline of Final Research Achievements |
Alzheimer’s Disease (AD) is the most prevailing dementia in Japan, and developing treatment for the disease is required. In this study, we focused on that tau pathology including their over-phosphorylation and aggregation, as AD causative factor, is regulated by lipid bilayers, and aim to elucidate the mechanism of tau pathology and develop the approach for their inhibition. As an accomplishment of this study, it is found that lipid X1, which specifically interact with tau, can regulate tau pathology in vivo. We established a platform to validating tau aggregation and phosphorylation at cell culture experiment. It is elucidated a new mechanism underlying toxicity of tau pathology.
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| Academic Significance and Societal Importance of the Research Achievements |
アルツハイマー病 (AD) の神経細胞死の進行は、タウの病変で形成する神経原線維変化（NFT）と一致している。本研究成果は、タウの病変形成のメカニズムを理解し、これを防ぐ方法を開発することに役立つ。特に新たに構築した培養細胞系でタウの凝集検証する実験系は、タウの病変を防ぐ薬剤探索への利用が期待でき、より簡便な手法による検出法を開発中である。
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