| Project/Area Number |
17K19884
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Health science and related fields
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| Research Institution | Tohoku University |
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Principal Investigator |
Kuranaga Erina 東北大学, 生命科学研究科, 教授 (90376591)
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| Project Period (FY) |
2017-06-30 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2018: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2017: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 神経変性 / ショウジョウバエ / 神経変性疾患 / 栄養因子 / プロテアソーム / 栄養 |
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| Outline of Final Research Achievements |
In this study, we aim to control the nutrient intake and its metabolites in order to reduce the onset and pathogenesis of neurodegenerative diseases. The aim of the study was to explore the mechanisms that can inhibit progression of the disease. We found that activation of the ubiquitin-proteasome system reduces symptoms in neurodegenerative disease systems. Confirmation. We screened for nutritional factors and drugs using life span extension as an indicator in neurodegenerative disease strains. Since glucose metabolism was assumed to be involved in the changes in lifespan, we screened for drugs that increase ATP production.The effectiveness of the drugs was examined using the following methods. The results showed that drugs that maintain ATP production were effective. We are planning to elucidate the action of these results in the future.
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| Academic Significance and Societal Importance of the Research Achievements |
疾患の発症メカニズムの理解には、疾患に関与する生体内タンパク質の同定やその機能解析がスタンダードかつ重要な方法である。しかし、そのタンパク質が臨床現場で実際に治療ターゲットとなりうるかに関しては改めて検討が必要であり、臨床のニーズから若干の乖離がある。本研究は栄養素という、神経変性疾患の研究ではあまり着目されておらず、かつ摂取の容易な細胞外物質を起点として解析を進めるため、全く新しい側面からの発症メカニズム解明と、臨床応用への橋渡しを同時に追求することが可能であると考えている。
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