| Project/Area Number |
18K19682
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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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| Review Section |
Medium-sized Section 58:Society medicine, nursing, and related fields
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| Research Institution | Hiroshima University |
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Principal Investigator |
Kotake Yaichiro 広島大学, 医系科学研究科(薬), 教授 (20335649)
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| Co-Investigator(Kenkyū-buntansha) |
宮良 政嗣 岐阜薬科大学, 薬学部, 研究員 (60816346)
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| Project Period (FY) |
2018-06-29 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2019: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2018: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 糖尿病 / パーキンソン病 / 低グルコース / MPTP |
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| Outline of Final Research Achievements |
We experimentally tried to evaluate epidemiological survey that the risk of Parkinson’s disease is high in diabetic patients. However, we were not able to show clear data. Whereas, we investigated the differences of the reactivity of parkinsonian toxin MPP+ against primary cortical neurons and neuroblastoma. As the results, MPP+ did not activate acetyl-CoA carboxylase (ACC) though it activated AMPK only in cortical neurons. Such differences in energy metabolism between primary neurons and neuroblastoma may lead to experimentally clarify that diabetes is associated with an increased risk of Parkinson's disease.
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| Academic Significance and Societal Importance of the Research Achievements |
糖尿病がパーキンソン病発症のリスクを高めるという疫学調査の動物実験による解明を試みたが、有意な結果は得られなかった。体重増加による運動機能低下とパーキンソン病態のそれを区別することが難しかったのがその一因として考えられる。一方、初代培養神経細胞と神経芽細胞腫はエネルギー代謝の面で異なる点が認められ、これは上記調査結果のメカニズムを考える上で有用な知見であると考えられる。
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