| Project/Area Number |
17K19190
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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 |
Biomolecular chemistry and related fields
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| Research Institution | Tohoku University |
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Principal Investigator |
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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: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2017: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | 神経変性疾患 / 細胞小器官 |
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| Outline of Final Research Achievements |
The accumulation of protein aggregates and dysfunctional mitochondria is a common feature of neurodegenerative diseases. The present study aimed to enable selective removal of dysfunctional mitochondria by selective autophagy.
Using an unpublished small molecule that locally recruits selective autophagy, I developed conditions to deliver this molecule to the outer mitochondrial membrane. Degradation of the dysfunctional mitochondria was observed and mitochondrial morphology, its membrane potential, and ATP production were found to be improved.
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| Academic Significance and Societal Importance of the Research Achievements |
疾患の原因となる物質を取り除く手法ができれば、直裁的な分子治療戦略になります。神経変性疾患では、根本的な治療法が存在しないことも多いため、今回の研究を企画しました。昨日が低下したミトコンドリアにオートファジーを呼び寄せることによって分解除去する可能性が示されました。今回の実験は、培養細胞を用いた基礎研究であり、疾患モデル動物など、より高次な評価系で検討を継続する必要があります。
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