Analysis of the relationship between an accumulation of mutant mtDNA and the mitochondrial quality control in Parkinsonism

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K21081
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Neurochemistry/Neuropharmacology; Laboratory animal science
• Research Institution: Shiga University of Medical Science
• Principal Investigator: Fuke Satoshi 滋賀医科大学, 医学部, 助教 (20422660)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: ミトコンドリア / パーキンソン病 / ミトコンドリアDNA / Parkin / Polg

Outline of Final Research Achievements

To elucidate the physiological significance of relationships between an accumulation of mutant mtDNA molecules and the mitochondrial quality control depending on mitophagy in Parkinson’s disease, a role of mitophagy due to Parkin in mtDNA dynamics was assessed. In a mouse neuroblastoma cell line (Neuro2a), we found that there are not a few Parkin-nonlocalized mitochondria that were undegraded after the induction of mitophagy by FCCP mitochondrial depolarizing agent. These result suggest that the mitochondrial depolarization is necessary but not enough for the removal of damaged mitochondria through mitophagy.

Free Research Field

分子神経生物学