Mitochondrial hyperactivity as a potential therapeutic target in Parkinson's disease. Author Danielle Mor, Coleen Murphy Publication Year 2020 Type Journal Article Abstract Mitochondrial dysfunction is thought to contribute to neurodegeneration in Parkinson's disease (PD), yet the cellular events that lead to mitochondrial disruption remain unclear. Post-mortem studies of PD patient brains and the use of complex I inhibitors to model the disease previously suggested a reduction in mitochondrial activity as a causative factor in PD, but this may represent an endpoint in the disease process. In our recent studies, we identified a novel link between branched-chain amino acid metabolism and PD, and uncovered mitochondrial hyperactivity as a potential alternative mechanism of PD pathogenesis. Increased mitochondrial activity may occur in a subset of PD patients, or may be a more common early event that precedes the ultimate loss of mitochondrial function. Therefore, it may be that any imbalance in mitochondrial activity, either increased or decreased, could cause a loss of mitochondrial homeostasis that leads to disease. An effective therapeutic strategy may be to target specific imbalances in activity at selective stages of PD or in specific patients, with any efforts to reduce mitochondrial activity constituting a surprising new avenue for PD treatment. Journal Transl Med Aging Volume 4 Pages 117-120 Date Published 2020 ISSN Number 2468-5011 DOI 10.1016/j.tma.2020.07.007 Alternate Journal Transl Med Aging PMCID PMC7653964 PMID 33178902 PubMedPubMed CentralGoogle ScholarBibTeXEndNote X3 XML