Mitochondrial hyperactivity as a potential therapeutic target in Parkinson's disease

Danielle E. Mor, Coleen T. Murphy

Research output: Contribution to journalArticle

1 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)117-120
Number of pages4
JournalTranslational Medicine of Aging
Volume4
DOIs
StatePublished - 2020

All Science Journal Classification (ASJC) codes

  • Geriatrics and Gerontology
  • Aging
  • Physiology
  • Cell Biology
  • Clinical Neurology

Keywords

  • Branched-chain amino acid metabolism
  • Hyperactive mitochondria
  • Mitochondrial homeostasis
  • Parkinson's disease

Fingerprint Dive into the research topics of 'Mitochondrial hyperactivity as a potential therapeutic target in Parkinson's disease'. Together they form a unique fingerprint.

  • Cite this