The Parkinson Disease Mitochondrial Hypothesis: Where Are We at?

Sandra Franco-Iborra, Miquel Vila, Celine Perier

Research output: Contribution to journalReview articleResearchpeer-review

100 Citations (Scopus)


© SAGE Publications. Parkinson's disease is a common, adult-onset neurodegenerative disorder whose pathogenesis is still under intense investigation. Substantial evidence from postmortem human brain tissue, genetic- and toxin-induced animal and cellular models indicates that mitochondrial dysfunction plays a central role in the pathophysiology of the disease. This review discusses our current understanding of Parkinson's disease-related mitochondrial dysfunction, including bioenergetic defects, mitochondrial DNA alterations, altered mitochondrial dynamics, activation of mitochondrial-dependent programmed cell death, and perturbations in mitochondrial tethering to the endoplasmic reticulum. Whether a primary or secondary event, mitochondrial dysfunction holds promise as a potential therapeutic target to halt the progression of neurodegeneration in Parkinson's disease.
Original languageEnglish
Pages (from-to)266-277
Issue number3
Publication statusPublished - 1 Jan 2016


  • apoptosis
  • complex I
  • fusion/fission
  • mitochondria-associated endoplasmic reticulum membranes
  • mtDNA


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