Mitochondrial alterations in Parkinson's disease: New clues

Miquel Vila, David Ramonet, Celine Perier

Research output: Contribution to journalReview articleResearchpeer-review

105 Citations (Scopus)

Abstract

Mitochondrial dysfunction has long been associated with Parkinson's disease (PD). In particular, complex I impairment and subsequent oxidative stress have been widely demonstrated in experimental models of PD and in post-mortem PD samples. A recent wave of new studies is providing novel clues to the potential involvement of mitochondria in PD. In particular, (i) mitochondria-dependent programmed cell death pathways have been shown to be critical to PD-related dopaminergic neurodegeneration, (ii) many disease-causing proteins associated with familial forms of PD have been demonstrated to interact either directly or indirectly with mitochondria, (iii) aging-related mitochondrial changes, such as alterations in mitochondrial DNA, are increasingly being associated with PD, and (iv) anomalies in mitochondrial dynamics and intra-neuronal distribution are emerging as critical participants in the pathogenesis of PD. These new findings are revitalizing the field and reinforcing the potential role of mitochondria in the pathogenesis of PD. Whether a primary or secondary event, or part of a multi-factorial pathogenic process, mitochondrial dysfunction remains at the forefront of PD research and holds the promise as a potential molecular target for the development of new therapeutic strategies for this devastating, currently incurable, disease. © 2008 The Authors.
Original languageEnglish
Pages (from-to)317-328
JournalJournal of Neurochemistry
Volume107
Issue number2
DOIs
Publication statusPublished - 1 Oct 2008

Keywords

  • α-synuclein
  • Apoptosis
  • Complex I
  • Fusion/fission
  • mtDNA
  • Phosphatase and tensin homologue-induced kinase 1

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