Mitochondrial therapies for Parkinson's disease

Bobby Thomas, M. Flint Beal

Research output: Contribution to journalArticle

28 Scopus citations

Abstract

Parkinson's disease (PD) is marked by widespread neurodegeneration in the brain in addition to a selective yet prominent and progressive loss of nigrostriatal dopaminergic neurons. Of the multiple theories suggested in the pathogenesis of PD, mitochondrial dysfunction takes a center stage in both sporadic and familial forms of illness. Deficits in mitochondrial functions due to impaired bioenergetics, aging associated increased generation of reactive oxygen species, damage to mitochondrial DNA, impaired calcium buffering, and alterations in mitochondrial morphology may contribute to improper functioning of the CNS leading to neurodegeneration. These mitochondrial alterations suggest that a potential target worth exploring for neuroprotective therapies are the ones that can preserve mitochondrial functions in PD. Here, we provide a recent update on potential drugs that are known to block mitochondrial dysfunctions in various experimental models and those that are currently under clinical trials for PD. We also review novel mitochondrial survival pathways that provide hope and promise for innovative neuroprotective therapies in the future that can be explored as possible therapeutic intervention for PD pathogenesis.

Original languageEnglish (US)
Pages (from-to)S155-S160
JournalMovement Disorders
Volume25
Issue numberSUPPL. 1
DOIs
StatePublished - Dec 20 2010

Keywords

  • Coenzyme Q10
  • Creatine
  • Mitochondrial dysfunction
  • PGC-1α
  • Parkinson's disease
  • Sirtuins

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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