4.6 Article Proceedings Paper

Mitochondrial Therapies for Parkinson's Disease

期刊

MOVEMENT DISORDERS
卷 25, 期 3, 页码 S155-S160

出版社

WILEY
DOI: 10.1002/mds.22781

关键词

Parkinson's disease; mitochondrial dysfunction; coenzyme Q10; creatine; PGC-1 alpha; sirtuins

资金

  1. NINDS NIH HHS [R01 NS060885, R21 NS062165] Funding Source: Medline
  2. NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R21NS062165, R01NS060885] Funding Source: NIH RePORTER

向作者/读者索取更多资源

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 clue 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. (C) 2010 Movement Disorder Society

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