期刊
BIOCHIMIE
卷 100, 期 -, 页码 177-183出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biochi.2013.07.033
关键词
Parkinson's disease; Mitophagy; Charcot-Marie-Tooth disease; Amyotrophic lateral; Sclerosis
资金
- Agence Nationale de la Recherche
- Association pour la recherche sur la SLA et les autres maladies du motoneurone (ARSla)
- Thierry Latran Foundation
- Association pour la recherche et le developpement de moyens de lutte contre les maladies neurodegeneratives (AREMANE)
- Helmholtz Institute
- ALS association [2235]
- Mercator Professorship(DFG)
- contrat d'interface INSERM/AP-HP
Mutations causing genetic forms of Parkinson's disease or hereditary neuropathies have been recently shown to affect key molecular players involved in the recycling of defective mitochondria, most notably PARKIN, PINK1, Mitofusin 2 or dynein heavy chain. Interestingly, the same pathways are also indirectly targeted by multiple other mutations involved in familial forms of amyotrophic lateral sclerosis, Huntington's disease or Alzheimer's disease. These recent genetic results strongly reinforce the notion that defective mitochondrial physiology might cause neurodegeneration. Mitochondrial dysfunction has however been observed in virtually every neurodegenerative disease and appears not restricted to the most vulnerable neuronal populations affected by a given disease. Thus, the mechanisms linking defective mitochondrial quality control to death of selective neuronal populations remain to be identified. This review provides an update on the most recent literature on mitochondrial quality control and its impairment during neurodegenerative diseases. (C) 2013 Elsevier Masson SAS. All rights reserved.
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