Mitochondrial quality control turns out to be the principal suspect in parkin and PINK1-related autosomal recessive Parkinson's disease.
Identifieur interne : 000776 ( PubMed/Corpus ); précédent : 000775; suivant : 000777Mitochondrial quality control turns out to be the principal suspect in parkin and PINK1-related autosomal recessive Parkinson's disease.
Auteurs : Olga Corti ; Alexis BriceSource :
- Current opinion in neurobiology [ 1873-6882 ] ; 2013.
English descriptors
- KwdEn :
- Animals, Humans, Mitochondria (genetics), Mitochondria (metabolism), Parkinson Disease (genetics), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Protein Kinases (genetics), Protein Kinases (metabolism), Ubiquitin-Protein Ligases (genetics), Ubiquitin-Protein Ligases (metabolism).
- MESH :
- chemical , genetics : Protein Kinases, Ubiquitin-Protein Ligases.
- genetics : Mitochondria, Parkinson Disease.
- metabolism : Mitochondria, Parkinson Disease, Protein Kinases, Ubiquitin-Protein Ligases.
- physiopathology : Parkinson Disease.
- Animals, Humans.
Abstract
Mitochondrial dysfunction has long been suspected to play a key role in neurodegeneration in Parkinson's disease. PINK1 and Parkin, the products of two genes responsible for autosomal recessive Parkinsonian syndromes with early onset, act as a quality control system on the outer mitochondrial membrane to preserve mitochondrial integrity. While doing so, they interact with multiple molecular actors in processes regulating mitochondrial biology and cell survival. The physiological conditions that mobilize these processes in neurons, and the mechanisms underlying their integration and spatiotemporal coordination, remain to be elucidated. Understanding how dysfunction of these house-keeping pathways leads to the preferential degeneration of a specific neuronal population in Parkinson's disease is a major challenge for future research.
DOI: 10.1016/j.conb.2012.11.002
PubMed: 23206589
Links to Exploration step
pubmed:23206589Le document en format XML
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<author><name sortKey="Brice, Alexis" sort="Brice, Alexis" uniqKey="Brice A" first="Alexis" last="Brice">Alexis Brice</name>
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<front><div type="abstract" xml:lang="en">Mitochondrial dysfunction has long been suspected to play a key role in neurodegeneration in Parkinson's disease. PINK1 and Parkin, the products of two genes responsible for autosomal recessive Parkinsonian syndromes with early onset, act as a quality control system on the outer mitochondrial membrane to preserve mitochondrial integrity. While doing so, they interact with multiple molecular actors in processes regulating mitochondrial biology and cell survival. The physiological conditions that mobilize these processes in neurons, and the mechanisms underlying their integration and spatiotemporal coordination, remain to be elucidated. Understanding how dysfunction of these house-keeping pathways leads to the preferential degeneration of a specific neuronal population in Parkinson's disease is a major challenge for future research.</div>
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<Abstract><AbstractText>Mitochondrial dysfunction has long been suspected to play a key role in neurodegeneration in Parkinson's disease. PINK1 and Parkin, the products of two genes responsible for autosomal recessive Parkinsonian syndromes with early onset, act as a quality control system on the outer mitochondrial membrane to preserve mitochondrial integrity. While doing so, they interact with multiple molecular actors in processes regulating mitochondrial biology and cell survival. The physiological conditions that mobilize these processes in neurons, and the mechanisms underlying their integration and spatiotemporal coordination, remain to be elucidated. Understanding how dysfunction of these house-keeping pathways leads to the preferential degeneration of a specific neuronal population in Parkinson's disease is a major challenge for future research.</AbstractText>
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