Mitochondrial quality control in neurodegenerative diseases.
Identifieur interne : 001195 ( Ncbi/Merge ); précédent : 001194; suivant : 001196Mitochondrial quality control in neurodegenerative diseases.
Auteurs : Luc Dupuis [France]Source :
- Biochimie [ 1638-6183 ] ; 2014.
English descriptors
- KwdEn :
- Autophagy (genetics), Dyneins (genetics), Dyneins (metabolism), GTP Phosphohydrolases (genetics), GTP Phosphohydrolases (metabolism), Gene Expression Regulation, Humans, Mitochondria (genetics), Mitochondria (metabolism), Mitochondria (pathology), Mitochondrial Proteins (genetics), Mitochondrial Proteins (metabolism), Mutation, Neurodegenerative Diseases (genetics), Neurodegenerative Diseases (metabolism), Neurodegenerative Diseases (pathology), Neurons (metabolism), Neurons (pathology), Protein Kinases (genetics), Protein Kinases (metabolism), Signal Transduction, Ubiquitin-Protein Ligases (genetics), Ubiquitin-Protein Ligases (metabolism).
- MESH :
- chemical , genetics : Dyneins, GTP Phosphohydrolases, Mitochondrial Proteins, Protein Kinases, Ubiquitin-Protein Ligases.
- genetics : Autophagy, Mitochondria, Neurodegenerative Diseases.
- chemical , metabolism : Dyneins, GTP Phosphohydrolases, Mitochondria, Mitochondrial Proteins, Neurodegenerative Diseases, Neurons, Protein Kinases, Ubiquitin-Protein Ligases.
- pathology : Mitochondria, Neurodegenerative Diseases, Neurons.
- Gene Expression Regulation, Humans, Mutation, Signal Transduction.
Abstract
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.
DOI: 10.1016/j.biochi.2013.07.033
PubMed: 23958438
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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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23958438</PMID><DateCreated><Year>2014</Year><Month>03</Month><Day>24</Day></DateCreated><DateCompleted><Year>2014</Year><Month>11</Month><Day>06</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1638-6183</ISSN><JournalIssue CitedMedium="Internet"><Volume>100</Volume><PubDate><Year>2014</Year><Month>May</Month></PubDate></JournalIssue><Title>Biochimie</Title><ISOAbbreviation>Biochimie</ISOAbbreviation></Journal><ArticleTitle>Mitochondrial quality control in neurodegenerative diseases.</ArticleTitle><Pagination><MedlinePgn>177-83</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.biochi.2013.07.033</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0300-9084(13)00278-2</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>Copyright © 2013 Elsevier Masson SAS. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dupuis</LastName><ForeName>Luc</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>INSERM, U1118, Strasbourg F-67085, France; Université de Strasbourg, Fédération de Médecine Translationnelle (FMTS), UMRS1118, Strasbourg F-67085, France. 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