Ubiquitin-proteasome system and Parkinson's disease.
Identifieur interne : 002A98 ( PubMed/Corpus ); précédent : 002A97; suivant : 002A99Ubiquitin-proteasome system and Parkinson's disease.
Auteurs : C Warren Olanow ; Kevin St P. McnaughtSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2006.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Proteasome Endopeptidase Complex, Ubiquitin.
- genetics : Parkinson Disease.
- metabolism : Central Nervous System, Parkinson Disease, Proteasome Endopeptidase Complex, Ubiquitin.
- Age Factors, Animals, Humans, Models, Biological, Mutation.
Abstract
Increasing genetic, pathological, and experimental evidence suggest that neurodegeneration in both familial and sporadic forms of Parkinson's disease (PD) may be related to a defect in the capacity of the ubiquitin-proteasome system (UPS) to clear unwanted proteins, resulting in protein accumulation, aggregation, and cytotoxicity. This concept is supported by in vitro and in vivo laboratory experiments which show that inhibition of UPS function can cause neurodegeneration coupled with the formation of Lewy body-like inclusions. This hypothesis could account for the presence of protein aggregates and Lewy bodies in PD, the other biochemical features seen in the disorder, and the age-related vulnerability of the substantia nigra pars compacta. It also suggests novel targets for putative neuroprotective therapies for PD.
DOI: 10.1002/mds.21013
PubMed: 16972273
Links to Exploration step
pubmed:16972273Le document en format XML
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<author><name sortKey="Olanow, C Warren" sort="Olanow, C Warren" uniqKey="Olanow C" first="C Warren" last="Olanow">C Warren Olanow</name>
<affiliation><nlm:affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York10029, USA. warren.olanow@mssm.edu</nlm:affiliation>
</affiliation>
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<author><name sortKey="Mcnaught, Kevin St P" sort="Mcnaught, Kevin St P" uniqKey="Mcnaught K" first="Kevin St P" last="Mcnaught">Kevin St P. Mcnaught</name>
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<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age Factors</term>
<term>Animals</term>
<term>Central Nervous System (metabolism)</term>
<term>Humans</term>
<term>Models, Biological</term>
<term>Mutation</term>
<term>Parkinson Disease (genetics)</term>
<term>Parkinson Disease (metabolism)</term>
<term>Proteasome Endopeptidase Complex (genetics)</term>
<term>Proteasome Endopeptidase Complex (metabolism)</term>
<term>Ubiquitin (genetics)</term>
<term>Ubiquitin (metabolism)</term>
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<term>Proteasome Endopeptidase Complex</term>
<term>Ubiquitin</term>
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<keywords scheme="MESH" xml:lang="en"><term>Age Factors</term>
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<term>Models, Biological</term>
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<front><div type="abstract" xml:lang="en">Increasing genetic, pathological, and experimental evidence suggest that neurodegeneration in both familial and sporadic forms of Parkinson's disease (PD) may be related to a defect in the capacity of the ubiquitin-proteasome system (UPS) to clear unwanted proteins, resulting in protein accumulation, aggregation, and cytotoxicity. This concept is supported by in vitro and in vivo laboratory experiments which show that inhibition of UPS function can cause neurodegeneration coupled with the formation of Lewy body-like inclusions. This hypothesis could account for the presence of protein aggregates and Lewy bodies in PD, the other biochemical features seen in the disorder, and the age-related vulnerability of the substantia nigra pars compacta. It also suggests novel targets for putative neuroprotective therapies for PD.</div>
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<Title>Movement disorders : official journal of the Movement Disorder Society</Title>
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<Abstract><AbstractText>Increasing genetic, pathological, and experimental evidence suggest that neurodegeneration in both familial and sporadic forms of Parkinson's disease (PD) may be related to a defect in the capacity of the ubiquitin-proteasome system (UPS) to clear unwanted proteins, resulting in protein accumulation, aggregation, and cytotoxicity. This concept is supported by in vitro and in vivo laboratory experiments which show that inhibition of UPS function can cause neurodegeneration coupled with the formation of Lewy body-like inclusions. This hypothesis could account for the presence of protein aggregates and Lewy bodies in PD, the other biochemical features seen in the disorder, and the age-related vulnerability of the substantia nigra pars compacta. It also suggests novel targets for putative neuroprotective therapies for PD.</AbstractText>
</Abstract>
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<ForeName>C Warren</ForeName>
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<NumberOfReferences>232</NumberOfReferences>
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