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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Mcnaught</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2006">2006</date><idno type="doi">10.1002/mds.21013</idno><idno type="RBID">pubmed:16972273</idno><idno type="pmid">16972273</idno><idno type="wicri:Area/PubMed/Corpus">002A98</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Ubiquitin-proteasome system and Parkinson's disease.</title><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></author><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></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><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></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Proteasome Endopeptidase Complex</term><term>Ubiquitin</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Central Nervous System</term><term>Parkinson Disease</term><term>Proteasome Endopeptidase Complex</term><term>Ubiquitin</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age Factors</term><term>Animals</term><term>Humans</term><term>Models, Biological</term><term>Mutation</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">16972273</PMID><DateCreated><Year>2006</Year><Month>12</Month><Day>05</Day></DateCreated><DateCompleted><Year>2007</Year><Month>02</Month><Day>20</Day></DateCompleted><DateRevised><Year>2007</Year><Month>12</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>21</Volume><Issue>11</Issue><PubDate><Year>2006</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Ubiquitin-proteasome system and Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1806-23</MedlinePgn></Pagination><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><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Olanow</LastName><ForeName>C Warren</ForeName><Initials>CW</Initials><AffiliationInfo><Affiliation>Department of Neurology, Mount Sinai School of Medicine, New York, New York10029, USA. warren.olanow@mssm.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McNaught</LastName><ForeName>Kevin St P</ForeName><Initials>KS</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>1 RO1 NS045999-01</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D025801">Ubiquitin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.25.1</RegistryNumber><NameOfSubstance UI="D046988">Proteasome Endopeptidase Complex</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000367">Age Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002490">Central Nervous System</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008954">Models, Biological</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009154">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D046988">Proteasome Endopeptidase Complex</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D025801">Ubiquitin</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>232</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>9</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>2</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>9</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.21013</ArticleId><ArticleId IdType="pubmed">16972273</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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