Etiology of Parkinson's disease.
Identifieur interne : 000292 ( Ncbi/Merge ); précédent : 000291; suivant : 000293Etiology of Parkinson's disease.
Auteurs : Zhigao Huang [Canada] ; Raúl De La Fuente-Fernández ; A Jon StoesslSource :
- The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques [ 0317-1671 ] ; 2003.
English descriptors
- KwdEn :
- Cell Death (physiology), Comorbidity, Environmental Exposure (statistics & numerical data), Environmental Pollution (statistics & numerical data), Humans, Incidence, Parkinson Disease (epidemiology), Parkinson Disease (etiology), Parkinson Disease (genetics), Protein Processing, Post-Translational (genetics), Risk Factors, Smoking (epidemiology), Ubiquitin (metabolism).
- MESH :
- chemical , metabolism : Ubiquitin.
- epidemiology : Parkinson Disease, Smoking.
- etiology : Parkinson Disease.
- genetics : Parkinson Disease, Protein Processing, Post-Translational.
- physiology : Cell Death.
- statistics & numerical data : Environmental Exposure, Environmental Pollution.
- Comorbidity, Humans, Incidence, Risk Factors.
Abstract
There is growing recognition that Parkinson's disease (PD) is likely to arise from the combined effects of genetic predisposition as well as largely unidentified environmental factors. The relative contribution of each varies from one individual to another. Even in situations where more than one family member is affected, the predominant influence may be environmental. Although responsible for only a small minority of cases of PD, recently identified genetic mutations have provided tremendous insights into the basis for neurodegeneration and have led to growing recognition of the importance of abnormal protein handling in Parkinson's as well as other neurodegenerative disorders. Abnormal protein handling may increase susceptibility to oxidative stress; conversely, numerous other factors, including oxidative stress and impaired mitochondrial function can lead to impaired protein degradation. A limited number of environmental factors are known to be toxic to the substantia nigra; in contrast, some factors such as caffeine intake and cigarette smoking may protect against the development of PD, although the mechanisms are not established. We review the various genetic and environmental factors thought to be involved in PD, as well as the mechanisms that contribute to selective nigral cell death.
PubMed: 12691472
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The relative contribution of each varies from one individual to another. Even in situations where more than one family member is affected, the predominant influence may be environmental. Although responsible for only a small minority of cases of PD, recently identified genetic mutations have provided tremendous insights into the basis for neurodegeneration and have led to growing recognition of the importance of abnormal protein handling in Parkinson's as well as other neurodegenerative disorders. Abnormal protein handling may increase susceptibility to oxidative stress; conversely, numerous other factors, including oxidative stress and impaired mitochondrial function can lead to impaired protein degradation. A limited number of environmental factors are known to be toxic to the substantia nigra; in contrast, some factors such as caffeine intake and cigarette smoking may protect against the development of PD, although the mechanisms are not established. We review the various genetic and environmental factors thought to be involved in PD, as well as the mechanisms that contribute to selective nigral cell death.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12691472</PMID><DateCreated><Year>2003</Year><Month>04</Month><Day>14</Day></DateCreated><DateCompleted><Year>2003</Year><Month>05</Month><Day>08</Day></DateCompleted><DateRevised><Year>2005</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0317-1671</ISSN><JournalIssue CitedMedium="Print"><Volume>30 Suppl 1</Volume><PubDate><Year>2003</Year><Month>Mar</Month></PubDate></JournalIssue><Title>The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques</Title><ISOAbbreviation>Can J Neurol Sci</ISOAbbreviation></Journal><ArticleTitle>Etiology of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>S10-8</MedlinePgn></Pagination><Abstract><AbstractText>There is growing recognition that Parkinson's disease (PD) is likely to arise from the combined effects of genetic predisposition as well as largely unidentified environmental factors. The relative contribution of each varies from one individual to another. Even in situations where more than one family member is affected, the predominant influence may be environmental. Although responsible for only a small minority of cases of PD, recently identified genetic mutations have provided tremendous insights into the basis for neurodegeneration and have led to growing recognition of the importance of abnormal protein handling in Parkinson's as well as other neurodegenerative disorders. Abnormal protein handling may increase susceptibility to oxidative stress; conversely, numerous other factors, including oxidative stress and impaired mitochondrial function can lead to impaired protein degradation. A limited number of environmental factors are known to be toxic to the substantia nigra; in contrast, some factors such as caffeine intake and cigarette smoking may protect against the development of PD, although the mechanisms are not established. We review the various genetic and environmental factors thought to be involved in PD, as well as the mechanisms that contribute to selective nigral cell death.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Zhigao</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, BC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de la Fuente-Fernández</LastName><ForeName>Raúl</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Stoessl</LastName><ForeName>A Jon</ForeName><Initials>AJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Can J Neurol Sci</MedlineTA><NlmUniqueID>0415227</NlmUniqueID><ISSNLinking>0317-1671</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D025801">Ubiquitin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015897" MajorTopicYN="N">Comorbidity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004781" MajorTopicYN="N">Environmental Exposure</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004787" MajorTopicYN="N">Environmental Pollution</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011499" MajorTopicYN="N">Protein Processing, Post-Translational</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012907" MajorTopicYN="N">Smoking</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D025801" MajorTopicYN="N">Ubiquitin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>144</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>4</Month><Day>15</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>5</Month><Day>9</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2003</Year><Month>4</Month><Day>15</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12691472</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="De La Fuente Fernandez, Raul" sort="De La Fuente Fernandez, Raul" uniqKey="De La Fuente Fernandez R" first="Raúl" last="De La Fuente-Fernández">Raúl De La Fuente-Fernández</name><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A Jon" last="Stoessl">A Jon Stoessl</name></noCountry><country name="Canada"><noRegion><name sortKey="Huang, Zhigao" sort="Huang, Zhigao" uniqKey="Huang Z" first="Zhigao" last="Huang">Zhigao Huang</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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