Etiology of Parkinson's disease.
Identifieur interne : 001694 ( PubMed/Curation ); précédent : 001693; suivant : 001695Etiology of Parkinson's disease.
Auteurs : A J Stoessl [Canada]Source :
- The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques [ 0317-1671 ] ; 1999.
English descriptors
- KwdEn :
- Aging (physiology), Apoptosis (physiology), Free Radicals, Humans, Immune System Diseases (complications), Incidence, Infection (complications), Mitochondria (physiology), Nerve Growth Factors (physiology), Parkinson Disease (epidemiology), Parkinson Disease (etiology), Parkinson Disease (genetics), Prevalence.
- MESH :
- chemical , physiology : Nerve Growth Factors.
- chemical : Free Radicals.
- complications : Immune System Diseases, Infection.
- epidemiology : Parkinson Disease.
- etiology : Parkinson Disease.
- genetics : Parkinson Disease.
- physiology : Aging, Apoptosis, Mitochondria.
- Humans, Incidence, Prevalence.
Abstract
Controversy over the etiology and pathogenesis of Parkinson's disease (PD) has continued for many years and while the details have changed, the uncertainty persists. Although heritability was most emphatically refuted a decade ago by many investigators, recent progress firmly indicates that genetic factors at least play a role, although probably to a variable degree from one individual to another. Evidence for a variety of other etiological factors is amassed from epidemiological studies, animal models, molecular and cellular biology. Genetic factors, infectious and immunological abnormalities, the effects of ageing, toxins (endogenous as well as exogenous) and other environmental factors may all contribute to the development of PD. Loss of nigral dopaminergic neurons may be mediated by varying combinations of oxidative free radical toxicity, impaired mitochondrial function, "weak excitotoxicity" and abnormal handling of cytoskeletal proteins, all of which may shift the balance regulating apoptotic cell death.
PubMed: 10451754
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Although heritability was most emphatically refuted a decade ago by many investigators, recent progress firmly indicates that genetic factors at least play a role, although probably to a variable degree from one individual to another. Evidence for a variety of other etiological factors is amassed from epidemiological studies, animal models, molecular and cellular biology. Genetic factors, infectious and immunological abnormalities, the effects of ageing, toxins (endogenous as well as exogenous) and other environmental factors may all contribute to the development of PD. Loss of nigral dopaminergic neurons may be mediated by varying combinations of oxidative free radical toxicity, impaired mitochondrial function, "weak excitotoxicity" and abnormal handling of cytoskeletal proteins, all of which may shift the balance regulating apoptotic cell death.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10451754</PMID><DateCreated><Year>1999</Year><Month>09</Month><Day>28</Day></DateCreated><DateCompleted><Year>1999</Year><Month>09</Month><Day>28</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>26 Suppl 2</Volume><PubDate><Year>1999</Year><Month>Aug</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>S5-12</MedlinePgn></Pagination><Abstract><AbstractText>Controversy over the etiology and pathogenesis of Parkinson's disease (PD) has continued for many years and while the details have changed, the uncertainty persists. Although heritability was most emphatically refuted a decade ago by many investigators, recent progress firmly indicates that genetic factors at least play a role, although probably to a variable degree from one individual to another. Evidence for a variety of other etiological factors is amassed from epidemiological studies, animal models, molecular and cellular biology. Genetic factors, infectious and immunological abnormalities, the effects of ageing, toxins (endogenous as well as exogenous) and other environmental factors may all contribute to the development of PD. Loss of nigral dopaminergic neurons may be mediated by varying combinations of oxidative free radical toxicity, impaired mitochondrial function, "weak excitotoxicity" and abnormal handling of cytoskeletal proteins, all of which may shift the balance regulating apoptotic cell death.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Stoessl</LastName><ForeName>A J</ForeName><Initials>AJ</Initials><AffiliationInfo><Affiliation>Neurodegenerative Disorders Centre, Vancouver Hospital & Health Sciences Centre, British Columbia, Canada.</Affiliation></AffiliationInfo></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="D005609">Free Radicals</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009414">Nerve Growth Factors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="N">Aging</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005609" MajorTopicYN="N">Free Radicals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007154" MajorTopicYN="N">Immune System Diseases</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007239" MajorTopicYN="N">Infection</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009414" MajorTopicYN="N">Nerve Growth Factors</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></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="D015995" MajorTopicYN="N">Prevalence</DescriptorName></MeshHeading></MeshHeadingList><NumberOfReferences>117</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>8</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1999</Year><Month>8</Month><Day>19</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1999</Year><Month>8</Month><Day>19</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10451754</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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