Etiopathogenesis of Parkinson disease: a new beginning?
Identifieur interne : 000128 ( PubMed/Corpus ); précédent : 000127; suivant : 000129Etiopathogenesis of Parkinson disease: a new beginning?
Auteurs : Weidong Le ; Shen Chen ; Joseph JankovicSource :
- The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry [ 1073-8584 ] ; 2009.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Dopamine.
- etiology : Parkinson Disease.
- genetics : Parkinson Disease.
- metabolism : Neurons.
- pathology : Brain, Neurons, Parkinson Disease.
- Animals, Humans.
Abstract
Parkinson disease (PD) probably represents a syndrome of different disorders and origins converging into a relatively uniform neurodegenerative process. Although clinical-pathological studies have suggested that the presymptomatic phase of PD may be relatively short, perhaps less than a decade, the authors postulate that the pathogenic mechanisms may begin much earlier, possibly even in the prenatal period. Thus, some patients with PD may be born with a fewer than normal number of dopaminergic (and nondopaminergic) neurons as a result of genetic or other abnormalities sustained during the prenatal or perinatal period; as a result of normal age-related neuronal attrition, they eventually reach the critical threshold (60% or more) of neuronal loss needed for onset of PD to become clinically manifest. The authors review the emerging evidence that genetic disruption of normal development, coupled with subsequent environmental factors (the so called multiple-hit hypothesis), plays an important role in the etiopathogenesis of PD.
DOI: 10.1177/1073858408319974
PubMed: 19008336
Links to Exploration step
pubmed:19008336Le document en format XML
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Although clinical-pathological studies have suggested that the presymptomatic phase of PD may be relatively short, perhaps less than a decade, the authors postulate that the pathogenic mechanisms may begin much earlier, possibly even in the prenatal period. Thus, some patients with PD may be born with a fewer than normal number of dopaminergic (and nondopaminergic) neurons as a result of genetic or other abnormalities sustained during the prenatal or perinatal period; as a result of normal age-related neuronal attrition, they eventually reach the critical threshold (60% or more) of neuronal loss needed for onset of PD to become clinically manifest. The authors review the emerging evidence that genetic disruption of normal development, coupled with subsequent environmental factors (the so called multiple-hit hypothesis), plays an important role in the etiopathogenesis of PD.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">19008336</PMID><DateCreated><Year>2009</Year><Month>02</Month><Day>16</Day></DateCreated><DateCompleted><Year>2009</Year><Month>04</Month><Day>15</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1073-8584</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><Issue>1</Issue><PubDate><Year>2009</Year><Month>Feb</Month></PubDate></JournalIssue><Title>The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry</Title><ISOAbbreviation>Neuroscientist</ISOAbbreviation></Journal><ArticleTitle>Etiopathogenesis of Parkinson disease: a new beginning?</ArticleTitle><Pagination><MedlinePgn>28-35</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1177/1073858408319974</ELocationID><Abstract><AbstractText>Parkinson disease (PD) probably represents a syndrome of different disorders and origins converging into a relatively uniform neurodegenerative process. Although clinical-pathological studies have suggested that the presymptomatic phase of PD may be relatively short, perhaps less than a decade, the authors postulate that the pathogenic mechanisms may begin much earlier, possibly even in the prenatal period. Thus, some patients with PD may be born with a fewer than normal number of dopaminergic (and nondopaminergic) neurons as a result of genetic or other abnormalities sustained during the prenatal or perinatal period; as a result of normal age-related neuronal attrition, they eventually reach the critical threshold (60% or more) of neuronal loss needed for onset of PD to become clinically manifest. The authors review the emerging evidence that genetic disruption of normal development, coupled with subsequent environmental factors (the so called multiple-hit hypothesis), plays an important role in the etiopathogenesis of PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Weidong Le</LastName><AffiliationInfo><Affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shen Chen</LastName></Author><Author ValidYN="Y"><LastName>Jankovic</LastName><ForeName>Joseph</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2008</Year><Month>11</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neuroscientist</MedlineTA><NlmUniqueID>9504819</NlmUniqueID><ISSNLinking>1073-8584</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004298">Dopamine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009474">Neurons</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>90</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="aheadofprint"><Year>2008</Year><Month>11</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>11</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>4</Month><Day>16</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>11</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pii">1073858408319974</ArticleId><ArticleId IdType="doi">10.1177/1073858408319974</ArticleId><ArticleId IdType="pubmed">19008336</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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