Glial cells and inflammation in Parkinson's disease: a role in neurodegeneration?
Identifieur interne : 001345 ( PubMed/Checkpoint ); précédent : 001344; suivant : 001346Glial cells and inflammation in Parkinson's disease: a role in neurodegeneration?
Auteurs : E C Hirsch [France] ; S. Hunot ; P. Damier ; B. FaucheuxSource :
- Annals of neurology [ 0364-5134 ] ; 1998.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Dopamine, Free Radical Scavengers.
- chemical , physiology : Dopamine.
- metabolism : Neurons.
- physiology : Neuroglia, Neurons.
- physiopathology : Nerve Degeneration, Neuritis, Parkinson Disease.
- Humans.
Abstract
The data reviewed here show that, in Parkinson's disease (PD), some dopaminergic neurons are more vulnerable than others to the pathologic process. The glial cells surrounding dopaminergic neurons may be involved in this selective vulnerability. One subpopulation of glial cells, in particular, may play a neuroprotective role by metabolizing dopamine and scavenging oxygen free radicals that are associated with dopamine metabolism. Another subpopulation of glial cells may be deleterious to dopaminergic neurons. This effect may be mediated by the production of nitric oxide and cytokines, which may in turn account for the oxidative stress observed in the substantia nigra of patients with PD. Finally, this inflammatory reaction may result in the induction of apoptosis.
PubMed: 9749582
Affiliations:
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Damier</name></author><author><name sortKey="Faucheux, B" sort="Faucheux, B" uniqKey="Faucheux B" first="B" last="Faucheux">B. 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Hunot</name></author><author><name sortKey="Damier, P" sort="Damier, P" uniqKey="Damier P" first="P" last="Damier">P. Damier</name></author><author><name sortKey="Faucheux, B" sort="Faucheux, B" uniqKey="Faucheux B" first="B" last="Faucheux">B. Faucheux</name></author></analytic><series><title level="j">Annals of neurology</title><idno type="ISSN">0364-5134</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dopamine (metabolism)</term><term>Dopamine (physiology)</term><term>Free Radical Scavengers (metabolism)</term><term>Humans</term><term>Nerve Degeneration (physiopathology)</term><term>Neuritis (physiopathology)</term><term>Neuroglia (physiology)</term><term>Neurons (metabolism)</term><term>Neurons (physiology)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Free Radical Scavengers</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Neuroglia</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Nerve Degeneration</term><term>Neuritis</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The data reviewed here show that, in Parkinson's disease (PD), some dopaminergic neurons are more vulnerable than others to the pathologic process. The glial cells surrounding dopaminergic neurons may be involved in this selective vulnerability. One subpopulation of glial cells, in particular, may play a neuroprotective role by metabolizing dopamine and scavenging oxygen free radicals that are associated with dopamine metabolism. Another subpopulation of glial cells may be deleterious to dopaminergic neurons. This effect may be mediated by the production of nitric oxide and cytokines, which may in turn account for the oxidative stress observed in the substantia nigra of patients with PD. Finally, this inflammatory reaction may result in the induction of apoptosis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9749582</PMID><DateCreated><Year>1998</Year><Month>10</Month><Day>07</Day></DateCreated><DateCompleted><Year>1998</Year><Month>10</Month><Day>07</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0364-5134</ISSN><JournalIssue CitedMedium="Print"><Volume>44</Volume><Issue>3 Suppl 1</Issue><PubDate><Year>1998</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Annals of neurology</Title><ISOAbbreviation>Ann. Neurol.</ISOAbbreviation></Journal><ArticleTitle>Glial cells and inflammation in Parkinson's disease: a role in neurodegeneration?</ArticleTitle><Pagination><MedlinePgn>S115-20</MedlinePgn></Pagination><Abstract><AbstractText>The data reviewed here show that, in Parkinson's disease (PD), some dopaminergic neurons are more vulnerable than others to the pathologic process. The glial cells surrounding dopaminergic neurons may be involved in this selective vulnerability. One subpopulation of glial cells, in particular, may play a neuroprotective role by metabolizing dopamine and scavenging oxygen free radicals that are associated with dopamine metabolism. Another subpopulation of glial cells may be deleterious to dopaminergic neurons. This effect may be mediated by the production of nitric oxide and cytokines, which may in turn account for the oxidative stress observed in the substantia nigra of patients with PD. Finally, this inflammatory reaction may result in the induction of apoptosis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>E C</ForeName><Initials>EC</Initials><AffiliationInfo><Affiliation>INSERM U 289, Hôpital de la Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hunot</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Damier</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Faucheux</LastName><ForeName>B</ForeName><Initials>B</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</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>Ann Neurol</MedlineTA><NlmUniqueID>7707449</NlmUniqueID><ISSNLinking>0364-5134</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016166">Free Radical Scavengers</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016166" MajorTopicYN="N">Free Radical Scavengers</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009410" MajorTopicYN="N">Nerve Degeneration</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009443" MajorTopicYN="N">Neuritis</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009457" MajorTopicYN="N">Neuroglia</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>61</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1998</Year><Month>9</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1998</Year><Month>9</Month><Day>28</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1998</Year><Month>9</Month><Day>28</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9749582</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement></list><tree><noCountry><name sortKey="Damier, P" sort="Damier, P" uniqKey="Damier P" first="P" last="Damier">P. Damier</name><name sortKey="Faucheux, B" sort="Faucheux, B" uniqKey="Faucheux B" first="B" last="Faucheux">B. Faucheux</name><name sortKey="Hunot, S" sort="Hunot, S" uniqKey="Hunot S" first="S" last="Hunot">S. Hunot</name></noCountry><country name="France"><region name="Île-de-France"><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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