Association of interleukin-1 beta polymorphisms with idiopathic Parkinson's disease.
Identifieur interne : 001482 ( PubMed/Checkpoint ); précédent : 001481; suivant : 001483Association of interleukin-1 beta polymorphisms with idiopathic Parkinson's disease.
Auteurs : Patrick L. Mcgeer [Canada] ; Koji Yasojima ; Edith G. McgeerSource :
- Neuroscience letters [ 0304-3940 ] ; 2002.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Interleukin-1.
- genetics : Parkinson Disease.
- immunology : Brain, Parkinson Disease, Polymorphism, Genetic.
- pathology : Brain, Parkinson Disease.
- Aged, Aged, 80 and over, Autopsy, Genotype, Humans.
Abstract
Activated microglia surround degenerating substantia nigra neurons in Parkinson's disease (PD). Such microglia produce high levels of interleukin-1 beta (IL-1 beta) and interleukin-1 alpha (IL-1 alpha). T and C alleles exist for the IL-1 beta-511 regulatory region as well as for the IL-1 alpha-889 regulatory region. The T genotypes of both have been reported to increase the risk of Alzheimer's disease (AD) (Arch. Neurol. 58 (2001) 1790). Since the lesions of PD and AD have similar neuroinflammatory characteristics (Neurology 38 (1988) 1285), we genotyped 100 PD and 100 control postmortem brains for the same polymorphisms. We found a significant increase of the IL-1 beta T genotype in PD cases compared with controls (chi(2)=9.65, P=0.0019). A significant increase was not found for the IL-alpha T genotype (chi(2)=1.32, P=0.23), although there was a trend towards more frequent expression of the T allele.
PubMed: 12052540
Affiliations:
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pubmed:12052540Le document en format XML
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Mcgeer</name><affiliation wicri:level="1"><nlm:affiliation>Kinsmen Laboratory of Neurological Research and the Movement Disorders Center, University of British Columbia, Vancouver, B.C., Canada. mcgeerpl@interchange.ubc.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Kinsmen Laboratory of Neurological Research and the Movement Disorders Center, University of British Columbia, Vancouver, B.C.</wicri:regionArea><wicri:noRegion>B.C.</wicri:noRegion></affiliation></author><author><name sortKey="Yasojima, Koji" sort="Yasojima, Koji" uniqKey="Yasojima K" first="Koji" last="Yasojima">Koji Yasojima</name></author><author><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G" last="Mcgeer">Edith G. 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Mcgeer</name><affiliation wicri:level="1"><nlm:affiliation>Kinsmen Laboratory of Neurological Research and the Movement Disorders Center, University of British Columbia, Vancouver, B.C., Canada. mcgeerpl@interchange.ubc.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Kinsmen Laboratory of Neurological Research and the Movement Disorders Center, University of British Columbia, Vancouver, B.C.</wicri:regionArea><wicri:noRegion>B.C.</wicri:noRegion></affiliation></author><author><name sortKey="Yasojima, Koji" sort="Yasojima, Koji" uniqKey="Yasojima K" first="Koji" last="Yasojima">Koji Yasojima</name></author><author><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G" last="Mcgeer">Edith G. Mcgeer</name></author></analytic><series><title level="j">Neuroscience letters</title><idno type="ISSN">0304-3940</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Autopsy</term><term>Brain (immunology)</term><term>Brain (pathology)</term><term>Genotype</term><term>Humans</term><term>Interleukin-1 (genetics)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (immunology)</term><term>Parkinson Disease (pathology)</term><term>Polymorphism, Genetic (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interleukin-1</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term><term>Polymorphism, Genetic</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Autopsy</term><term>Genotype</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Activated microglia surround degenerating substantia nigra neurons in Parkinson's disease (PD). Such microglia produce high levels of interleukin-1 beta (IL-1 beta) and interleukin-1 alpha (IL-1 alpha). T and C alleles exist for the IL-1 beta-511 regulatory region as well as for the IL-1 alpha-889 regulatory region. The T genotypes of both have been reported to increase the risk of Alzheimer's disease (AD) (Arch. Neurol. 58 (2001) 1790). Since the lesions of PD and AD have similar neuroinflammatory characteristics (Neurology 38 (1988) 1285), we genotyped 100 PD and 100 control postmortem brains for the same polymorphisms. We found a significant increase of the IL-1 beta T genotype in PD cases compared with controls (chi(2)=9.65, P=0.0019). A significant increase was not found for the IL-alpha T genotype (chi(2)=1.32, P=0.23), although there was a trend towards more frequent expression of the T allele.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12052540</PMID><DateCreated><Year>2002</Year><Month>06</Month><Day>07</Day></DateCreated><DateCompleted><Year>2002</Year><Month>08</Month><Day>28</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0304-3940</ISSN><JournalIssue CitedMedium="Print"><Volume>326</Volume><Issue>1</Issue><PubDate><Year>2002</Year><Month>Jun</Month><Day>21</Day></PubDate></JournalIssue><Title>Neuroscience letters</Title><ISOAbbreviation>Neurosci. Lett.</ISOAbbreviation></Journal><ArticleTitle>Association of interleukin-1 beta polymorphisms with idiopathic Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>67-9</MedlinePgn></Pagination><Abstract><AbstractText>Activated microglia surround degenerating substantia nigra neurons in Parkinson's disease (PD). Such microglia produce high levels of interleukin-1 beta (IL-1 beta) and interleukin-1 alpha (IL-1 alpha). T and C alleles exist for the IL-1 beta-511 regulatory region as well as for the IL-1 alpha-889 regulatory region. The T genotypes of both have been reported to increase the risk of Alzheimer's disease (AD) (Arch. Neurol. 58 (2001) 1790). Since the lesions of PD and AD have similar neuroinflammatory characteristics (Neurology 38 (1988) 1285), we genotyped 100 PD and 100 control postmortem brains for the same polymorphisms. We found a significant increase of the IL-1 beta T genotype in PD cases compared with controls (chi(2)=9.65, P=0.0019). A significant increase was not found for the IL-alpha T genotype (chi(2)=1.32, P=0.23), although there was a trend towards more frequent expression of the T allele.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>McGeer</LastName><ForeName>Patrick L</ForeName><Initials>PL</Initials><AffiliationInfo><Affiliation>Kinsmen Laboratory of Neurological Research and the Movement Disorders Center, University of British Columbia, Vancouver, B.C., Canada. mcgeerpl@interchange.ubc.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yasojima</LastName><ForeName>Koji</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>McGeer</LastName><ForeName>Edith G</ForeName><Initials>EG</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Neurosci Lett</MedlineTA><NlmUniqueID>7600130</NlmUniqueID><ISSNLinking>0304-3940</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007375">Interleukin-1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001344" MajorTopicYN="N">Autopsy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007375" MajorTopicYN="N">Interleukin-1</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011110" MajorTopicYN="Y">Polymorphism, Genetic</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>6</Month><Day>8</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>8</Month><Day>29</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>6</Month><Day>8</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12052540</ArticleId><ArticleId IdType="pii">S0304394002003002</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G" last="Mcgeer">Edith G. Mcgeer</name><name sortKey="Yasojima, Koji" sort="Yasojima, Koji" uniqKey="Yasojima K" first="Koji" last="Yasojima">Koji Yasojima</name></noCountry><country name="Canada"><noRegion><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L" last="Mcgeer">Patrick L. Mcgeer</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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