Association between Parkinson's disease and polymorphisms in the nNOS and iNOS genes in a community-based case-control study.
Identifieur interne : 001099 ( PubMed/Curation ); précédent : 001098; suivant : 001100Association between Parkinson's disease and polymorphisms in the nNOS and iNOS genes in a community-based case-control study.
Auteurs : Clotilde Levecque [France] ; Alexis Elbaz ; Jacqueline Clavel ; Florence Richard ; Jean-Sébastien Vidal ; Philippe Amouyel ; Christophe Tzourio ; Annick Alpérovitch ; Marie-Christine Chartier-HarlinSource :
- Human molecular genetics [ 0964-6906 ] ; 2003.
English descriptors
- KwdEn :
- Case-Control Studies, Genetic Predisposition to Disease, Humans, Neutrophils (enzymology), Neutrophils (metabolism), Nitrates (metabolism), Nitric Oxide (metabolism), Nitric Oxide Synthase (genetics), Nitric Oxide Synthase (metabolism), Nitric Oxide Synthase Type I, Nitric Oxide Synthase Type II, Parkinson Disease (enzymology), Parkinson Disease (genetics), Parkinson Disease (metabolism), Smoking (adverse effects), Smoking (epidemiology).
- MESH :
- chemical , genetics : Nitric Oxide Synthase.
- chemical , metabolism : Nitrates, Nitric Oxide, Nitric Oxide Synthase.
- adverse effects : Smoking.
- enzymology : Neutrophils, Parkinson Disease.
- epidemiology : Smoking.
- genetics : Parkinson Disease.
- metabolism : Neutrophils, Parkinson Disease.
- Case-Control Studies, Genetic Predisposition to Disease, Humans, Nitric Oxide Synthase Type I, Nitric Oxide Synthase Type II.
Abstract
Excess of nitric oxide (NO) has been shown to exert neurotoxic impacts in the brain. Moreover, inhibition of two NO-synthesizing enzymes, neuronal NOS (nNOS) and inducible NOS (iNOS), displays neuroprotective effects in the MPTP model of Parkinson's disease (PD). These data suggest a possible involvement of NOS as factors controlling the resistance of the nigral dopaminergic neurons to environmental insults. Therefore, we investigated whether polymorphisms present in these genes could contribute to the risk of developing PD. We carried out a community-based case-control study among subjects enrolled in the Mutualité Sociale Agricole, the French health insurance organization for workers connected to agriculture. Two-hundred and nine PD patients and 488 controls of European (mostly French) ancestry and matched for age, sex and region of residency were included in this study. Associations were observed with polymorphisms present in exon 22 of iNOS (OR for AA carriers=0.50, 95% CI=0.29-0.86, P=0.01) and in exon 29 of nNOS (OR for carriers of the T allele=1.53, 95% CI=1.08-2.16, P=0.02); no association was observed with a polymorphism in exon 18 of nNOS (OR for carriers of the T allele=1.20, 95% CI=0.85-1.69, P=0.30). Moreover, a significant interaction of the nNOS polymorphisms with current and ever cigarette smoking was found (nNOS 18, P=0.05; nNOS 29, P=0.04). All together, these data favour an involvement of these two genes as new modifier genes in PD.
PubMed: 12490535
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Lille</wicri:regionArea></affiliation></author><author><name sortKey="Elbaz, Alexis" sort="Elbaz, Alexis" uniqKey="Elbaz A" first="Alexis" last="Elbaz">Alexis Elbaz</name></author><author><name sortKey="Clavel, Jacqueline" sort="Clavel, Jacqueline" uniqKey="Clavel J" first="Jacqueline" last="Clavel">Jacqueline Clavel</name></author><author><name sortKey="Richard, Florence" sort="Richard, Florence" uniqKey="Richard F" first="Florence" last="Richard">Florence Richard</name></author><author><name sortKey="Vidal, Jean Sebastien" sort="Vidal, Jean Sebastien" uniqKey="Vidal J" first="Jean-Sébastien" last="Vidal">Jean-Sébastien Vidal</name></author><author><name sortKey="Amouyel, Philippe" sort="Amouyel, Philippe" uniqKey="Amouyel P" first="Philippe" last="Amouyel">Philippe Amouyel</name></author><author><name sortKey="Tzourio, Christophe" sort="Tzourio, Christophe" uniqKey="Tzourio C" first="Christophe" last="Tzourio">Christophe Tzourio</name></author><author><name sortKey="Alperovitch, Annick" sort="Alperovitch, Annick" uniqKey="Alperovitch A" first="Annick" last="Alpérovitch">Annick Alpérovitch</name></author><author><name sortKey="Chartier Harlin, Marie Christine" sort="Chartier Harlin, Marie Christine" uniqKey="Chartier Harlin M" first="Marie-Christine" last="Chartier-Harlin">Marie-Christine Chartier-Harlin</name></author></analytic><series><title level="j">Human molecular genetics</title><idno type="ISSN">0964-6906</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Case-Control Studies</term><term>Genetic Predisposition to Disease</term><term>Humans</term><term>Neutrophils (enzymology)</term><term>Neutrophils (metabolism)</term><term>Nitrates (metabolism)</term><term>Nitric Oxide (metabolism)</term><term>Nitric Oxide Synthase (genetics)</term><term>Nitric Oxide Synthase (metabolism)</term><term>Nitric Oxide Synthase Type I</term><term>Nitric Oxide Synthase Type II</term><term>Parkinson Disease (enzymology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Smoking (adverse effects)</term><term>Smoking (epidemiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Nitric Oxide Synthase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nitrates</term><term>Nitric Oxide</term><term>Nitric Oxide Synthase</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Smoking</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Neutrophils</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Smoking</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neutrophils</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Case-Control Studies</term><term>Genetic Predisposition to Disease</term><term>Humans</term><term>Nitric Oxide Synthase Type I</term><term>Nitric Oxide Synthase Type II</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Excess of nitric oxide (NO) has been shown to exert neurotoxic impacts in the brain. Moreover, inhibition of two NO-synthesizing enzymes, neuronal NOS (nNOS) and inducible NOS (iNOS), displays neuroprotective effects in the MPTP model of Parkinson's disease (PD). These data suggest a possible involvement of NOS as factors controlling the resistance of the nigral dopaminergic neurons to environmental insults. Therefore, we investigated whether polymorphisms present in these genes could contribute to the risk of developing PD. We carried out a community-based case-control study among subjects enrolled in the Mutualité Sociale Agricole, the French health insurance organization for workers connected to agriculture. Two-hundred and nine PD patients and 488 controls of European (mostly French) ancestry and matched for age, sex and region of residency were included in this study. Associations were observed with polymorphisms present in exon 22 of iNOS (OR for AA carriers=0.50, 95% CI=0.29-0.86, P=0.01) and in exon 29 of nNOS (OR for carriers of the T allele=1.53, 95% CI=1.08-2.16, P=0.02); no association was observed with a polymorphism in exon 18 of nNOS (OR for carriers of the T allele=1.20, 95% CI=0.85-1.69, P=0.30). Moreover, a significant interaction of the nNOS polymorphisms with current and ever cigarette smoking was found (nNOS 18, P=0.05; nNOS 29, P=0.04). All together, these data favour an involvement of these two genes as new modifier genes in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12490535</PMID><DateCreated><Year>2002</Year><Month>12</Month><Day>19</Day></DateCreated><DateCompleted><Year>2003</Year><Month>07</Month><Day>03</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0964-6906</ISSN><JournalIssue CitedMedium="Print"><Volume>12</Volume><Issue>1</Issue><PubDate><Year>2003</Year><Month>Jan</Month><Day>01</Day></PubDate></JournalIssue><Title>Human molecular genetics</Title><ISOAbbreviation>Hum. Mol. Genet.</ISOAbbreviation></Journal><ArticleTitle>Association between Parkinson's disease and polymorphisms in the nNOS and iNOS genes in a community-based case-control study.</ArticleTitle><Pagination><MedlinePgn>79-86</MedlinePgn></Pagination><Abstract><AbstractText>Excess of nitric oxide (NO) has been shown to exert neurotoxic impacts in the brain. Moreover, inhibition of two NO-synthesizing enzymes, neuronal NOS (nNOS) and inducible NOS (iNOS), displays neuroprotective effects in the MPTP model of Parkinson's disease (PD). These data suggest a possible involvement of NOS as factors controlling the resistance of the nigral dopaminergic neurons to environmental insults. Therefore, we investigated whether polymorphisms present in these genes could contribute to the risk of developing PD. We carried out a community-based case-control study among subjects enrolled in the Mutualité Sociale Agricole, the French health insurance organization for workers connected to agriculture. Two-hundred and nine PD patients and 488 controls of European (mostly French) ancestry and matched for age, sex and region of residency were included in this study. Associations were observed with polymorphisms present in exon 22 of iNOS (OR for AA carriers=0.50, 95% CI=0.29-0.86, P=0.01) and in exon 29 of nNOS (OR for carriers of the T allele=1.53, 95% CI=1.08-2.16, P=0.02); no association was observed with a polymorphism in exon 18 of nNOS (OR for carriers of the T allele=1.20, 95% CI=0.85-1.69, P=0.30). Moreover, a significant interaction of the nNOS polymorphisms with current and ever cigarette smoking was found (nNOS 18, P=0.05; nNOS 29, P=0.04). All together, these data favour an involvement of these two genes as new modifier genes in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Levecque</LastName><ForeName>Clotilde</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>INSERM Unit 508 Institut Pasteur de Lille, 59019 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Elbaz</LastName><ForeName>Alexis</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Clavel</LastName><ForeName>Jacqueline</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Richard</LastName><ForeName>Florence</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Vidal</LastName><ForeName>Jean-Sébastien</ForeName><Initials>JS</Initials></Author><Author ValidYN="Y"><LastName>Amouyel</LastName><ForeName>Philippe</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Tzourio</LastName><ForeName>Christophe</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Alpérovitch</LastName><ForeName>Annick</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Chartier-Harlin</LastName><ForeName>Marie-Christine</ForeName><Initials>MC</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Hum Mol Genet</MedlineTA><NlmUniqueID>9208958</NlmUniqueID><ISSNLinking>0964-6906</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009566">Nitrates</NameOfSubstance></Chemical><Chemical><RegistryNumber>31C4KY9ESH</RegistryNumber><NameOfSubstance UI="D009569">Nitric Oxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="C496320">NOS1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="C496319">NOS2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="D019001">Nitric Oxide Synthase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="D052248">Nitric Oxide Synthase Type I</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="D052247">Nitric Oxide Synthase Type II</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="N">Genetic Predisposition to 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UI="D052248" MajorTopicYN="N">Nitric Oxide Synthase Type I</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D052247" MajorTopicYN="N">Nitric Oxide Synthase Type II</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012907" MajorTopicYN="N">Smoking</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>12</Month><Day>20</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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