Association between Parkinson's disease and polymorphisms in the nNOS and iNOS genes in a community-based case–control study
Identifieur interne : 001963 ( Main/Corpus ); précédent : 001962; suivant : 001964Association between Parkinson's disease and polymorphisms in the nNOS and iNOS genes in a community-based case–control study
Auteurs : Clotilde Levecque ; Alexis Elbaz ; Jacqueline Clavel ; Florence Richard ; Jean-Se Bastien Vidal ; Philippe Amouyel ; Christophe Tzourio ; Annick Alpe Rovitch ; Marie-Christine Chartier-HarlinSource :
- Human Molecular Genetics [ 0964-6906 ] ; 2003-01-01.
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.
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DOI: 10.1093/hmg/ddg009
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sort="Clavel, Jacqueline" uniqKey="Clavel J" first="Jacqueline" last="Clavel">Jacqueline Clavel</name><affiliation><mods:affiliation>INSERM Unit 170, Villejuif, France and</mods:affiliation></affiliation></author><author><name sortKey="Richard, Florence" sort="Richard, Florence" uniqKey="Richard F" first="Florence" last="Richard">Florence Richard</name><affiliation><mods:affiliation>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</mods:affiliation></affiliation></author><author><name sortKey="Vidal, Jean Se Bastien" sort="Vidal, Jean Se Bastien" uniqKey="Vidal J" first="Jean-Se Bastien" last="Vidal">Jean-Se Bastien Vidal</name><affiliation><mods:affiliation>Service de Neurologie, Hôpital Saint-Antoine, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Amouyel, Philippe" sort="Amouyel, Philippe" uniqKey="Amouyel P" first="Philippe" last="Amouyel">Philippe Amouyel</name><affiliation><mods:affiliation>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</mods:affiliation></affiliation></author><author><name sortKey="Tzourio, Christophe" sort="Tzourio, Christophe" uniqKey="Tzourio C" first="Christophe" last="Tzourio">Christophe Tzourio</name><affiliation><mods:affiliation>INSERM Unit 360 Hôpital de la Salpêtrière, Paris, France,</mods:affiliation></affiliation></author><author><name sortKey="Alpe Rovitch, Annick" sort="Alpe Rovitch, Annick" uniqKey="Alpe Rovitch A" first="Annick" last="Alpe Rovitch">Annick Alpe Rovitch</name><affiliation><mods:affiliation>INSERM Unit 360 Hôpital de la Salpêtrière, Paris, France,</mods:affiliation></affiliation></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><affiliation><mods:affiliation>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Human Molecular Genetics</title><title level="j" type="abbrev">Hum. Mol. Genet.</title><idno type="ISSN">0964-6906</idno><idno type="eISSN">1460-2083</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2003-01-01">2003-01-01</date><biblScope unit="volume">12</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="79">79</biblScope><biblScope unit="page" to="86">86</biblScope></imprint><idno type="ISSN">0964-6906</idno></series><idno type="istex">C9F803C4DECDD03181C94FB6A3FFE350F6AF70F9</idno><idno type="DOI">10.1093/hmg/ddg009</idno><idno type="local">ddg009</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0964-6906</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></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><istex><corpusName>oup</corpusName><author><json:item><name>Clotilde Levecque</name><affiliations><json:string>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</json:string></affiliations></json:item><json:item><name>Alexis Elbaz</name><affiliations><json:string>INSERM Unit 360 Hôpital de la Salpêtrière, Paris, France,</json:string></affiliations></json:item><json:item><name>Jacqueline Clavel</name><affiliations><json:string>INSERM Unit 170, Villejuif, France and</json:string></affiliations></json:item><json:item><name>Florence Richard</name><affiliations><json:string>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</json:string></affiliations></json:item><json:item><name>Jean-Sébastien Vidal</name><affiliations><json:string>Service de Neurologie, Hôpital Saint-Antoine, Paris, France</json:string></affiliations></json:item><json:item><name>Philippe Amouyel</name><affiliations><json:string>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</json:string></affiliations></json:item><json:item><name>Christophe Tzourio</name><affiliations><json:string>INSERM Unit 360 Hôpital de la Salpêtrière, Paris, France,</json:string></affiliations></json:item><json:item><name>Annick Alpérovitch</name><affiliations><json:string>INSERM Unit 360 Hôpital de la Salpêtrière, Paris, France,</json:string></affiliations></json:item><json:item><name>Marie-Christine Chartier-Harlin</name><affiliations><json:string>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Article</value></json:item></subject><language><json:string>eng</json:string></language><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). 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Mol. Genet.</title><idno type="pISSN">0964-6906</idno><idno type="eISSN">1460-2083</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2003-01-01"></date><biblScope unit="volume">12</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="79">79</biblScope><biblScope unit="page" to="86">86</biblScope></imprint></monogr><idno type="istex">C9F803C4DECDD03181C94FB6A3FFE350F6AF70F9</idno><idno type="DOI">10.1093/hmg/ddg009</idno><idno type="local">ddg009</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2003</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>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.</p></abstract></profileDesc><revisionDesc><change when="2003-01-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-15">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/C9F803C4DECDD03181C94FB6A3FFE350F6AF70F9/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="US-ASCII"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">hmg</journal-id><journal-id journal-id-type="nlm-ta">Hum Mol Genet</journal-id><journal-id journal-id-type="publisher-id">hmg</journal-id><journal-title>Human Molecular Genetics</journal-title><abbrev-journal-title abbrev-type="publisher">Hum. Mol. Genet.</abbrev-journal-title><issn pub-type="ppub">0964-6906</issn><issn pub-type="epub">1460-2083</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">ddg009</article-id><article-id pub-id-type="doi">10.1093/hmg/ddg009</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Association between Parkinson's disease and polymorphisms in the nNOS and iNOS genes in a community-based case–control study</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Levecque</surname><given-names>Clotilde</given-names></name><xref rid="AF1">1</xref><xref rid="FN2">†</xref></contrib><contrib contrib-type="author"><name><surname>Elbaz</surname><given-names>Alexis</given-names></name><xref rid="AF2">2</xref><xref rid="FN2">†</xref></contrib><contrib contrib-type="author"><name><surname>Clavel</surname><given-names>Jacqueline</given-names></name><xref rid="AF3">3</xref></contrib><contrib contrib-type="author"><name><surname>Richard</surname><given-names>Florence</given-names></name><xref rid="AF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Vidal</surname><given-names>Jean-Sébastien</given-names></name><xref rid="AF4">4</xref></contrib><contrib contrib-type="author"><name><surname>Amouyel</surname><given-names>Philippe</given-names></name><xref rid="AF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Tzourio</surname><given-names>Christophe</given-names></name><xref rid="AF2">2</xref></contrib><contrib contrib-type="author"><name><surname>Alpérovitch</surname><given-names>Annick</given-names></name><xref rid="AF2">2</xref></contrib><contrib contrib-type="author"><name><surname>Chartier-Harlin</surname><given-names>Marie-Christine</given-names></name><xref rid="AF1">1</xref><xref rid="FN1">*</xref></contrib><aff id="AF1"><sup>1</sup>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</aff><aff id="AF2"><sup>2</sup>INSERM Unit 360 Hôpital de la Salpêtrière, Paris, France,</aff><aff id="AF3"><sup>3</sup>INSERM Unit 170, Villejuif, France and</aff><aff id="AF4"><sup>4</sup>Service de Neurologie, Hôpital Saint-Antoine, Paris, France</aff></contrib-group><pub-date pub-type="ppub"><day>1</day><month>01</month><year>2003</year></pub-date><volume>12</volume><issue>1</issue><fpage>79</fpage><lpage>86</lpage><history><date date-type="accepted"><day>11</day><month>11</month><year>2002</year></date><date date-type="received"><day>16</day><month>09</month><year>2002</year></date></history><permissions><copyright-year>2003</copyright-year></permissions><abstract xml:lang="en"><p>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, <italic>P</italic>=0.01) and in exon 29 of nNOS (OR for carriers of the T allele=1.53, 95% CI=1.08–2.16, <italic>P</italic>=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, <italic>P</italic>=0.30). Moreover, a significant interaction of the nNOS polymorphisms with current and ever cigarette smoking was found (nNOS 18, <italic>P</italic>=0.05; nNOS 29, <italic>P</italic>=0.04). All together, these data favour an involvement of these two genes as new modifier genes in PD.</p></abstract><custom-meta-wrap><custom-meta><meta-name>hwp-legacy-fpage</meta-name><meta-value>79</meta-value></custom-meta><custom-meta><meta-name>hwp-legacy-dochead</meta-name><meta-value>Article</meta-value></custom-meta></custom-meta-wrap></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Association between Parkinson's disease and polymorphisms in the nNOS and iNOS genes in a community-based case–control study</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Association between Parkinson's disease and polymorphisms in the nNOS and iNOS genes in a community-based case–control study</title></titleInfo><name type="personal"><namePart type="given">Clotilde</namePart><namePart type="family">Levecque</namePart><affiliation>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alexis</namePart><namePart type="family">Elbaz</namePart><affiliation>INSERM Unit 360 Hôpital de la Salpêtrière, Paris, France,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jacqueline</namePart><namePart type="family">Clavel</namePart><affiliation>INSERM Unit 170, Villejuif, France and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Florence</namePart><namePart type="family">Richard</namePart><affiliation>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean-Sébastien</namePart><namePart type="family">Vidal</namePart><affiliation>Service de Neurologie, Hôpital Saint-Antoine, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">Amouyel</namePart><affiliation>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christophe</namePart><namePart type="family">Tzourio</namePart><affiliation>INSERM Unit 360 Hôpital de la Salpêtrière, Paris, France,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Annick</namePart><namePart type="family">Alpérovitch</namePart><affiliation>INSERM Unit 360 Hôpital de la Salpêtrière, Paris, France,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marie-Christine</namePart><namePart type="family">Chartier-Harlin</namePart><affiliation>INSERM Unit 508 Institut Pasteur de Lille, Lille, France,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2003-01-01</dateIssued><copyrightDate encoding="w3cdtf">2003</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract 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.</abstract><relatedItem type="host"><titleInfo><title>Human Molecular Genetics</title></titleInfo><titleInfo type="abbreviated"><title>Hum. Mol. Genet.</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0964-6906</identifier><identifier type="eISSN">1460-2083</identifier><identifier type="PublisherID">hmg</identifier><identifier type="PublisherID-hwp">hmg</identifier><identifier type="PublisherID-nlm-ta">Hum Mol Genet</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>12</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>79</start><end>86</end></extent></part></relatedItem><identifier type="istex">C9F803C4DECDD03181C94FB6A3FFE350F6AF70F9</identifier><identifier type="DOI">10.1093/hmg/ddg009</identifier><identifier type="local">ddg009</identifier><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/C9F803C4DECDD03181C94FB6A3FFE350F6AF70F9/annexes/jpeg</uri></json:item><json:item><original>true</original><mimetype>image/gif</mimetype><extension>gif</extension><uri>https://api.istex.fr/document/C9F803C4DECDD03181C94FB6A3FFE350F6AF70F9/annexes/gif</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/C9F803C4DECDD03181C94FB6A3FFE350F6AF70F9/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">BIOCHEMISTRY & MOLECULAR BIOLOGY</classCode><classCode scheme="WOS">GENETICS & HEREDITY</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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