Association study of the NEDD9 gene with the risk of developing Alzheimer's and Parkinson's disease
Identifieur interne : 001E81 ( Main/Corpus ); précédent : 001E80; suivant : 001E82Association study of the NEDD9 gene with the risk of developing Alzheimer's and Parkinson's disease
Auteurs : Julien Chapuis ; Frdric Moisan ; Georges Mellick ; Alexis Elbaz ; Peter Silburn ; Florence Pasquier ; Didier Hannequin ; Corinne Lendon ; Dominique Campion ; Philippe Amouyel ; Jean-Charles LambertSource :
- Human Molecular Genetics [ 0964-6906 ] ; 2008-09-15.
Abstract
Alzheimer's disease (AD) and Parkinson's disease (PD), the two most common neurodegenerative disorders in the elderly, have been hypothesized to share genetic determinants. Recently, Li et al. proposed that a variant in the NEDD9 gene may be one of these common genetic factors. We attempted to confirm this initial observation by conducting an equivalent analysis in terms of pathologies and sample size. We genotyped the NEDD9 rs760678 SNP in three independent AD casecontrol studies (n 3176) and two independent PD casecontrol studies (n 1855). However, we failed to detect an association of this SNP with the risk of developing AD or PD, in any of these populations. In conclusion, these data indicate that the rs760678 SNP of the NEDD9 gene is at best a weak genetic determinant of AD or PD.
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DOI: 10.1093/hmg/ddn183
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Hannequin</name><affiliation><mods:affiliation>14, Faculty of Medicine, IFRMP, Rouen, France</mods:affiliation></affiliation></author><author><name sortKey="Lendon, Corinne" sort="Lendon, Corinne" uniqKey="Lendon C" first="Corinne" last="Lendon">Corinne Lendon</name><affiliation><mods:affiliation></mods:affiliation></affiliation></author><author><name sortKey="Campion, Dominique" sort="Campion, Dominique" uniqKey="Campion D" first="Dominique" last="Campion">Dominique Campion</name><affiliation><mods:affiliation>14, Faculty of Medicine, IFRMP, Rouen, 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></mods:affiliation></affiliation></author><author><name sortKey="Lambert, Jean Charles" sort="Lambert, Jean Charles" uniqKey="Lambert J" first="Jean-Charles" last="Lambert">Jean-Charles 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Recently, Li et al. proposed that a variant in the NEDD9 gene may be one of these common genetic factors. We attempted to confirm this initial observation by conducting an equivalent analysis in terms of pathologies and sample size. We genotyped the NEDD9 rs760678 SNP in three independent AD casecontrol studies (n 3176) and two independent PD casecontrol studies (n 1855). However, we failed to detect an association of this SNP with the risk of developing AD or PD, in any of these populations. In conclusion, these data indicate that the rs760678 SNP of the NEDD9 gene is at best a weak genetic determinant of AD or PD.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Julien Chapuis</name><affiliations><json:string>Inserm, U744, Institut Pasteur de Lille, Universit de Lille 2, Lille, France</json:string></affiliations></json:item><json:item><name>Frdric Moisan</name><affiliations><json:string>Inserm, U708, Hpital de la Salptrire, Paris, France</json:string><json:string>Universit Pierre et Marie Curie-Paris6, Paris, France</json:string></affiliations></json:item><json:item><name>Georges Mellick</name><affiliations><json:string>Eskitis Institue for Cell and Molecular Therapies, Griffith University, Queensland, Australia</json:string></affiliations></json:item><json:item><name>Alexis Elbaz</name><affiliations><json:string>Inserm, U708, Hpital de la Salptrire, Paris, France</json:string><json:string>Universit Pierre et Marie Curie-Paris6, Paris, France</json:string></affiliations></json:item><json:item><name>Peter Silburn</name><affiliations><json:string>Eskitis Institue for Cell and Molecular Therapies, Griffith University, Queensland, Australia</json:string></affiliations></json:item><json:item><name>Florence Pasquier</name><affiliations><json:string>EA2391, Department of Neurology, Memory Clinic, University Hospital of Lille, Lille, France</json:string></affiliations></json:item><json:item><name>Didier Hannequin</name><affiliations><json:string>Inserm, U614, Faculty of Medicine, IFRMP, Rouen, France</json:string></affiliations></json:item><json:item><name>Corinne Lendon</name><affiliations><json:string>Molecular Psychiatry Group, Queensland Institute of Medical Research, Brisbane, Australia</json:string></affiliations></json:item><json:item><name>Dominique Campion</name><affiliations><json:string>Inserm, U614, Faculty of Medicine, IFRMP, Rouen, France</json:string></affiliations></json:item><json:item><name>Philippe Amouyel</name><affiliations><json:string>Inserm, U744, Institut Pasteur de Lille, Universit de Lille 2, Lille, France</json:string></affiliations></json:item><json:item><name>Jean-Charles Lambert</name><affiliations><json:string>Inserm, U744, Institut Pasteur de Lille, Universit de Lille 2, Lille, France</json:string><json:string>E-mail: jean-charles.lambert@pasteur-lille.fr</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>ARTICLES</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Alzheimer's disease (AD) and Parkinson's disease (PD), the two most common neurodegenerative disorders in the elderly, have been hypothesized to share genetic determinants. Recently, Li et al. proposed that a variant in the NEDD9 gene may be one of these common genetic factors. We attempted to confirm this initial observation by conducting an equivalent analysis in terms of pathologies and sample size. We genotyped the NEDD9 rs760678 SNP in three independent AD casecontrol studies (n 3176) and two independent PD casecontrol studies (n 1855). However, we failed to detect an association of this SNP with the risk of developing AD or PD, in any of these populations. In conclusion, these data indicate that the rs760678 SNP of the NEDD9 gene is at best a weak genetic determinant of AD or PD.</abstract><qualityIndicators><score>4.442</score><pdfVersion>1.2</pdfVersion><pdfPageSize>612 x 797.953 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>1</keywordCount><abstractCharCount>796</abstractCharCount><pdfWordCount>2870</pdfWordCount><pdfCharCount>17763</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>131</abstractWordCount></qualityIndicators><title>Association study of the NEDD9 gene with the risk of developing Alzheimer's and Parkinson's disease</title><genre><json:string>research-article</json:string></genre><host><volume>17</volume><pages><last>2867</last><first>2863</first></pages><issn><json:string>0964-6906</json:string></issn><issue>18</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-2083</json:string></eissn><title>Human Molecular 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type="first">Philippe</forename><surname>Amouyel</surname></persName><affiliation></affiliation></author><author><persName><forename type="first">Jean-Charles</forename><surname>Lambert</surname></persName><email>jean-charles.lambert@pasteur-lille.fr</email><affiliation></affiliation></author></analytic><monogr><title level="j">Human Molecular Genetics</title><idno type="pISSN">0964-6906</idno><idno type="eISSN">1460-2083</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2008-09-15"></date><biblScope unit="volume">17</biblScope><biblScope unit="issue">18</biblScope><biblScope unit="page" from="2863">2863</biblScope><biblScope unit="page" to="2867">2867</biblScope></imprint></monogr><idno type="istex">A41BD80097BCF3CF1F839BFB926EC2C53657A76E</idno><idno type="DOI">10.1093/hmg/ddn183</idno><idno type="ArticleID">ddn183</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2008-06-25</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Alzheimer's disease (AD) and Parkinson's disease (PD), the two most common neurodegenerative disorders in the elderly, have been hypothesized to share genetic determinants. Recently, Li et al. proposed that a variant in the NEDD9 gene may be one of these common genetic factors. We attempted to confirm this initial observation by conducting an equivalent analysis in terms of pathologies and sample size. We genotyped the NEDD9 rs760678 SNP in three independent AD casecontrol studies (n 3176) and two independent PD casecontrol studies (n 1855). However, we failed to detect an association of this SNP with the risk of developing AD or PD, in any of these populations. In conclusion, these data indicate that the rs760678 SNP of the NEDD9 gene is at best a weak genetic determinant of AD or PD.</p></abstract></profileDesc><revisionDesc><change when="2008-06-25">Created</change><change when="2008-09-15">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/A41BD80097BCF3CF1F839BFB926EC2C53657A76E/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</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 article-type="research-article"><front><journal-meta><journal-id journal-id-type="publisher-id">hmg</journal-id><journal-id journal-id-type="hwp">hmg</journal-id><journal-title>Human Molecular Genetics</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="doi">10.1093/hmg/ddn183</article-id><article-id pub-id-type="publisher-id">ddn183</article-id><article-categories><subj-group subj-group-type="heading"><subject>ARTICLES</subject></subj-group></article-categories><title-group><article-title>Association study of the <italic>NEDD9</italic> gene with the risk of developing Alzheimer's and Parkinson's disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Chapuis</surname><given-names>Julien</given-names></name><xref ref-type="aff" rid="af1">1</xref></contrib><contrib contrib-type="author"><name><surname>Moisan</surname><given-names>Frédéric</given-names></name><xref ref-type="aff" rid="af2">2</xref><xref ref-type="aff" rid="af3">3</xref></contrib><contrib contrib-type="author"><name><surname>Mellick</surname><given-names>Georges</given-names></name><xref ref-type="aff" rid="af4">4</xref></contrib><contrib contrib-type="author"><name><surname>Elbaz</surname><given-names>Alexis</given-names></name><xref ref-type="aff" rid="af2">2</xref><xref ref-type="aff" rid="af3">3</xref></contrib><contrib contrib-type="author"><name><surname>Silburn</surname><given-names>Peter</given-names></name><xref ref-type="aff" rid="af4">4</xref></contrib><contrib contrib-type="author"><name><surname>Pasquier</surname><given-names>Florence</given-names></name><xref ref-type="aff" rid="af5">5</xref></contrib><contrib contrib-type="author"><name><surname>Hannequin</surname><given-names>Didier</given-names></name><xref ref-type="aff" rid="af6">6</xref></contrib><contrib contrib-type="author"><name><surname>Lendon</surname><given-names>Corinne</given-names></name><xref ref-type="aff" rid="af7">7</xref></contrib><contrib contrib-type="author"><name><surname>Campion</surname><given-names>Dominique</given-names></name><xref ref-type="aff" rid="af6">6</xref></contrib><contrib contrib-type="author"><name><surname>Amouyel</surname><given-names>Philippe</given-names></name><xref ref-type="aff" rid="af1">1</xref></contrib><contrib contrib-type="author"><name><surname>Lambert</surname><given-names>Jean-Charles</given-names></name><xref ref-type="aff" rid="af1">1</xref><xref ref-type="corresp" rid="cor1">*</xref></contrib></contrib-group><aff id="af1"><label>1</label><addr-line>Inserm, U744, Institut Pasteur de Lille</addr-line>, <institution>Université de Lille 2</institution>, <addr-line>Lille</addr-line>, <country>France</country></aff><aff id="af2"><label>2</label><addr-line>Inserm, U708, Hôpital de la Salpêtrière, Paris</addr-line>, <country>France</country></aff><aff id="af3"><label>3</label><institution>Université Pierre et Marie Curie-Paris6</institution>, <addr-line>Paris</addr-line>, <country>France</country></aff><aff id="af4"><label>4</label><addr-line>Eskitis Institue for Cell and Molecular Therapies</addr-line>, <institution>Griffith University</institution>, <addr-line>Queensland</addr-line>, <country>Australia</country></aff><aff id="af5"><label>5</label><addr-line>EA2391, Department of Neurology, Memory Clinic</addr-line>, <institution>University Hospital of Lille</institution>, <addr-line>Lille</addr-line>, <country>France</country></aff><aff id="af6"><label>6</label><addr-line>Inserm, U614, Faculty of Medicine, IFRMP, Rouen</addr-line>, <country>France</country></aff><aff id="af7"><label>7</label><addr-line>Molecular Psychiatry Group</addr-line>, <institution>Queensland Institute of Medical Research</institution>, <addr-line>Brisbane</addr-line>, <country>Australia</country></aff><author-notes><corresp id="cor1"><label>*</label>To whom correspondence should be addressed at: <addr-line>unité INSERM 744</addr-line>, <institution>Institut Pasteur de Lille</institution>, <addr-line>BP 245, 1, rue du professeur Calmette, 59019 Lille cédex</addr-line>, <country>France</country>. Tel: <phone>+33 320 877391</phone>; Fax: <fax>+33 320 877894</fax>; Email: <email>jean-charles.lambert@pasteur-lille.fr</email></corresp></author-notes><pub-date pub-type="ppub"><day>15</day><month>9</month><year>2008</year></pub-date><pub-date pub-type="epub"><day>25</day><month>6</month><year>2008</year></pub-date><volume>17</volume><issue>18</issue><fpage>2863</fpage><lpage>2867</lpage><history><date date-type="received"><day>26</day><month>5</month><year>2008</year></date><date date-type="accepted"><day>22</day><month>6</month><year>2008</year></date></history><copyright-statement>© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</copyright-statement><copyright-year>2008</copyright-year><abstract><p>Alzheimer's disease (AD) and Parkinson's disease (PD), the two most common neurodegenerative disorders in the elderly, have been hypothesized to share genetic determinants. Recently, Li <italic>et al</italic>. proposed that a variant in the <italic>NEDD9</italic> gene may be one of these common genetic factors. We attempted to confirm this initial observation by conducting an equivalent analysis in terms of pathologies and sample size. We genotyped the <italic>NEDD9</italic> rs760678 SNP in three independent AD case–control studies (<italic>n</italic> = 3176) and two independent PD case–control studies (<italic>n</italic> = 1855). However, we failed to detect an association of this SNP with the risk of developing AD or PD, in any of these populations. In conclusion, these data indicate that the rs760678 SNP of the <italic>NEDD9</italic> gene is at best a weak genetic determinant of AD or PD.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Association study of the NEDD9 gene with the risk of developing Alzheimer's and Parkinson's disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Association study of the NEDD9 gene with the risk of developing Alzheimer's and Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Julien</namePart><namePart type="family">Chapuis</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Frdric</namePart><namePart type="family">Moisan</namePart><affiliation></affiliation><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Georges</namePart><namePart type="family">Mellick</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alexis</namePart><namePart type="family">Elbaz</namePart><affiliation></affiliation><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">Silburn</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Florence</namePart><namePart type="family">Pasquier</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Didier</namePart><namePart type="family">Hannequin</namePart><affiliation>14, Faculty of Medicine, IFRMP, Rouen, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Corinne</namePart><namePart type="family">Lendon</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dominique</namePart><namePart type="family">Campion</namePart><affiliation>14, Faculty of Medicine, IFRMP, Rouen, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">Amouyel</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean-Charles</namePart><namePart type="family">Lambert</namePart><affiliation></affiliation><affiliation>E-mail: jean-charles.lambert@pasteur-lille.fr</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">2008-09-15</dateIssued><dateCreated encoding="w3cdtf">2008-06-25</dateCreated><copyrightDate encoding="w3cdtf">2008</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>Alzheimer's disease (AD) and Parkinson's disease (PD), the two most common neurodegenerative disorders in the elderly, have been hypothesized to share genetic determinants. Recently, Li et al. proposed that a variant in the NEDD9 gene may be one of these common genetic factors. We attempted to confirm this initial observation by conducting an equivalent analysis in terms of pathologies and sample size. We genotyped the NEDD9 rs760678 SNP in three independent AD casecontrol studies (n 3176) and two independent PD casecontrol studies (n 1855). However, we failed to detect an association of this SNP with the risk of developing AD or PD, in any of these populations. In conclusion, these data indicate that the rs760678 SNP of the NEDD9 gene is at best a weak genetic determinant of AD or PD.</abstract><relatedItem type="host"><titleInfo><title>Human Molecular Genetics</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><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>18</number></detail><extent unit="pages"><start>2863</start><end>2867</end></extent></part></relatedItem><identifier type="istex">A41BD80097BCF3CF1F839BFB926EC2C53657A76E</identifier><identifier type="DOI">10.1093/hmg/ddn183</identifier><identifier type="ArticleID">ddn183</identifier><accessCondition type="use and reproduction" contentType="copyright">The Author 2008. Published by Oxford University Press. All rights reserved. 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