SNCA, MAPT, and GSK3B in Parkinson disease: a gene–gene interaction study
Identifieur interne : 000732 ( Main/Corpus ); précédent : 000731; suivant : 000733SNCA, MAPT, and GSK3B in Parkinson disease: a gene–gene interaction study
Auteurs : C. Wider ; C. Vilari O-Güell ; M. G. Heckman ; B. Jasinska-Myga ; A. I. Ortolaza-Soto ; N. N. Diehl ; J. E. Crook ; S. A. Cobb ; J. A. Bacon ; J. O. Aasly ; J. M. Gibson ; T. Lynch ; R. J. Uitti ; Z. K. Wszolek ; M. J. Farrer ; O. A. RossSource :
- European Journal of Neurology [ 1351-5101 ] ; 2011-06.
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Abstract
Background and purpose: Recent evidence suggests that variation in the SNCA, MAPT, and GSK3B genes interacts in affecting risk for Parkinson disease (PD). In the current study, we attempt to validate previously published findings, evaluating gene–gene interactions between SNCA, MAPT, and GSK3B in association with PD. Methods: Three Caucasian PD patient–control series from the United States, Ireland, and Norway (combined n = 1020 patients and 1095 controls) were genotyped for SNCA rs356219, MAPT H1/H2‐discriminating SNP rs1052553, and GSK3B rs334558 and rs6438552. Results: Our findings indicate that as previously reported, the SNCA rs356219‐G allele and MAPT rs1052553 (H1 haplotype) were both associated with an increased risk of PD, whilst contrary to previous reports, GSK3B variants were not. No pair‐wise interaction was observed between SNCA, MAPT, and GSK3B; the risk effects of SNCA rs356219‐G and MAPT rs1052553‐H1 were seen in a similar manner across genotypes of other variants, with no evidence suggesting synergistic, antagonistic, or deferential effects. Conclusions: In the Caucasian patient–control series examined, risk for PD was influenced by variation in SNCA and MAPT but not GSK3B. Additionally, those three genes did not interact in determining disease risk.
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DOI: 10.1111/j.1468-1331.2010.03297.x
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Vilari O-Güell</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Heckman, M G" sort="Heckman, M G" uniqKey="Heckman M" first="M. G." last="Heckman">M. G. Heckman</name><affiliation><mods:affiliation>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Jasinska Yga, B" sort="Jasinska Yga, B" uniqKey="Jasinska Yga B" first="B." last="Jasinska-Myga">B. Jasinska-Myga</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Medical University of Silesia, Katowice, Poland</mods:affiliation></affiliation></author><author><name sortKey="Ortolaza Oto, A I" sort="Ortolaza Oto, A I" uniqKey="Ortolaza Oto A" first="A. 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Wszolek</name><affiliation><mods:affiliation>Department of Neurology, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Farrer, M J" sort="Farrer, M J" uniqKey="Farrer M" first="M. J." last="Farrer">M. J. Farrer</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Ross, O A" sort="Ross, O A" uniqKey="Ross O" first="O. A." last="Ross">O. A. Ross</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A57633AA3A8126E755E495E6F81A87D2F72ABC6C</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1111/j.1468-1331.2010.03297.x</idno><idno type="url">https://api.istex.fr/document/A57633AA3A8126E755E495E6F81A87D2F72ABC6C/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000732</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">SNCA, MAPT, and GSK3B in Parkinson disease: a gene–gene interaction study</title><author><name sortKey="Wider, C" sort="Wider, C" uniqKey="Wider C" first="C." last="Wider">C. Wider</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Clinical Neurosciences, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Vilari O Ell, C" sort="Vilari O Ell, C" uniqKey="Vilari O Ell C" first="C." last="Vilari O-Güell">C. Vilari O-Güell</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Heckman, M G" sort="Heckman, M G" uniqKey="Heckman M" first="M. G." last="Heckman">M. G. Heckman</name><affiliation><mods:affiliation>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Jasinska Yga, B" sort="Jasinska Yga, B" uniqKey="Jasinska Yga B" first="B." last="Jasinska-Myga">B. Jasinska-Myga</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Medical University of Silesia, Katowice, Poland</mods:affiliation></affiliation></author><author><name sortKey="Ortolaza Oto, A I" sort="Ortolaza Oto, A I" uniqKey="Ortolaza Oto A" first="A. I." last="Ortolaza-Soto">A. I. Ortolaza-Soto</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Diehl, N N" sort="Diehl, N N" uniqKey="Diehl N" first="N. N." last="Diehl">N. N. Diehl</name><affiliation><mods:affiliation>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Crook, J E" sort="Crook, J E" uniqKey="Crook J" first="J. E." last="Crook">J. E. Crook</name><affiliation><mods:affiliation>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Cobb, S A" sort="Cobb, S A" uniqKey="Cobb S" first="S. A." last="Cobb">S. A. Cobb</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Bacon, J A" sort="Bacon, J A" uniqKey="Bacon J" first="J. A." last="Bacon">J. A. Bacon</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Aasly, J O" sort="Aasly, J O" uniqKey="Aasly J" first="J. O." last="Aasly">J. O. Aasly</name><affiliation><mods:affiliation>Department of Neuroscience, Norwegian University of Science and Technology, Trondheim, Norway</mods:affiliation></affiliation></author><author><name sortKey="Gibson, J M" sort="Gibson, J M" uniqKey="Gibson J" first="J. M." last="Gibson">J. M. Gibson</name><affiliation><mods:affiliation>Department of Neurology, Royal Victoria Hospital, Belfast, Ireland</mods:affiliation></affiliation></author><author><name sortKey="Lynch, T" sort="Lynch, T" uniqKey="Lynch T" first="T." last="Lynch">T. Lynch</name><affiliation><mods:affiliation>Dublin Neurological Institute at the Mater Misericordiae Hospital and University College Dublin Conway Neuroscience Investigator, Dublin, Ireland</mods:affiliation></affiliation></author><author><name sortKey="Uitti, R J" sort="Uitti, R J" uniqKey="Uitti R" first="R. J." last="Uitti">R. J. Uitti</name><affiliation><mods:affiliation>Department of Neurology, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Wszolek, Z K" sort="Wszolek, Z K" uniqKey="Wszolek Z" first="Z. K." last="Wszolek">Z. K. Wszolek</name><affiliation><mods:affiliation>Department of Neurology, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Farrer, M J" sort="Farrer, M J" uniqKey="Farrer M" first="M. J." last="Farrer">M. J. Farrer</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Ross, O A" sort="Ross, O A" uniqKey="Ross O" first="O. A." last="Ross">O. A. Ross</name><affiliation><mods:affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neurology</title><idno type="ISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-06">2011-06</date><biblScope unit="volume">18</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="876">876</biblScope><biblScope unit="page" to="881">881</biblScope></imprint><idno type="ISSN">1351-5101</idno></series><idno type="istex">A57633AA3A8126E755E495E6F81A87D2F72ABC6C</idno><idno type="DOI">10.1111/j.1468-1331.2010.03297.x</idno><idno type="ArticleID">ENE3297</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1351-5101</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>GSK3B</term><term>MAPT</term><term>Parkinson disease</term><term>SNCA</term><term>genetics</term><term>gene–gene interaction</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background and purpose: Recent evidence suggests that variation in the SNCA, MAPT, and GSK3B genes interacts in affecting risk for Parkinson disease (PD). In the current study, we attempt to validate previously published findings, evaluating gene–gene interactions between SNCA, MAPT, and GSK3B in association with PD. Methods: Three Caucasian PD patient–control series from the United States, Ireland, and Norway (combined n = 1020 patients and 1095 controls) were genotyped for SNCA rs356219, MAPT H1/H2‐discriminating SNP rs1052553, and GSK3B rs334558 and rs6438552. Results: Our findings indicate that as previously reported, the SNCA rs356219‐G allele and MAPT rs1052553 (H1 haplotype) were both associated with an increased risk of PD, whilst contrary to previous reports, GSK3B variants were not. No pair‐wise interaction was observed between SNCA, MAPT, and GSK3B; the risk effects of SNCA rs356219‐G and MAPT rs1052553‐H1 were seen in a similar manner across genotypes of other variants, with no evidence suggesting synergistic, antagonistic, or deferential effects. Conclusions: In the Caucasian patient–control series examined, risk for PD was influenced by variation in SNCA and MAPT but not GSK3B. Additionally, those three genes did not interact in determining disease risk.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>C. Wider</name><affiliations><json:string>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</json:string><json:string>Department of Clinical Neurosciences, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland</json:string></affiliations></json:item><json:item><name>C. Vilariño‐Güell</name><affiliations><json:string>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</json:string></affiliations></json:item><json:item><name>M. G. Heckman</name><affiliations><json:string>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</json:string></affiliations></json:item><json:item><name>B. Jasinska‐Myga</name><affiliations><json:string>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</json:string><json:string>Department of Neurology, Medical University of Silesia, Katowice, Poland</json:string></affiliations></json:item><json:item><name>A. I. Ortolaza‐Soto</name><affiliations><json:string>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</json:string></affiliations></json:item><json:item><name>N. N. Diehl</name><affiliations><json:string>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</json:string></affiliations></json:item><json:item><name>J. E. Crook</name><affiliations><json:string>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</json:string></affiliations></json:item><json:item><name>S. A. Cobb</name><affiliations><json:string>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</json:string></affiliations></json:item><json:item><name>J. A. Bacon</name><affiliations><json:string>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</json:string></affiliations></json:item><json:item><name>J. O. Aasly</name><affiliations><json:string>Department of Neuroscience, Norwegian University of Science and Technology, Trondheim, Norway</json:string></affiliations></json:item><json:item><name>J. M. Gibson</name><affiliations><json:string>Department of Neurology, Royal Victoria Hospital, Belfast, Ireland</json:string></affiliations></json:item><json:item><name>T. Lynch</name><affiliations><json:string>Dublin Neurological Institute at the Mater Misericordiae Hospital and University College Dublin Conway Neuroscience Investigator, Dublin, Ireland</json:string></affiliations></json:item><json:item><name>R. J. Uitti</name><affiliations><json:string>Department of Neurology, Mayo Clinic, Jacksonville, FL, USA</json:string></affiliations></json:item><json:item><name>Z. K. Wszolek</name><affiliations><json:string>Department of Neurology, Mayo Clinic, Jacksonville, FL, USA</json:string></affiliations></json:item><json:item><name>M. J. Farrer</name><affiliations><json:string>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</json:string></affiliations></json:item><json:item><name>O. A. Ross</name><affiliations><json:string>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>gene–gene interaction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>genetics</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>GSK3B</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MAPT</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SNCA</value></json:item></subject><articleId><json:string>ENE3297</json:string></articleId><language><json:string>eng</json:string></language><abstract>Background and purpose: Recent evidence suggests that variation in the SNCA, MAPT, and GSK3B genes interacts in affecting risk for Parkinson disease (PD). In the current study, we attempt to validate previously published findings, evaluating gene–gene interactions between SNCA, MAPT, and GSK3B in association with PD. Methods: Three Caucasian PD patient–control series from the United States, Ireland, and Norway (combined n = 1020 patients and 1095 controls) were genotyped for SNCA rs356219, MAPT H1/H2‐discriminating SNP rs1052553, and GSK3B rs334558 and rs6438552. Results: Our findings indicate that as previously reported, the SNCA rs356219‐G allele and MAPT rs1052553 (H1 haplotype) were both associated with an increased risk of PD, whilst contrary to previous reports, GSK3B variants were not. No pair‐wise interaction was observed between SNCA, MAPT, and GSK3B; the risk effects of SNCA rs356219‐G and MAPT rs1052553‐H1 were seen in a similar manner across genotypes of other variants, with no evidence suggesting synergistic, antagonistic, or deferential effects. Conclusions: In the Caucasian patient–control series examined, risk for PD was influenced by variation in SNCA and MAPT but not GSK3B. Additionally, those three genes did not interact in determining disease risk.</abstract><qualityIndicators><score>5.356</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>1292</abstractCharCount><pdfWordCount>3136</pdfWordCount><pdfCharCount>21491</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>185</abstractWordCount></qualityIndicators><title>SNCA, MAPT, and GSK3B in Parkinson disease: a gene–gene interaction study</title><genre><json:string>article</json:string></genre><host><volume>18</volume><publisherId><json:string>ENE</json:string></publisherId><pages><total>6</total><last>881</last><first>876</first></pages><issn><json:string>1351-5101</json:string></issn><issue>6</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-1331</json:string></eissn><title>European Journal of Neurology</title><doi><json:string>10.1111/(ISSN)1468-1331</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1111/j.1468-1331.2010.03297.x</json:string></doi><id>A57633AA3A8126E755E495E6F81A87D2F72ABC6C</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/A57633AA3A8126E755E495E6F81A87D2F72ABC6C/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/A57633AA3A8126E755E495E6F81A87D2F72ABC6C/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/A57633AA3A8126E755E495E6F81A87D2F72ABC6C/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">SNCA, MAPT, and GSK3B in Parkinson disease: a gene–gene interaction study</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">SNCA, MAPT, and GSK3B in Parkinson disease: a gene–gene interaction study</title><author><persName><forename type="first">C.</forename><surname>Wider</surname></persName><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation><affiliation>Department of Clinical Neurosciences, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland</affiliation></author><author><persName><forename type="first">C.</forename><surname>Vilariño‐Güell</surname></persName><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation></author><author><persName><forename type="first">M. G.</forename><surname>Heckman</surname></persName><affiliation>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</affiliation></author><author><persName><forename type="first">B.</forename><surname>Jasinska‐Myga</surname></persName><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation><affiliation>Department of Neurology, Medical University of Silesia, Katowice, Poland</affiliation></author><author><persName><forename type="first">A. I.</forename><surname>Ortolaza‐Soto</surname></persName><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation></author><author><persName><forename type="first">N. N.</forename><surname>Diehl</surname></persName><affiliation>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</affiliation></author><author><persName><forename type="first">J. E.</forename><surname>Crook</surname></persName><affiliation>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</affiliation></author><author><persName><forename type="first">S. A.</forename><surname>Cobb</surname></persName><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation></author><author><persName><forename type="first">J. A.</forename><surname>Bacon</surname></persName><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation></author><author><persName><forename type="first">J. O.</forename><surname>Aasly</surname></persName><affiliation>Department of Neuroscience, Norwegian University of Science and Technology, Trondheim, Norway</affiliation></author><author><persName><forename type="first">J. M.</forename><surname>Gibson</surname></persName><affiliation>Department of Neurology, Royal Victoria Hospital, Belfast, Ireland</affiliation></author><author><persName><forename type="first">T.</forename><surname>Lynch</surname></persName><affiliation>Dublin Neurological Institute at the Mater Misericordiae Hospital and University College Dublin Conway Neuroscience Investigator, Dublin, Ireland</affiliation></author><author><persName><forename type="first">R. J.</forename><surname>Uitti</surname></persName><affiliation>Department of Neurology, Mayo Clinic, Jacksonville, FL, USA</affiliation></author><author><persName><forename type="first">Z. K.</forename><surname>Wszolek</surname></persName><affiliation>Department of Neurology, Mayo Clinic, Jacksonville, FL, USA</affiliation></author><author><persName><forename type="first">M. J.</forename><surname>Farrer</surname></persName><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation></author><author><persName><forename type="first">O. A.</forename><surname>Ross</surname></persName><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation></author></analytic><monogr><title level="j">European Journal of Neurology</title><idno type="pISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><idno type="DOI">10.1111/(ISSN)1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-06"></date><biblScope unit="volume">18</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="876">876</biblScope><biblScope unit="page" to="881">881</biblScope></imprint></monogr><idno type="istex">A57633AA3A8126E755E495E6F81A87D2F72ABC6C</idno><idno type="DOI">10.1111/j.1468-1331.2010.03297.x</idno><idno type="ArticleID">ENE3297</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Background and purpose: Recent evidence suggests that variation in the SNCA, MAPT, and GSK3B genes interacts in affecting risk for Parkinson disease (PD). In the current study, we attempt to validate previously published findings, evaluating gene–gene interactions between SNCA, MAPT, and GSK3B in association with PD. Methods: Three Caucasian PD patient–control series from the United States, Ireland, and Norway (combined n = 1020 patients and 1095 controls) were genotyped for SNCA rs356219, MAPT H1/H2‐discriminating SNP rs1052553, and GSK3B rs334558 and rs6438552. Results: Our findings indicate that as previously reported, the SNCA rs356219‐G allele and MAPT rs1052553 (H1 haplotype) were both associated with an increased risk of PD, whilst contrary to previous reports, GSK3B variants were not. No pair‐wise interaction was observed between SNCA, MAPT, and GSK3B; the risk effects of SNCA rs356219‐G and MAPT rs1052553‐H1 were seen in a similar manner across genotypes of other variants, with no evidence suggesting synergistic, antagonistic, or deferential effects. Conclusions: In the Caucasian patient–control series examined, risk for PD was influenced by variation in SNCA and MAPT but not GSK3B. Additionally, those three genes did not interact in determining disease risk.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>gene–gene interaction</term></item><item><term>genetics</term></item><item><term>GSK3B</term></item><item><term>MAPT</term></item><item><term>Parkinson disease</term></item><item><term>SNCA</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2011-06">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/A57633AA3A8126E755E495E6F81A87D2F72ABC6C/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1468-1331</doi><issn type="print">1351-5101</issn><issn type="electronic">1468-1331</issn><idGroup><id type="product" value="ENE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROLOGY">European Journal of Neurology</title></titleGroup></publicationMeta><publicationMeta level="part" position="06106"><doi origin="wiley">10.1111/ene.2011.18.issue-6</doi><numberingGroup><numbering type="journalVolume" number="18">18</numbering><numbering type="journalIssue" number="6">6</numbering></numberingGroup><coverDate startDate="2011-06">June 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="13" status="forIssue"><doi origin="wiley">10.1111/j.1468-1331.2010.03297.x</doi><idGroup><id type="unit" value="ENE3297"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><copyright>© 2010 The Author(s). European Journal of Neurology © 2010 EFNS</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.4.9 mode:FullText" date="2011-05-09"></event><event type="publishedOnlineEarlyUnpaginated" date="2010-12-15"></event><event type="firstOnline" date="2010-12-15"></event><event type="publishedOnlineFinalForm" date="2011-05-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-24"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="876">876</numbering><numbering type="pageLast" number="881">881</numbering></numberingGroup><correspondenceTo>C. Wider, MD, Department of Clinical Neurosciences, Centre Hospitalier Universitaire Vaudois (CHUV), Bugnon 46, 1011 Lausanne, Switzerland (tel.: +41 79 556 8117; fax: +41 21 314 1244; e‐mail: <email>christian.wider@chuv.ch</email>).</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ENE.ENE3297.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 12 October 2010 Accepted 3 November 2010</unparsedEditorialHistory><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="4"></count></countGroup><titleGroup><title type="main"><i>SNCA</i>, <i>MAPT</i>, and <i>GSK3B</i> in Parkinson disease: a gene–gene interaction study</title><title type="shortAuthors">C. Wider <i>et al.</i></title><title type="short"><i>SNCA</i>, <i>MAPT</i> and <i>GSK3B</i> in Parkinson disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>C.</givenNames><familyName>Wider</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>C.</givenNames><familyName>Vilariño‐Güell</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a3"><personName><givenNames>M. G.</givenNames><familyName>Heckman</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1 #a4"><personName><givenNames>B.</givenNames><familyName>Jasinska‐Myga</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>A. I.</givenNames><familyName>Ortolaza‐Soto</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a3"><personName><givenNames>N. N.</givenNames><familyName>Diehl</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a3"><personName><givenNames>J. E.</givenNames><familyName>Crook</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a1"><personName><givenNames>S. A.</givenNames><familyName>Cobb</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a1"><personName><givenNames>J. A.</givenNames><familyName>Bacon</familyName></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a5"><personName><givenNames>J. O.</givenNames><familyName>Aasly</familyName></personName></creator><creator creatorRole="author" xml:id="cr11" affiliationRef="#a6"><personName><givenNames>J. M.</givenNames><familyName>Gibson</familyName></personName></creator><creator creatorRole="author" xml:id="cr12" affiliationRef="#a7"><personName><givenNames>T.</givenNames><familyName>Lynch</familyName></personName></creator><creator creatorRole="author" xml:id="cr13" affiliationRef="#a8"><personName><givenNames>R. J.</givenNames><familyName>Uitti</familyName></personName></creator><creator creatorRole="author" xml:id="cr14" affiliationRef="#a8"><personName><givenNames>Z. K.</givenNames><familyName>Wszolek</familyName></personName></creator><creator creatorRole="author" xml:id="cr15" affiliationRef="#a1"><personName><givenNames>M. J.</givenNames><familyName>Farrer</familyName></personName></creator><creator creatorRole="author" xml:id="cr16" affiliationRef="#a1"><personName><givenNames>O. A.</givenNames><familyName>Ross</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="CH"><unparsedAffiliation>Department of Clinical Neurosciences, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="US"><unparsedAffiliation>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="PL"><unparsedAffiliation>Department of Neurology, Medical University of Silesia, Katowice, Poland</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="NO"><unparsedAffiliation>Department of Neuroscience, Norwegian University of Science and Technology, Trondheim, Norway</unparsedAffiliation></affiliation><affiliation xml:id="a6" countryCode="IE"><unparsedAffiliation>Department of Neurology, Royal Victoria Hospital, Belfast, Ireland</unparsedAffiliation></affiliation><affiliation xml:id="a7" countryCode="IE"><unparsedAffiliation>Dublin Neurological Institute at the Mater Misericordiae Hospital and University College Dublin Conway Neuroscience Investigator, Dublin, Ireland</unparsedAffiliation></affiliation><affiliation xml:id="a8" countryCode="US"><unparsedAffiliation>Department of Neurology, Mayo Clinic, Jacksonville, FL, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">gene–gene interaction</keyword><keyword xml:id="k2">genetics</keyword><keyword xml:id="k3"><i>GSK3B</i></keyword><keyword xml:id="k4"><i>MAPT</i></keyword><keyword xml:id="k5">Parkinson disease</keyword><keyword xml:id="k6"><i>SNCA</i></keyword></keywordGroup><supportingInformation><p><b>Table S1.</b> Allele and genotype frequencies in the US series.</p><p><b>Table S2.</b> Allele and genotype frequencies in the Irish series.</p><p><b>Table S3.</b> Allele and genotype frequencies in the Norwegian series.</p><supportingInfoItem><mediaResource alt="supporting info item" href="urn-x:wiley:13515101:media:ene3297:ENE_3297_sm_Table1-3"></mediaResource><caption>Supporting info item</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><p><b>Background and purpose: </b> Recent evidence suggests that variation in the <i>SNCA</i>, <i>MAPT</i>, and <i>GSK3B</i> genes interacts in affecting risk for Parkinson disease (PD). In the current study, we attempt to validate previously published findings, evaluating gene–gene interactions between <i>SNCA</i>, <i>MAPT</i>, and <i>GSK3B</i> in association with PD.</p><p><b>Methods: </b> Three Caucasian PD patient–control series from the United States, Ireland, and Norway (combined <i>n</i> = 1020 patients and 1095 controls) were genotyped for <i>SNCA</i> rs356219, <i>MAPT</i> H1/H2‐discriminating SNP rs1052553, and <i>GSK3B</i> rs334558 and rs6438552.</p><p><b>Results: </b> Our findings indicate that as previously reported, the <i>SNCA</i> rs356219‐G allele and <i>MAPT</i> rs1052553 (H1 haplotype) were both associated with an increased risk of PD, whilst contrary to previous reports, <i>GSK3B</i> variants were not. No pair‐wise interaction was observed between <i>SNCA</i>, <i>MAPT</i>, and <i>GSK3B</i>; the risk effects of <i>SNCA</i> rs356219‐G and <i>MAPT</i> rs1052553‐H1 were seen in a similar manner across genotypes of other variants, with no evidence suggesting synergistic, antagonistic, or deferential effects.</p><p><b>Conclusions: </b> In the Caucasian patient–control series examined, risk for PD was influenced by variation in <i>SNCA</i> and <i>MAPT</i> but not <i>GSK3B</i>. Additionally, those three genes did not interact in determining disease risk.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>SNCA, MAPT, and GSK3B in Parkinson disease: a gene–gene interaction study</title></titleInfo><titleInfo type="abbreviated"><title>SNCA, MAPT and GSK3B in Parkinson disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>,</title></titleInfo><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Wider</namePart><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation><affiliation>Department of Clinical Neurosciences, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Vilariño‐Güell</namePart><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. G.</namePart><namePart type="family">Heckman</namePart><affiliation>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Jasinska‐Myga</namePart><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation><affiliation>Department of Neurology, Medical University of Silesia, Katowice, Poland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. I.</namePart><namePart type="family">Ortolaza‐Soto</namePart><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N. N.</namePart><namePart type="family">Diehl</namePart><affiliation>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. E.</namePart><namePart type="family">Crook</namePart><affiliation>Biostatistics Unit, Mayo Clinic, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S. A.</namePart><namePart type="family">Cobb</namePart><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. A.</namePart><namePart type="family">Bacon</namePart><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. O.</namePart><namePart type="family">Aasly</namePart><affiliation>Department of Neuroscience, Norwegian University of Science and Technology, Trondheim, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. M.</namePart><namePart type="family">Gibson</namePart><affiliation>Department of Neurology, Royal Victoria Hospital, Belfast, Ireland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Lynch</namePart><affiliation>Dublin Neurological Institute at the Mater Misericordiae Hospital and University College Dublin Conway Neuroscience Investigator, Dublin, Ireland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R. J.</namePart><namePart type="family">Uitti</namePart><affiliation>Department of Neurology, Mayo Clinic, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Z. K.</namePart><namePart type="family">Wszolek</namePart><affiliation>Department of Neurology, Mayo Clinic, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. J.</namePart><namePart type="family">Farrer</namePart><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O. A.</namePart><namePart type="family">Ross</namePart><affiliation>Division of Neurogenetics, Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2011-06</dateIssued><edition>Received 12 October 2010 Accepted 3 November 2010</edition><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="tables">4</extent></physicalDescription><abstract lang="en">Background and purpose: Recent evidence suggests that variation in the SNCA, MAPT, and GSK3B genes interacts in affecting risk for Parkinson disease (PD). In the current study, we attempt to validate previously published findings, evaluating gene–gene interactions between SNCA, MAPT, and GSK3B in association with PD. Methods: Three Caucasian PD patient–control series from the United States, Ireland, and Norway (combined n = 1020 patients and 1095 controls) were genotyped for SNCA rs356219, MAPT H1/H2‐discriminating SNP rs1052553, and GSK3B rs334558 and rs6438552. Results: Our findings indicate that as previously reported, the SNCA rs356219‐G allele and MAPT rs1052553 (H1 haplotype) were both associated with an increased risk of PD, whilst contrary to previous reports, GSK3B variants were not. No pair‐wise interaction was observed between SNCA, MAPT, and GSK3B; the risk effects of SNCA rs356219‐G and MAPT rs1052553‐H1 were seen in a similar manner across genotypes of other variants, with no evidence suggesting synergistic, antagonistic, or deferential effects. Conclusions: In the Caucasian patient–control series examined, risk for PD was influenced by variation in SNCA and MAPT but not GSK3B. Additionally, those three genes did not interact in determining disease risk.</abstract><subject lang="en"><genre>Keywords</genre><topic>gene–gene interaction</topic><topic>genetics</topic><topic>GSK3B</topic><topic>MAPT</topic><topic>Parkinson disease</topic><topic>SNCA</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neurology</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Table S1. Allele and genotype frequencies in the US series. Table S2. Allele and genotype frequencies in the Irish series. Table S3. Allele and genotype frequencies in the Norwegian series. Table S1. Allele and genotype frequencies in the US series. Table S2. Allele and genotype frequencies in the Irish series. Table S3. Allele and genotype frequencies in the Norwegian series. Table S1. Allele and genotype frequencies in the US series. Table S2. Allele and genotype frequencies in the Irish series. Table S3. Allele and genotype frequencies in the Norwegian series.Supporting Info Item: Supporting info item - </note><identifier type="ISSN">1351-5101</identifier><identifier type="eISSN">1468-1331</identifier><identifier type="DOI">10.1111/(ISSN)1468-1331</identifier><identifier type="PublisherID">ENE</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>876</start><end>881</end><total>6</total></extent></part></relatedItem><identifier type="istex">A57633AA3A8126E755E495E6F81A87D2F72ABC6C</identifier><identifier type="DOI">10.1111/j.1468-1331.2010.03297.x</identifier><identifier type="ArticleID">ENE3297</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2010 The Author(s). 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