Genomewide association study for susceptibility genes contributing to familial Parkinson disease.
Identifieur interne : 000130 ( PubMed/Corpus ); précédent : 000129; suivant : 000131Genomewide association study for susceptibility genes contributing to familial Parkinson disease.
Auteurs : Nathan Pankratz ; Jemma. Wilk ; Jeanne. Latourelle ; Anita. Destefano ; Cheryl Halter ; Elizabeth. Pugh ; Kimberly. Doheny ; James. Gusella ; William. Nichols ; Tatiana Foroud ; Richard. MyersSource :
- Human genetics ; 2009.
English descriptors
- KwdEn :
- Adult, Aged, Case-Control Studies, Diacylglycerol Kinase (genetics), Female, Genes, Recessive, Genetic Predisposition to Disease, Humans, Intracellular Signaling Peptides and Proteins (genetics), Logistic Models, Male, Middle Aged, Models, Genetic, Parkinson Disease (genetics), Polymorphism, Single Nucleotide, Protein-Serine-Threonine Kinases (genetics), alpha-Synuclein (genetics), tau Proteins (genetics).
- MESH :
- chemical , genetics : Diacylglycerol Kinase, Intracellular Signaling Peptides and Proteins, Protein-Serine-Threonine Kinases, alpha-Synuclein, tau Proteins.
- genetics : Parkinson Disease.
- Adult, Aged, Case-Control Studies, Female, Genes, Recessive, Genetic Predisposition to Disease, Humans, Logistic Models, Male, Middle Aged, Models, Genetic, Polymorphism, Single Nucleotide.
Abstract
Five genes have been identified that contribute to Mendelian forms of Parkinson disease (PD); however, mutations have been found in fewer than 5% of patients, suggesting that additional genes contribute to disease risk. Unlike previous studies that focused primarily on sporadic PD, we have performed the first genomewide association study (GWAS) in familial PD. Genotyping was performed with the Illumina HumanCNV370Duo array in 857 familial PD cases and 867 controls. A logistic model was employed to test for association under additive and recessive modes of inheritance after adjusting for gender and age. No result met genomewide significance based on a conservative Bonferroni correction. The strongest association result was with SNPs in the GAK/DGKQ region on chromosome 4 (additive model: p = 3.4 x 10(-6); OR = 1.69). Consistent evidence of association was also observed to the chromosomal regions containing SNCA (additive model: p = 5.5 x 10(-5); OR = 1.35) and MAPT (recessive model: p = 2.0 x 10(-5); OR = 0.56). Both of these genes have been implicated previously in PD susceptibility; however, neither was identified in previous GWAS studies of PD. Meta-analysis was performed using data from a previous case-control GWAS, and yielded improved p values for several regions, including GAK/DGKQ (additive model: p = 2.5 x 10(-7)) and the MAPT region (recessive model: p = 9.8 x 10(-6); additive model: p = 4.8 x 10(-5)). These data suggest the identification of new susceptibility alleles for PD in the GAK/DGKQ region, and also provide further support for the role of SNCA and MAPT in PD susceptibility.
DOI: 10.1007/s00439-008-0582-9
PubMed: 18985386
Links to Exploration step
pubmed:18985386Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Genomewide association study for susceptibility genes contributing to familial Parkinson disease.</title><author><name sortKey="Pankratz, Nathan" sort="Pankratz, Nathan" uniqKey="Pankratz N" first="Nathan" last="Pankratz">Nathan Pankratz</name><affiliation><nlm:affiliation>Indiana University School of Medicine, Health Information and Translational Sciences Building, Indianapolis, IN 46202-3002, USA. npankrat@iupui.edu</nlm:affiliation></affiliation></author><author><name sortKey="Wilk, Jemma B" sort="Wilk, Jemma B" uniqKey="Wilk J" first="Jemma" last="Wilk">Jemma. Wilk</name></author><author><name sortKey="Latourelle, Jeanne C" sort="Latourelle, Jeanne C" uniqKey="Latourelle J" first="Jeanne" last="Latourelle">Jeanne. Latourelle</name></author><author><name sortKey="Destefano, Anita L" sort="Destefano, Anita L" uniqKey="Destefano A" first="Anita" last="Destefano">Anita. Destefano</name></author><author><name sortKey="Halter, Cheryl" sort="Halter, Cheryl" uniqKey="Halter C" first="Cheryl" last="Halter">Cheryl Halter</name></author><author><name sortKey="Pugh, Elizabeth W" sort="Pugh, Elizabeth W" uniqKey="Pugh E" first="Elizabeth" last="Pugh">Elizabeth. Pugh</name></author><author><name sortKey="Doheny, Kimberly F" sort="Doheny, Kimberly F" uniqKey="Doheny K" first="Kimberly" last="Doheny">Kimberly. Doheny</name></author><author><name sortKey="Gusella, James F" sort="Gusella, James F" uniqKey="Gusella J" first="James" last="Gusella">James. Gusella</name></author><author><name sortKey="Nichols, William C" sort="Nichols, William C" uniqKey="Nichols W" first="William" last="Nichols">William. Nichols</name></author><author><name sortKey="Foroud, Tatiana" sort="Foroud, Tatiana" uniqKey="Foroud T" first="Tatiana" last="Foroud">Tatiana Foroud</name></author><author><name sortKey="Myers, Richard H" sort="Myers, Richard H" uniqKey="Myers R" first="Richard" last="Myers">Richard. Myers</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="doi">10.1007/s00439-008-0582-9</idno><idno type="RBID">pubmed:18985386</idno><idno type="pmid">18985386</idno><idno type="wicri:Area/PubMed/Corpus">000130</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Genomewide association study for susceptibility genes contributing to familial Parkinson disease.</title><author><name sortKey="Pankratz, Nathan" sort="Pankratz, Nathan" uniqKey="Pankratz N" first="Nathan" last="Pankratz">Nathan Pankratz</name><affiliation><nlm:affiliation>Indiana University School of Medicine, Health Information and Translational Sciences Building, Indianapolis, IN 46202-3002, USA. npankrat@iupui.edu</nlm:affiliation></affiliation></author><author><name sortKey="Wilk, Jemma B" sort="Wilk, Jemma B" uniqKey="Wilk J" first="Jemma" last="Wilk">Jemma. Wilk</name></author><author><name sortKey="Latourelle, Jeanne C" sort="Latourelle, Jeanne C" uniqKey="Latourelle J" first="Jeanne" last="Latourelle">Jeanne. Latourelle</name></author><author><name sortKey="Destefano, Anita L" sort="Destefano, Anita L" uniqKey="Destefano A" first="Anita" last="Destefano">Anita. Destefano</name></author><author><name sortKey="Halter, Cheryl" sort="Halter, Cheryl" uniqKey="Halter C" first="Cheryl" last="Halter">Cheryl Halter</name></author><author><name sortKey="Pugh, Elizabeth W" sort="Pugh, Elizabeth W" uniqKey="Pugh E" first="Elizabeth" last="Pugh">Elizabeth. Pugh</name></author><author><name sortKey="Doheny, Kimberly F" sort="Doheny, Kimberly F" uniqKey="Doheny K" first="Kimberly" last="Doheny">Kimberly. Doheny</name></author><author><name sortKey="Gusella, James F" sort="Gusella, James F" uniqKey="Gusella J" first="James" last="Gusella">James. Gusella</name></author><author><name sortKey="Nichols, William C" sort="Nichols, William C" uniqKey="Nichols W" first="William" last="Nichols">William. Nichols</name></author><author><name sortKey="Foroud, Tatiana" sort="Foroud, Tatiana" uniqKey="Foroud T" first="Tatiana" last="Foroud">Tatiana Foroud</name></author><author><name sortKey="Myers, Richard H" sort="Myers, Richard H" uniqKey="Myers R" first="Richard" last="Myers">Richard. Myers</name></author></analytic><series><title level="j">Human genetics</title><idno type="e-ISSN">1432-1203</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Case-Control Studies</term><term>Diacylglycerol Kinase (genetics)</term><term>Female</term><term>Genes, Recessive</term><term>Genetic Predisposition to Disease</term><term>Humans</term><term>Intracellular Signaling Peptides and Proteins (genetics)</term><term>Logistic Models</term><term>Male</term><term>Middle Aged</term><term>Models, Genetic</term><term>Parkinson Disease (genetics)</term><term>Polymorphism, Single Nucleotide</term><term>Protein-Serine-Threonine Kinases (genetics)</term><term>alpha-Synuclein (genetics)</term><term>tau Proteins (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Diacylglycerol Kinase</term><term>Intracellular Signaling Peptides and Proteins</term><term>Protein-Serine-Threonine Kinases</term><term>alpha-Synuclein</term><term>tau Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Case-Control Studies</term><term>Female</term><term>Genes, Recessive</term><term>Genetic Predisposition to Disease</term><term>Humans</term><term>Logistic Models</term><term>Male</term><term>Middle Aged</term><term>Models, Genetic</term><term>Polymorphism, Single Nucleotide</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Five genes have been identified that contribute to Mendelian forms of Parkinson disease (PD); however, mutations have been found in fewer than 5% of patients, suggesting that additional genes contribute to disease risk. Unlike previous studies that focused primarily on sporadic PD, we have performed the first genomewide association study (GWAS) in familial PD. Genotyping was performed with the Illumina HumanCNV370Duo array in 857 familial PD cases and 867 controls. A logistic model was employed to test for association under additive and recessive modes of inheritance after adjusting for gender and age. No result met genomewide significance based on a conservative Bonferroni correction. The strongest association result was with SNPs in the GAK/DGKQ region on chromosome 4 (additive model: p = 3.4 x 10(-6); OR = 1.69). Consistent evidence of association was also observed to the chromosomal regions containing SNCA (additive model: p = 5.5 x 10(-5); OR = 1.35) and MAPT (recessive model: p = 2.0 x 10(-5); OR = 0.56). Both of these genes have been implicated previously in PD susceptibility; however, neither was identified in previous GWAS studies of PD. Meta-analysis was performed using data from a previous case-control GWAS, and yielded improved p values for several regions, including GAK/DGKQ (additive model: p = 2.5 x 10(-7)) and the MAPT region (recessive model: p = 9.8 x 10(-6); additive model: p = 4.8 x 10(-5)). These data suggest the identification of new susceptibility alleles for PD in the GAK/DGKQ region, and also provide further support for the role of SNCA and MAPT in PD susceptibility.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">18985386</PMID><DateCreated><Year>2008</Year><Month>12</Month><Day>22</Day></DateCreated><DateCompleted><Year>2009</Year><Month>01</Month><Day>07</Day></DateCompleted><DateRevised><Year>2014</Year><Month>09</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-1203</ISSN><JournalIssue CitedMedium="Internet"><Volume>124</Volume><Issue>6</Issue><PubDate><Year>2009</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Human genetics</Title><ISOAbbreviation>Hum. Genet.</ISOAbbreviation></Journal><ArticleTitle>Genomewide association study for susceptibility genes contributing to familial Parkinson disease.</ArticleTitle><Pagination><MedlinePgn>593-605</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00439-008-0582-9</ELocationID><Abstract><AbstractText>Five genes have been identified that contribute to Mendelian forms of Parkinson disease (PD); however, mutations have been found in fewer than 5% of patients, suggesting that additional genes contribute to disease risk. Unlike previous studies that focused primarily on sporadic PD, we have performed the first genomewide association study (GWAS) in familial PD. Genotyping was performed with the Illumina HumanCNV370Duo array in 857 familial PD cases and 867 controls. A logistic model was employed to test for association under additive and recessive modes of inheritance after adjusting for gender and age. No result met genomewide significance based on a conservative Bonferroni correction. The strongest association result was with SNPs in the GAK/DGKQ region on chromosome 4 (additive model: p = 3.4 x 10(-6); OR = 1.69). Consistent evidence of association was also observed to the chromosomal regions containing SNCA (additive model: p = 5.5 x 10(-5); OR = 1.35) and MAPT (recessive model: p = 2.0 x 10(-5); OR = 0.56). Both of these genes have been implicated previously in PD susceptibility; however, neither was identified in previous GWAS studies of PD. Meta-analysis was performed using data from a previous case-control GWAS, and yielded improved p values for several regions, including GAK/DGKQ (additive model: p = 2.5 x 10(-7)) and the MAPT region (recessive model: p = 9.8 x 10(-6); additive model: p = 4.8 x 10(-5)). These data suggest the identification of new susceptibility alleles for PD in the GAK/DGKQ region, and also provide further support for the role of SNCA and MAPT in PD susceptibility.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pankratz</LastName><ForeName>Nathan</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Indiana University School of Medicine, Health Information and Translational Sciences Building, Indianapolis, IN 46202-3002, USA. npankrat@iupui.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wilk</LastName><ForeName>Jemma B</ForeName><Initials>JB</Initials></Author><Author ValidYN="Y"><LastName>Latourelle</LastName><ForeName>Jeanne C</ForeName><Initials>JC</Initials></Author><Author ValidYN="Y"><LastName>DeStefano</LastName><ForeName>Anita L</ForeName><Initials>AL</Initials></Author><Author ValidYN="Y"><LastName>Halter</LastName><ForeName>Cheryl</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Pugh</LastName><ForeName>Elizabeth W</ForeName><Initials>EW</Initials></Author><Author ValidYN="Y"><LastName>Doheny</LastName><ForeName>Kimberly F</ForeName><Initials>KF</Initials></Author><Author ValidYN="Y"><LastName>Gusella</LastName><ForeName>James F</ForeName><Initials>JF</Initials></Author><Author ValidYN="Y"><LastName>Nichols</LastName><ForeName>William C</ForeName><Initials>WC</Initials></Author><Author ValidYN="Y"><LastName>Foroud</LastName><ForeName>Tatiana</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Myers</LastName><ForeName>Richard H</ForeName><Initials>RH</Initials></Author><Author ValidYN="Y"><CollectiveName>PSG-PROGENI and GenePD Investigators, Coordinators and Molecular Genetic Laboratories</CollectiveName></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>GTB07001</GrantID><Agency>Telethon</Agency><Country>Italy</Country></Grant><Grant><GrantID>HHSN268200782096C</GrantID><Agency>PHS 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Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2008</Year><Month>11</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Hum Genet</MedlineTA><NlmUniqueID>7613873</NlmUniqueID><ISSNLinking>0340-6717</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D047908">Intracellular Signaling Peptides and Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C054369">MAPT protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C497604">SNCA protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.107</RegistryNumber><NameOfSubstance UI="D019852">Diacylglycerol Kinase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C486325">GAK protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D017346">Protein-Serine-Threonine Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Am J Hum Genet. 2006 Jun;78(6):1081-2</RefSource><PMID Version="1">16685659</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 2006 Jun;63(6):826-32</RefSource><PMID Version="1">16769863</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>JAMA. 2006 Aug 9;296(6):661-70</RefSource><PMID 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