Testing association between LRRK2 and Parkinson’s disease and investigating linkage disequilibrium
Background: We and others recently identified the gene underlying PARK8 linked Parkinson’s disease (PD). This gene, LRRK2, contains mutations that cause an autosomal dominant PD, including a mutation, G2019S, which is the most common PD causing mutation identified to date. Common genetic variability...
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| Veröffentlicht in: | Journal of medical genetics 2006-02, Vol.43 (2), p.e09-e09 |
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| creator | Paisán-Ruíz, C Evans, E W Jain, S Xiromerisiou, G Gibbs, J R Eerola, J Gourbali, V Hellström, O Duckworth, J Papadimitriou, A Tienari, P J Hadjigeorgiou, G M Singleton, A B |
| description | Background: We and others recently identified the gene underlying PARK8 linked Parkinson’s disease (PD). This gene, LRRK2, contains mutations that cause an autosomal dominant PD, including a mutation, G2019S, which is the most common PD causing mutation identified to date. Common genetic variability in genes that contain PD causing mutations has previously been implicated as a risk factor for typical sporadic disease. Methods: We undertook a case-control association analysis of LRRK2 in two independent European PD cohorts using 31 tagging single nucleotide polymorphisms (tSNPs) and five potentially functional SNPs. To assess the structure of this locus in different populations, we have performed linkage disequilibrium (LD) analysis using these variants in a human diversity panel. Results: We show that common genetic variability in LRRK2 is not associated with risk for PD in the European populations studied here. We also show inter-population variability in the strength of LD across this locus. Conclusions: To our knowledge this is the first comprehensive analysis of common variability within LRRK2 as a risk factor for PD. |
| doi_str_mv | 10.1136/jmg.2005.036889 |
| format | Article |
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This gene, LRRK2, contains mutations that cause an autosomal dominant PD, including a mutation, G2019S, which is the most common PD causing mutation identified to date. Common genetic variability in genes that contain PD causing mutations has previously been implicated as a risk factor for typical sporadic disease. Methods: We undertook a case-control association analysis of LRRK2 in two independent European PD cohorts using 31 tagging single nucleotide polymorphisms (tSNPs) and five potentially functional SNPs. To assess the structure of this locus in different populations, we have performed linkage disequilibrium (LD) analysis using these variants in a human diversity panel. Results: We show that common genetic variability in LRRK2 is not associated with risk for PD in the European populations studied here. We also show inter-population variability in the strength of LD across this locus. Conclusions: To our knowledge this is the first comprehensive analysis of common variability within LRRK2 as a risk factor for PD.</description><identifier>ISSN: 0022-2593</identifier><identifier>ISSN: 1468-6244</identifier><identifier>EISSN: 1468-6244</identifier><identifier>DOI: 10.1136/jmg.2005.036889</identifier><identifier>PMID: 16467219</identifier><identifier>CODEN: JMDGAE</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd</publisher><subject>Adult ; Age ; Aged ; dardarin ; Disequilibrium ; Electronic Letter ; Female ; Genes ; Genetic Markers ; Genetic Predisposition to Disease - genetics ; Haplotypes ; Humans ; Kinases ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 ; linkage disequilibrium ; Linkage Disequilibrium - genetics ; LRRK2 ; Male ; Middle Aged ; Multiculturalism & pluralism ; Mutation ; Otolaryngology ; Parkinson Disease - genetics ; Parkinson's disease ; Polymorphism, Single Nucleotide - genetics ; Population ; Protein-Serine-Threonine Kinases - genetics ; single nucleotide polymorphism ; SNP ; Studies ; tagging SNP ; tSNP</subject><ispartof>Journal of medical genetics, 2006-02, Vol.43 (2), p.e09-e09</ispartof><rights>Copyright 2006 Journal of Medical Genetics</rights><rights>Copyright: 2006 Copyright 2006 Journal of Medical Genetics</rights><rights>Copyright ©2006 BMJ Publishing Group Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b523t-e4cbf9c8e431fa66b471a1cd40e6055f949c1d67ee4b226a2dfb05dc6f888123</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://jmg.bmj.com/content/43/2/e09.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttps://jmg.bmj.com/content/43/2/e09.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,230,314,723,776,780,881,3182,23551,27903,27904,53769,53771,77346,77377</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16467219$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Paisán-Ruíz, C</creatorcontrib><creatorcontrib>Evans, E W</creatorcontrib><creatorcontrib>Jain, S</creatorcontrib><creatorcontrib>Xiromerisiou, G</creatorcontrib><creatorcontrib>Gibbs, J R</creatorcontrib><creatorcontrib>Eerola, J</creatorcontrib><creatorcontrib>Gourbali, V</creatorcontrib><creatorcontrib>Hellström, O</creatorcontrib><creatorcontrib>Duckworth, J</creatorcontrib><creatorcontrib>Papadimitriou, A</creatorcontrib><creatorcontrib>Tienari, P J</creatorcontrib><creatorcontrib>Hadjigeorgiou, G M</creatorcontrib><creatorcontrib>Singleton, A B</creatorcontrib><title>Testing association between LRRK2 and Parkinson’s disease and investigating linkage disequilibrium</title><title>Journal of medical genetics</title><addtitle>J Med Genet</addtitle><description>Background: We and others recently identified the gene underlying PARK8 linked Parkinson’s disease (PD). This gene, LRRK2, contains mutations that cause an autosomal dominant PD, including a mutation, G2019S, which is the most common PD causing mutation identified to date. Common genetic variability in genes that contain PD causing mutations has previously been implicated as a risk factor for typical sporadic disease. Methods: We undertook a case-control association analysis of LRRK2 in two independent European PD cohorts using 31 tagging single nucleotide polymorphisms (tSNPs) and five potentially functional SNPs. To assess the structure of this locus in different populations, we have performed linkage disequilibrium (LD) analysis using these variants in a human diversity panel. Results: We show that common genetic variability in LRRK2 is not associated with risk for PD in the European populations studied here. We also show inter-population variability in the strength of LD across this locus. Conclusions: To our knowledge this is the first comprehensive analysis of common variability within LRRK2 as a risk factor for PD.</description><subject>Adult</subject><subject>Age</subject><subject>Aged</subject><subject>dardarin</subject><subject>Disequilibrium</subject><subject>Electronic Letter</subject><subject>Female</subject><subject>Genes</subject><subject>Genetic Markers</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Haplotypes</subject><subject>Humans</subject><subject>Kinases</subject><subject>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</subject><subject>linkage disequilibrium</subject><subject>Linkage Disequilibrium - genetics</subject><subject>LRRK2</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Multiculturalism & pluralism</subject><subject>Mutation</subject><subject>Otolaryngology</subject><subject>Parkinson Disease - genetics</subject><subject>Parkinson's disease</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Population</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>single nucleotide polymorphism</subject><subject>SNP</subject><subject>Studies</subject><subject>tagging SNP</subject><subject>tSNP</subject><issn>0022-2593</issn><issn>1468-6244</issn><issn>1468-6244</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc1u1DAURi0EokNhzQ5FQmKBlKn_YjsbJDSiFHVEUTVC7CwnuQmeJk5rJwV2vEZfr0-CMxkV6KYrL-7x5_v5IPSS4CUhTBxtu2ZJMc6WmAml8kdoQbhQqaCcP0YLjClNaZazA_QshC3GhEkinqIDIriQlOQLVG0gDNY1iQmhL60ZbO-SAoYfAC5Zn5-f0sS4Kvli_IV1oXe3v29CUtkAJsBuYt31lNCYXUpr3YVpYEdcjba1hbdj9xw9qU0b4MX-PESb4w-b1Um6Pvv4afV-nRYZZUMKvCzqvFTAGamNEAWXxJCy4hgEzrI653lJKiEBeEGpMLSqC5xVpaiVUoSyQ_Rujr0ciw6qEtzgTasvve2M_6V7Y_X_E2e_66a_1jSL_8FVDHizD_D91Rhr6c6GEtrWOOjHoIUUcTWGHwRJzhlnGY_g63vgth-9i5-giVQkesByWvxopkrfh-ChvtuZYD151tGznjzr2XO88erfqn_5vdgIpDNgwwA_7-ZRY2zBZKY_f13pY3n6TaqTjZ4avZ35ots--PofHgXC2w</recordid><startdate>20060201</startdate><enddate>20060201</enddate><creator>Paisán-Ruíz, C</creator><creator>Evans, E W</creator><creator>Jain, S</creator><creator>Xiromerisiou, G</creator><creator>Gibbs, J R</creator><creator>Eerola, J</creator><creator>Gourbali, V</creator><creator>Hellström, O</creator><creator>Duckworth, J</creator><creator>Papadimitriou, A</creator><creator>Tienari, P J</creator><creator>Hadjigeorgiou, G M</creator><creator>Singleton, A B</creator><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group LTD</general><general>BMJ Group</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20060201</creationdate><title>Testing association between LRRK2 and Parkinson’s disease and investigating linkage disequilibrium</title><author>Paisán-Ruíz, C ; Evans, E W ; Jain, S ; Xiromerisiou, G ; Gibbs, J R ; Eerola, J ; Gourbali, V ; Hellström, O ; Duckworth, J ; Papadimitriou, A ; Tienari, P J ; Hadjigeorgiou, G M ; Singleton, A B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b523t-e4cbf9c8e431fa66b471a1cd40e6055f949c1d67ee4b226a2dfb05dc6f888123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Age</topic><topic>Aged</topic><topic>dardarin</topic><topic>Disequilibrium</topic><topic>Electronic Letter</topic><topic>Female</topic><topic>Genes</topic><topic>Genetic Markers</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Haplotypes</topic><topic>Humans</topic><topic>Kinases</topic><topic>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</topic><topic>linkage disequilibrium</topic><topic>Linkage Disequilibrium - genetics</topic><topic>LRRK2</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Multiculturalism & pluralism</topic><topic>Mutation</topic><topic>Otolaryngology</topic><topic>Parkinson Disease - genetics</topic><topic>Parkinson's disease</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Population</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>single nucleotide polymorphism</topic><topic>SNP</topic><topic>Studies</topic><topic>tagging SNP</topic><topic>tSNP</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Paisán-Ruíz, C</creatorcontrib><creatorcontrib>Evans, E W</creatorcontrib><creatorcontrib>Jain, S</creatorcontrib><creatorcontrib>Xiromerisiou, G</creatorcontrib><creatorcontrib>Gibbs, J R</creatorcontrib><creatorcontrib>Eerola, J</creatorcontrib><creatorcontrib>Gourbali, V</creatorcontrib><creatorcontrib>Hellström, O</creatorcontrib><creatorcontrib>Duckworth, J</creatorcontrib><creatorcontrib>Papadimitriou, A</creatorcontrib><creatorcontrib>Tienari, P J</creatorcontrib><creatorcontrib>Hadjigeorgiou, G M</creatorcontrib><creatorcontrib>Singleton, A B</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of medical genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Paisán-Ruíz, C</au><au>Evans, E W</au><au>Jain, S</au><au>Xiromerisiou, G</au><au>Gibbs, J R</au><au>Eerola, J</au><au>Gourbali, V</au><au>Hellström, O</au><au>Duckworth, J</au><au>Papadimitriou, A</au><au>Tienari, P J</au><au>Hadjigeorgiou, G M</au><au>Singleton, A B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Testing association between LRRK2 and Parkinson’s disease and investigating linkage disequilibrium</atitle><jtitle>Journal of medical genetics</jtitle><addtitle>J Med Genet</addtitle><date>2006-02-01</date><risdate>2006</risdate><volume>43</volume><issue>2</issue><spage>e09</spage><epage>e09</epage><pages>e09-e09</pages><issn>0022-2593</issn><issn>1468-6244</issn><eissn>1468-6244</eissn><coden>JMDGAE</coden><abstract>Background: We and others recently identified the gene underlying PARK8 linked Parkinson’s disease (PD). This gene, LRRK2, contains mutations that cause an autosomal dominant PD, including a mutation, G2019S, which is the most common PD causing mutation identified to date. Common genetic variability in genes that contain PD causing mutations has previously been implicated as a risk factor for typical sporadic disease. Methods: We undertook a case-control association analysis of LRRK2 in two independent European PD cohorts using 31 tagging single nucleotide polymorphisms (tSNPs) and five potentially functional SNPs. To assess the structure of this locus in different populations, we have performed linkage disequilibrium (LD) analysis using these variants in a human diversity panel. Results: We show that common genetic variability in LRRK2 is not associated with risk for PD in the European populations studied here. We also show inter-population variability in the strength of LD across this locus. Conclusions: To our knowledge this is the first comprehensive analysis of common variability within LRRK2 as a risk factor for PD.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd</pub><pmid>16467219</pmid><doi>10.1136/jmg.2005.036889</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Age Aged dardarin Disequilibrium Electronic Letter Female Genes Genetic Markers Genetic Predisposition to Disease - genetics Haplotypes Humans Kinases Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 linkage disequilibrium Linkage Disequilibrium - genetics LRRK2 Male Middle Aged Multiculturalism & pluralism Mutation Otolaryngology Parkinson Disease - genetics Parkinson's disease Polymorphism, Single Nucleotide - genetics Population Protein-Serine-Threonine Kinases - genetics single nucleotide polymorphism SNP Studies tagging SNP tSNP |
| title | Testing association between LRRK2 and Parkinson’s disease and investigating linkage disequilibrium |
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