Association analysis of 528 intra-genic SNPs in a region of chromosome 10 linked to late onset Alzheimer's disease
Late‐onset Alzheimer's disease (LOAD) is a genetically complex neurodegenerative disorder. Currently, only the ε4 allele of the Apolipoprotein E gene has been identified unequivocally as a genetic susceptibility factor for LOAD. Others remain to be found. In 2002 we observed genome‐wide signifi...
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| Veröffentlicht in: | American journal of medical genetics. Part B, Neuropsychiatric genetics Neuropsychiatric genetics, 2008-09, Vol.147B (6), p.727-731 |
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| creator | Morgan, A.R. Hamilton, G. Turic, D. Jehu, L. Harold, D. Abraham, R. Hollingworth, P. Moskvina, V. Brayne, C. Rubinsztein, D.C. Lynch, A. Lawlor, B. Gill, M. O'Donovan, M. Powell, J. Lovestone, S. Williams, J. Owen, M.J. |
| description | Late‐onset Alzheimer's disease (LOAD) is a genetically complex neurodegenerative disorder. Currently, only the ε4 allele of the Apolipoprotein E gene has been identified unequivocally as a genetic susceptibility factor for LOAD. Others remain to be found. In 2002 we observed genome‐wide significant evidence of linkage to a region on chromosome 10q11.23–q21.3 [Myers et al. (2002) Am J Med Genet 114:235–244]. Our objective in this study was to test every gene within the maximum LOD‐1 linkage region, for association with LOAD. We obtained results for 528 SNPs from 67 genes, with an average density of 1 SNP every 10 kb within the genes. We demonstrated nominally significant association with LOAD for 4 SNPs: rs1881747 near DKK1 (P = 0.011, OR = 1.24), rs2279420 in ANK3 (P = 0.022, OR = 0.79), rs2306402 in CTNNA3 (P = 0.024, OR = 1.18), and rs5030882 in CXXC6 (P = 0.046, OR = 1.29) in 1,160 cases and 1,389 controls. These results would not survive correction for multiple testing but warrant attempts at confirmation in independent samples. © 2007 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/ajmg.b.30670 |
| format | Article |
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Currently, only the ε4 allele of the Apolipoprotein E gene has been identified unequivocally as a genetic susceptibility factor for LOAD. Others remain to be found. In 2002 we observed genome‐wide significant evidence of linkage to a region on chromosome 10q11.23–q21.3 [Myers et al. (2002) Am J Med Genet 114:235–244]. Our objective in this study was to test every gene within the maximum LOD‐1 linkage region, for association with LOAD. We obtained results for 528 SNPs from 67 genes, with an average density of 1 SNP every 10 kb within the genes. We demonstrated nominally significant association with LOAD for 4 SNPs: rs1881747 near DKK1 (P = 0.011, OR = 1.24), rs2279420 in ANK3 (P = 0.022, OR = 0.79), rs2306402 in CTNNA3 (P = 0.024, OR = 1.18), and rs5030882 in CXXC6 (P = 0.046, OR = 1.29) in 1,160 cases and 1,389 controls. These results would not survive correction for multiple testing but warrant attempts at confirmation in independent samples. © 2007 Wiley‐Liss, Inc.</description><identifier>ISSN: 1552-4841</identifier><identifier>EISSN: 1552-485X</identifier><identifier>DOI: 10.1002/ajmg.b.30670</identifier><identifier>PMID: 18163421</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult and adolescent clinical studies ; Age of Onset ; Aged ; Aged, 80 and over ; alpha Catenin - genetics ; Alzheimer Disease - epidemiology ; Alzheimer Disease - genetics ; Ankyrins - genetics ; association ; Biological and medical sciences ; Case-Control Studies ; chromosome 10 ; Chromosomes, Human, Pair 10 ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; DNA Mutational Analysis ; DNA-Binding Proteins - genetics ; Female ; Genetic Linkage ; Genetic Predisposition to Disease ; Genotype ; Humans ; Intercellular Signaling Peptides and Proteins - genetics ; late-onset Alzheimer's disease ; Male ; Medical genetics ; Medical sciences ; Middle Aged ; Mixed Function Oxygenases ; Neurology ; Organic mental disorders. Neuropsychology ; Polymorphism, Single Nucleotide ; Proto-Oncogene Proteins - genetics ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; SNP</subject><ispartof>American journal of medical genetics. Part B, Neuropsychiatric genetics, 2008-09, Vol.147B (6), p.727-731</ispartof><rights>Copyright © 2007 Wiley‐Liss, Inc.</rights><rights>2008 INIST-CNRS</rights><rights>2007 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4980-eb139a04b29575c6a09eaf4d90d2224f71880919bec8edb7ea2f6d7b1f9678c93</citedby><cites>FETCH-LOGICAL-c4980-eb139a04b29575c6a09eaf4d90d2224f71880919bec8edb7ea2f6d7b1f9678c93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fajmg.b.30670$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fajmg.b.30670$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20598950$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18163421$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morgan, A.R.</creatorcontrib><creatorcontrib>Hamilton, G.</creatorcontrib><creatorcontrib>Turic, D.</creatorcontrib><creatorcontrib>Jehu, L.</creatorcontrib><creatorcontrib>Harold, D.</creatorcontrib><creatorcontrib>Abraham, R.</creatorcontrib><creatorcontrib>Hollingworth, P.</creatorcontrib><creatorcontrib>Moskvina, V.</creatorcontrib><creatorcontrib>Brayne, C.</creatorcontrib><creatorcontrib>Rubinsztein, D.C.</creatorcontrib><creatorcontrib>Lynch, A.</creatorcontrib><creatorcontrib>Lawlor, B.</creatorcontrib><creatorcontrib>Gill, M.</creatorcontrib><creatorcontrib>O'Donovan, M.</creatorcontrib><creatorcontrib>Powell, J.</creatorcontrib><creatorcontrib>Lovestone, S.</creatorcontrib><creatorcontrib>Williams, J.</creatorcontrib><creatorcontrib>Owen, M.J.</creatorcontrib><title>Association analysis of 528 intra-genic SNPs in a region of chromosome 10 linked to late onset Alzheimer's disease</title><title>American journal of medical genetics. Part B, Neuropsychiatric genetics</title><addtitle>Am. J. Med. Genet</addtitle><description>Late‐onset Alzheimer's disease (LOAD) is a genetically complex neurodegenerative disorder. Currently, only the ε4 allele of the Apolipoprotein E gene has been identified unequivocally as a genetic susceptibility factor for LOAD. Others remain to be found. In 2002 we observed genome‐wide significant evidence of linkage to a region on chromosome 10q11.23–q21.3 [Myers et al. (2002) Am J Med Genet 114:235–244]. Our objective in this study was to test every gene within the maximum LOD‐1 linkage region, for association with LOAD. We obtained results for 528 SNPs from 67 genes, with an average density of 1 SNP every 10 kb within the genes. We demonstrated nominally significant association with LOAD for 4 SNPs: rs1881747 near DKK1 (P = 0.011, OR = 1.24), rs2279420 in ANK3 (P = 0.022, OR = 0.79), rs2306402 in CTNNA3 (P = 0.024, OR = 1.18), and rs5030882 in CXXC6 (P = 0.046, OR = 1.29) in 1,160 cases and 1,389 controls. These results would not survive correction for multiple testing but warrant attempts at confirmation in independent samples. © 2007 Wiley‐Liss, Inc.</description><subject>Adult and adolescent clinical studies</subject><subject>Age of Onset</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>alpha Catenin - genetics</subject><subject>Alzheimer Disease - epidemiology</subject><subject>Alzheimer Disease - genetics</subject><subject>Ankyrins - genetics</subject><subject>association</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>chromosome 10</subject><subject>Chromosomes, Human, Pair 10</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>DNA Mutational Analysis</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Female</subject><subject>Genetic Linkage</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>late-onset Alzheimer's disease</subject><subject>Male</subject><subject>Medical genetics</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mixed Function Oxygenases</subject><subject>Neurology</subject><subject>Organic mental disorders. Neuropsychology</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>SNP</subject><issn>1552-4841</issn><issn>1552-485X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0ctv1DAQB-AIgegDbpyRL5QLWfyIY_u4qmChKuX9uFmOM9m6deLiyaosfz1ZdllucPLI-mZGml9RPGJ0xijlz91Vv5w1M0FrRe8Uh0xKXlZafru7ryt2UBwhXlEqqFTqfnHANKtFxdlhkeeIyQc3hjQQN7i4xoAkdURyTcIwZlcuYQiefLx4h9MHcSTDcoMn4y9z6hOmHgijJIbhGloyJhLdCCQNCCOZx5-XEHrIT5G0AcEhPCjudS4iPNy9x8Xnly8-nb4qz98uXp_Oz0tfGU1LaJgwjlYNN1JJXztqwHVVa2jLOa86xbSmhpkGvIa2UeB4V7eqYZ2plfZGHBcn27k3OX1fAY62D-ghRjdAWqGtTaU5n47yP8hpzatayQk-20KfE2KGzt7k0Lu8tozaTRh2E4Zt7O8wJv54N3fV9ND-xbvrT-DJDjj0LnbZDT7g3nEqjTZyM0hs3W2IsP7nUjs_e7P4s77cdgUc4ce-y-VrWyuhpP16sbAfhDj7ori278UvkEKw_Q</recordid><startdate>20080905</startdate><enddate>20080905</enddate><creator>Morgan, A.R.</creator><creator>Hamilton, G.</creator><creator>Turic, D.</creator><creator>Jehu, L.</creator><creator>Harold, D.</creator><creator>Abraham, R.</creator><creator>Hollingworth, P.</creator><creator>Moskvina, V.</creator><creator>Brayne, C.</creator><creator>Rubinsztein, D.C.</creator><creator>Lynch, A.</creator><creator>Lawlor, B.</creator><creator>Gill, M.</creator><creator>O'Donovan, M.</creator><creator>Powell, J.</creator><creator>Lovestone, S.</creator><creator>Williams, J.</creator><creator>Owen, M.J.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><scope>IQODW</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>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20080905</creationdate><title>Association analysis of 528 intra-genic SNPs in a region of chromosome 10 linked to late onset Alzheimer's disease</title><author>Morgan, A.R. ; Hamilton, G. ; Turic, D. ; Jehu, L. ; Harold, D. ; Abraham, R. ; Hollingworth, P. ; Moskvina, V. ; Brayne, C. ; Rubinsztein, D.C. ; Lynch, A. ; Lawlor, B. ; Gill, M. ; O'Donovan, M. ; Powell, J. ; Lovestone, S. ; Williams, J. ; Owen, M.J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4980-eb139a04b29575c6a09eaf4d90d2224f71880919bec8edb7ea2f6d7b1f9678c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult and adolescent clinical studies</topic><topic>Age of Onset</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>alpha Catenin - genetics</topic><topic>Alzheimer Disease - epidemiology</topic><topic>Alzheimer Disease - genetics</topic><topic>Ankyrins - genetics</topic><topic>association</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>chromosome 10</topic><topic>Chromosomes, Human, Pair 10</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>DNA Mutational Analysis</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Female</topic><topic>Genetic Linkage</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Humans</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>late-onset Alzheimer's disease</topic><topic>Male</topic><topic>Medical genetics</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mixed Function Oxygenases</topic><topic>Neurology</topic><topic>Organic mental disorders. Neuropsychology</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. 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Part B, Neuropsychiatric genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morgan, A.R.</au><au>Hamilton, G.</au><au>Turic, D.</au><au>Jehu, L.</au><au>Harold, D.</au><au>Abraham, R.</au><au>Hollingworth, P.</au><au>Moskvina, V.</au><au>Brayne, C.</au><au>Rubinsztein, D.C.</au><au>Lynch, A.</au><au>Lawlor, B.</au><au>Gill, M.</au><au>O'Donovan, M.</au><au>Powell, J.</au><au>Lovestone, S.</au><au>Williams, J.</au><au>Owen, M.J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association analysis of 528 intra-genic SNPs in a region of chromosome 10 linked to late onset Alzheimer's disease</atitle><jtitle>American journal of medical genetics. Part B, Neuropsychiatric genetics</jtitle><addtitle>Am. J. Med. Genet</addtitle><date>2008-09-05</date><risdate>2008</risdate><volume>147B</volume><issue>6</issue><spage>727</spage><epage>731</epage><pages>727-731</pages><issn>1552-4841</issn><eissn>1552-485X</eissn><abstract>Late‐onset Alzheimer's disease (LOAD) is a genetically complex neurodegenerative disorder. Currently, only the ε4 allele of the Apolipoprotein E gene has been identified unequivocally as a genetic susceptibility factor for LOAD. Others remain to be found. In 2002 we observed genome‐wide significant evidence of linkage to a region on chromosome 10q11.23–q21.3 [Myers et al. (2002) Am J Med Genet 114:235–244]. Our objective in this study was to test every gene within the maximum LOD‐1 linkage region, for association with LOAD. We obtained results for 528 SNPs from 67 genes, with an average density of 1 SNP every 10 kb within the genes. We demonstrated nominally significant association with LOAD for 4 SNPs: rs1881747 near DKK1 (P = 0.011, OR = 1.24), rs2279420 in ANK3 (P = 0.022, OR = 0.79), rs2306402 in CTNNA3 (P = 0.024, OR = 1.18), and rs5030882 in CXXC6 (P = 0.046, OR = 1.29) in 1,160 cases and 1,389 controls. These results would not survive correction for multiple testing but warrant attempts at confirmation in independent samples. © 2007 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>18163421</pmid><doi>10.1002/ajmg.b.30670</doi><tpages>5</tpages></addata></record> |
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| subjects | Adult and adolescent clinical studies Age of Onset Aged Aged, 80 and over alpha Catenin - genetics Alzheimer Disease - epidemiology Alzheimer Disease - genetics Ankyrins - genetics association Biological and medical sciences Case-Control Studies chromosome 10 Chromosomes, Human, Pair 10 Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases DNA Mutational Analysis DNA-Binding Proteins - genetics Female Genetic Linkage Genetic Predisposition to Disease Genotype Humans Intercellular Signaling Peptides and Proteins - genetics late-onset Alzheimer's disease Male Medical genetics Medical sciences Middle Aged Mixed Function Oxygenases Neurology Organic mental disorders. Neuropsychology Polymorphism, Single Nucleotide Proto-Oncogene Proteins - genetics Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry SNP |
| title | Association analysis of 528 intra-genic SNPs in a region of chromosome 10 linked to late onset Alzheimer's disease |
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