Support of association between BRD1 and both schizophrenia and bipolar affective disorder
A recent study published by our group implicated the bromodomain containing protein 1 (BRD1) gene located at chromosome 22q13.33 with schizophrenia (SZ) and bipolar affective disorder (BPD) susceptibility and provided evidence suggesting a possible role for BRD1 in neurodevelopment. The present stud...
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| Veröffentlicht in: | American journal of medical genetics. Part B, Neuropsychiatric genetics Neuropsychiatric genetics, 2010-03, Vol.153B (2), p.582-591 |
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| container_title | American journal of medical genetics. Part B, Neuropsychiatric genetics |
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| creator | Nyegaard, Mette Severinsen, Jacob E. Als, Thomas D. Hedemand, Anne Straarup, Steen Nordentoft, Merete McQuillin, Andrew Bass, Nicholas Lawrence, Jacob Thirumalai, Srinivasa Pereira, Ana C.P. Kandaswamy, Radhika Lydall, Gregory J. Sklar, Pamela Scolnick, Edward Purcell, Shaun Curtis, David Gurling, Hugh M.D. Mortensen, Preben B. Mors, Ole Børglum, Anders D. |
| description | A recent study published by our group implicated the bromodomain containing protein 1 (BRD1) gene located at chromosome 22q13.33 with schizophrenia (SZ) and bipolar affective disorder (BPD) susceptibility and provided evidence suggesting a possible role for BRD1 in neurodevelopment. The present study reports an association analysis of BRD1 and the neighboring gene ZBED4 using a Caucasian case–control sample from Denmark and England (UK/DK sample: 490 patients with BPD, 527 patients with SZ, and 601 control individuals), and genotypes obtained from a BPD genome wide association (GWA) study of an overlapping English sample comprising 506 patients with BPD and 510 control individuals (UCL sample). In the UK/DK sample we genotyped 11 SNPs in the BRD1 region, of which six showed association with SZ (minimal single marker P‐values of 0.0014), including two SNPs that previously showed association in a Scottish population [Severinsen et al. (2006); Mol Psychiatry 11(12): 1126–1138]. Haplotype analysis revealed specific risk as well as protective haplotypes with a minimal P‐value of 0.0027. None of the 11 SNPs showed association with BPD. However, analyzing seven BRD1 SNPs obtained from the BPD GWA study, positive associations with BPD was observed with all markers (minimal P‐value of 0.0014). The associations reported add further support for the implication of BRD1 with SZ and BPD susceptibility. © 2009 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/ajmg.b.31023 |
| format | Article |
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The present study reports an association analysis of BRD1 and the neighboring gene ZBED4 using a Caucasian case–control sample from Denmark and England (UK/DK sample: 490 patients with BPD, 527 patients with SZ, and 601 control individuals), and genotypes obtained from a BPD genome wide association (GWA) study of an overlapping English sample comprising 506 patients with BPD and 510 control individuals (UCL sample). In the UK/DK sample we genotyped 11 SNPs in the BRD1 region, of which six showed association with SZ (minimal single marker P‐values of 0.0014), including two SNPs that previously showed association in a Scottish population [Severinsen et al. (2006); Mol Psychiatry 11(12): 1126–1138]. Haplotype analysis revealed specific risk as well as protective haplotypes with a minimal P‐value of 0.0027. None of the 11 SNPs showed association with BPD. However, analyzing seven BRD1 SNPs obtained from the BPD GWA study, positive associations with BPD was observed with all markers (minimal P‐value of 0.0014). The associations reported add further support for the implication of BRD1 with SZ and BPD susceptibility. © 2009 Wiley‐Liss, Inc.</description><identifier>ISSN: 1552-4841</identifier><identifier>EISSN: 1552-485X</identifier><identifier>DOI: 10.1002/ajmg.b.31023</identifier><identifier>PMID: 19693800</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>22q13 ; Alleles ; association ; Bipolar Disorder - genetics ; Case-Control Studies ; complex disorder ; Family Health ; Genetic Markers ; Genetic Predisposition to Disease ; Genetic Variation ; Genetics ; Genotype ; Haplotypes ; Histone Chaperones ; Humans ; Models, Genetic ; neuronal development ; Nuclear Proteins - genetics ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Schizophrenia - genetics</subject><ispartof>American journal of medical genetics. Part B, Neuropsychiatric genetics, 2010-03, Vol.153B (2), p.582-591</ispartof><rights>Copyright © 2009 Wiley‐Liss, Inc.</rights><rights>(c) 2009 Wiley-Liss, Inc.</rights><rights>Copyright © 2009 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4703-183be2035fa3bdb1b31fd2f8dfda4a0e64d23f39cfcee0d6c7f7edeb407d900f3</citedby><cites>FETCH-LOGICAL-c4703-183be2035fa3bdb1b31fd2f8dfda4a0e64d23f39cfcee0d6c7f7edeb407d900f3</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.31023$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fajmg.b.31023$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27922,27923,45572,45573</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19693800$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nyegaard, Mette</creatorcontrib><creatorcontrib>Severinsen, Jacob E.</creatorcontrib><creatorcontrib>Als, Thomas D.</creatorcontrib><creatorcontrib>Hedemand, Anne</creatorcontrib><creatorcontrib>Straarup, Steen</creatorcontrib><creatorcontrib>Nordentoft, Merete</creatorcontrib><creatorcontrib>McQuillin, Andrew</creatorcontrib><creatorcontrib>Bass, Nicholas</creatorcontrib><creatorcontrib>Lawrence, Jacob</creatorcontrib><creatorcontrib>Thirumalai, Srinivasa</creatorcontrib><creatorcontrib>Pereira, Ana C.P.</creatorcontrib><creatorcontrib>Kandaswamy, Radhika</creatorcontrib><creatorcontrib>Lydall, Gregory J.</creatorcontrib><creatorcontrib>Sklar, Pamela</creatorcontrib><creatorcontrib>Scolnick, Edward</creatorcontrib><creatorcontrib>Purcell, Shaun</creatorcontrib><creatorcontrib>Curtis, David</creatorcontrib><creatorcontrib>Gurling, Hugh M.D.</creatorcontrib><creatorcontrib>Mortensen, Preben B.</creatorcontrib><creatorcontrib>Mors, Ole</creatorcontrib><creatorcontrib>Børglum, Anders D.</creatorcontrib><title>Support of association between BRD1 and both schizophrenia and bipolar affective disorder</title><title>American journal of medical genetics. Part B, Neuropsychiatric genetics</title><addtitle>Am. J. Med. Genet</addtitle><description>A recent study published by our group implicated the bromodomain containing protein 1 (BRD1) gene located at chromosome 22q13.33 with schizophrenia (SZ) and bipolar affective disorder (BPD) susceptibility and provided evidence suggesting a possible role for BRD1 in neurodevelopment. The present study reports an association analysis of BRD1 and the neighboring gene ZBED4 using a Caucasian case–control sample from Denmark and England (UK/DK sample: 490 patients with BPD, 527 patients with SZ, and 601 control individuals), and genotypes obtained from a BPD genome wide association (GWA) study of an overlapping English sample comprising 506 patients with BPD and 510 control individuals (UCL sample). In the UK/DK sample we genotyped 11 SNPs in the BRD1 region, of which six showed association with SZ (minimal single marker P‐values of 0.0014), including two SNPs that previously showed association in a Scottish population [Severinsen et al. (2006); Mol Psychiatry 11(12): 1126–1138]. Haplotype analysis revealed specific risk as well as protective haplotypes with a minimal P‐value of 0.0027. None of the 11 SNPs showed association with BPD. However, analyzing seven BRD1 SNPs obtained from the BPD GWA study, positive associations with BPD was observed with all markers (minimal P‐value of 0.0014). The associations reported add further support for the implication of BRD1 with SZ and BPD susceptibility. © 2009 Wiley‐Liss, Inc.</description><subject>22q13</subject><subject>Alleles</subject><subject>association</subject><subject>Bipolar Disorder - genetics</subject><subject>Case-Control Studies</subject><subject>complex disorder</subject><subject>Family Health</subject><subject>Genetic Markers</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic Variation</subject><subject>Genetics</subject><subject>Genotype</subject><subject>Haplotypes</subject><subject>Histone Chaperones</subject><subject>Humans</subject><subject>Models, Genetic</subject><subject>neuronal development</subject><subject>Nuclear Proteins - genetics</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Schizophrenia - genetics</subject><issn>1552-4841</issn><issn>1552-485X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0U1v1DAQBmALgegH3DgjSxy4kMX2JHFy7AddQAUkCtpysux4zHrJxsFOKOXXk5KlSBzg5JH1zCuNXkIecbbgjInnerP9vDAL4EzAHbLPi0JkeVVc3r2dc75HDlLaMAaskPI-2eN1WUPF2D75dDH2fYgDDY7qlELj9eBDRw0OV4gdPX5_yqnuLDVhWNPUrP2P0K8jdl7P374PrY5UO4fN4L8htT6FaDE-IPecbhM-3L2H5OPZiw8nL7Pzd8tXJ0fnWZNLBhmvwKBgUDgNxhpugDsrXGWd1blmWOZWgIO6cQ0is2UjnUSLJmfS1ow5OCRP59w-hq8jpkFtfWqwbXWHYUxK5kXNcgHl_yVAWU2ynuSTv-QmjLGbzlC8qkVVFhWHST2bVRNDShGd6qPf6nitOFM33aibbpRRv7qZ-ONd6Gi2aP_gXRkTgBlc-Rav_xmmjl6_Wf6OzeYtnwb8frul4xdVSpCFWr1dqpVYXVyellwJ-Al6c6pk</recordid><startdate>201003</startdate><enddate>201003</enddate><creator>Nyegaard, Mette</creator><creator>Severinsen, Jacob E.</creator><creator>Als, Thomas D.</creator><creator>Hedemand, Anne</creator><creator>Straarup, Steen</creator><creator>Nordentoft, Merete</creator><creator>McQuillin, Andrew</creator><creator>Bass, Nicholas</creator><creator>Lawrence, Jacob</creator><creator>Thirumalai, Srinivasa</creator><creator>Pereira, Ana C.P.</creator><creator>Kandaswamy, Radhika</creator><creator>Lydall, Gregory J.</creator><creator>Sklar, Pamela</creator><creator>Scolnick, Edward</creator><creator>Purcell, Shaun</creator><creator>Curtis, David</creator><creator>Gurling, Hugh M.D.</creator><creator>Mortensen, Preben B.</creator><creator>Mors, Ole</creator><creator>Børglum, Anders D.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley Subscription Services, Inc</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>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>201003</creationdate><title>Support of association between BRD1 and both schizophrenia and bipolar affective disorder</title><author>Nyegaard, Mette ; 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Genet</addtitle><date>2010-03</date><risdate>2010</risdate><volume>153B</volume><issue>2</issue><spage>582</spage><epage>591</epage><pages>582-591</pages><issn>1552-4841</issn><eissn>1552-485X</eissn><abstract>A recent study published by our group implicated the bromodomain containing protein 1 (BRD1) gene located at chromosome 22q13.33 with schizophrenia (SZ) and bipolar affective disorder (BPD) susceptibility and provided evidence suggesting a possible role for BRD1 in neurodevelopment. The present study reports an association analysis of BRD1 and the neighboring gene ZBED4 using a Caucasian case–control sample from Denmark and England (UK/DK sample: 490 patients with BPD, 527 patients with SZ, and 601 control individuals), and genotypes obtained from a BPD genome wide association (GWA) study of an overlapping English sample comprising 506 patients with BPD and 510 control individuals (UCL sample). In the UK/DK sample we genotyped 11 SNPs in the BRD1 region, of which six showed association with SZ (minimal single marker P‐values of 0.0014), including two SNPs that previously showed association in a Scottish population [Severinsen et al. (2006); Mol Psychiatry 11(12): 1126–1138]. Haplotype analysis revealed specific risk as well as protective haplotypes with a minimal P‐value of 0.0027. None of the 11 SNPs showed association with BPD. However, analyzing seven BRD1 SNPs obtained from the BPD GWA study, positive associations with BPD was observed with all markers (minimal P‐value of 0.0014). The associations reported add further support for the implication of BRD1 with SZ and BPD susceptibility. © 2009 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>19693800</pmid><doi>10.1002/ajmg.b.31023</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 22q13 Alleles association Bipolar Disorder - genetics Case-Control Studies complex disorder Family Health Genetic Markers Genetic Predisposition to Disease Genetic Variation Genetics Genotype Haplotypes Histone Chaperones Humans Models, Genetic neuronal development Nuclear Proteins - genetics Oligonucleotide Array Sequence Analysis Polymorphism, Single Nucleotide Schizophrenia - genetics |
| title | Support of association between BRD1 and both schizophrenia and bipolar affective disorder |
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