Genome-wide association study of bipolar disorder in European American and African American individuals.
paper
Cited
Public
- Authors
- Smith, E N; Bloss, C S; Badner, J A; Barrett, T; Belmonte, P L; Berrettini, W; Byerley, W; Coryell, W; Craig, D; Edenberg, H J; Eskin, E; Foroud, T; Gershon, E; Greenwood, T A; Hipolito, M; Koller, D L; Lawson, W B; Liu, C; Lohoff, F; McInnis, M G; McMahon, F J; Mirel, D B; Murray, S S; Nievergelt, C; Nurnberger, J; Nwulia, E A; Paschall, J; Potash, J B; Rice, J; Schulze, T G; Scheftner, W; Panganiban, C; Zaitlen, N; Zandi, P P; ZΓΆllner, S; Schork, N J; Kelsoe, J R
- Year
- 2009
- Journal
- Molecular psychiatry
- PMID
- 19488044
- DOI
- 10.1038/mp.2009.43
- PMCID
- PMC3035981
To identify bipolar disorder (BD) genetic susceptibility factors, we conducted two genome-wide association (GWA) studies: one involving a sample of individuals of European ancestry (EA; n=1001 cases; n=1033 controls), and one involving a sample of individuals of African ancestry (AA; n=345 cases; n=670 controls). For the EA sample, single-nucleotide polymorphisms (SNPs) with the strongest statistical evidence for association included rs5907577 in an intergenic region at Xq27.1 (P=1.6 x 10(-6)) and rs10193871 in NAP5 at 2q21.2 (P=9.8 x 10(-6)). For the AA sample, SNPs with the strongest statistical evidence for association included rs2111504 in DPY19L3 at 19q13.11 (P=1.5 x 10(-6)) and rs2769605 in NTRK2 at 9q21.33 (P=4.5 x 10(-5)). We also investigated whether we could provide support for three regions previously associated with BD, and we showed that the ANK3 region replicates in our sample, along with some support for C15Orf53; other evidence implicates BD candidate genes such as SLITRK2. We also tested the hypothesis that BD susceptibility variants exhibit genetic background-dependent effects. SNPs with the strongest statistical evidence for genetic background effects included rs11208285 in ROR1 at 1p31.3 (P=1.4 x 10(-6)), rs4657247 in RGS5 at 1q23.3 (P=4.1 x 10(-6)), and rs7078071 in BTBD16 at 10q26.13 (P=4.5 x 10(-6)). This study is the first to conduct GWA of BD in individuals of AA and suggests that genetic variations that contribute to BD may vary as a function of ancestry.
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| Name | Type |
|---|---|
| 13q local | variant |
| 15q14 local | variant |
| 22q local | variant |
| 6q local | variant |
| 8q local | variant |
| AA | cohort |
| AA group | cohort |
| AA participants | cohort |
| AA set local | cohort |
| Admixture local | phenotype |
| African American | cohort |
| age | phenotype |
| ANK3 | gene |
| another study local | cohort |
| antidepressants | drug |
| Baum2008_GWAS local | cohort |
| Baum et al., 2008 local | cohort |
| Baum et al. (2008) sample local | cohort |
| BD | phenotype |
| Bdnf | gene |
| BDNF SNPs local | variant |
| Bipolar Consortium local | cohort |
| bipolar disorder | phenotype |
| Bipolar Genome Study (BiGS) local | cohort |
| blood pressure | phenotype |
| BTBD16 local | gene |
| C15orf53 | gene |
| CACNA1C | gene |
| Case-control replication cohort local | cohort |
| CEU | cohort |
| collaborative GWA study local | cohort |
| Combined EA and AA local | cohort |
| combined sample | cohort |
| controls | cohort |
| current sample | cohort |
| depression | phenotype |
| DNA | drug |
| DPY19L3 local | gene |
| EA | cohort |
| EA dataset | cohort |
| EA group | cohort |
| EA participants | cohort |
| EA population | cohort |
| EA sample | cohort |
| EA set local | cohort |
| EPHA6 local | gene |
| European ancestry | cohort |
| family-based sample | cohort |
| GAIN initiative | cohort |
| genetic background-dependent effects local | phenotype |
| Genomic control adjustment local | drug |
| GermanReplicationSample local | cohort |
| GWA study | cohort |
| haplotype heterogeneity local | phenotype |
| HapMap rel21 phased haplotypes local | cohort |
| HapMap subjects local | cohort |
| HGDP subjects local | cohort |
| human brain | anatomy |
| LAMP local | drug |
| lithium | drug |
| Logistic regression with LAMP-generated covariate local | drug |
| Logistic regression with MDS-generated covariates local | drug |
| mania | phenotype |
| NAP1L5 | gene |
| neurogenesis | phenotype |
| NTRK2 | gene |
| population structure | phenotype |
| present study | cohort |
| PresentStudy local | cohort |
| Previous GWA studies of BD local | cohort |
| previous GWA study local | cohort |
| primary EA sample local | cohort |
| Pritzker Neuropsychiatric Disorders Research Consortium local | cohort |
| Pritzker Study local | cohort |
| probands | cohort |
| replication sample | cohort |
| Rgs5 | gene |
| RIN2 local | gene |
| ROR1 local | gene |
| rs10193871 local | variant |
| rs13358880 local | variant |
| rs1495186 local | variant |
| rs1825828 local | variant |
| rs1938526 local | variant |
| rs2111504 local | variant |
| rs2172835 | variant |
| rs2769605 local | variant |
| rs4825220 local | variant |
| rs5907577 local | variant |
| rs6046396 local | variant |
| rs9804190 local | variant |
| sex | phenotype |
| Sklar et al. (2008) sample local | cohort |
| SLITRK1 | gene |
| SLITRK2 local | gene |
| SNP | cohort |
| SNP_BTBD16_top local | variant |
| SNP_RGS5_top local | variant |
| SNP_ROR1_top local | variant |
| STEP-BD | cohort |
| Structure | drug |
| study cohort | cohort |
| suicide | phenotype |
| Touretteβs syndrome | phenotype |
| Wellcome Trust case control consortium | cohort |
| WTCCC | cohort |
| X chromosome haplotype (7 Mb) local | variant |
| Xq27.1 local | gene |
| Yoruba | cohort |
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