@article{f120cc303a1e4eafaa8383a1d5be845a,
title = "Genome-wide association study of bipolar disorder in European American and African American individuals",
abstract = "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; n1001 cases; n1033 controls), and one involving a sample of individuals of African ancestry (AA; n345 cases; n670 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 (P1.6 × 10 6) and rs10193871 in NAP5 at 2q21.2 (P9.8 × 10 6). For the AA sample, SNPs with the strongest statistical evidence for association included rs2111504 in DPY19L3 at 19q13.11 (P1.5 × 10 6) and rs2769605 in NTRK2 at 9q21.33 (P4.5 × 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 (P1.4 × 10 6), rs4657247 in RGS5 at 1q23.3 (P4.1 × 10 6), and rs7078071 in BTBD16 at 10q26.13 (P4.5 × 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.",
keywords = "ANK3, Allelic heterogeneity, Bipolar Genome Study, GAIN, Genetic background",
author = "Smith, {E. N.} and Bloss, {C. S.} and Badner, {J. A.} and T. Barrett and Belmonte, {P. L.} and W. Berrettini and W. Byerley and W. Coryell and D. Craig and Edenberg, {H. J.} and E. Eskin and T. Foroud and E. Gershon and Greenwood, {T. A.} and M. Hipolito and Koller, {D. L.} and Lawson, {W. B.} and C. Liu and F. Lohoff and McInnis, {M. G.} and McMahon, {F. J.} and Mirel, {D. B.} and Murray, {S. S.} and C. Nievergelt and J. Nurnberger and Nwulia, {E. A.} and J. Paschall and Potash, {J. B.} and J. Rice and Schulze, {T. G.} and W. Scheftner and C. Panganiban and N. Zaitlen and Zandi, {P. P.} and S. Z{\"o}llner and Schork, {N. J.} and Kelsoe, {J. R.}",
note = "Funding Information: In the last several years, the development of genome-wide association (GWA) study designs and analysis methods have made it possible to search for multiple genetic variations underlying a condition like BD without a priori assumptions about the genes or genomic regions that might harbor susceptibility variations.12 The GWA study approach has revealed a number of genetic variations that are unequivocally associated with many different traits and diseases.13,14 The US National Institutes of Mental Health– sponsored Genetics Initiative for Bipolar Disorder Consortium (Bipolar Consortium) collected over 3500 subjects with BD during 1990–2008. A genetic component of the Bipolar Consortium, termed the {\textquoteleft}Bipolar Genome Study{\textquoteright} (BiGS), was initiated in 2006 to conduct a GWA study of BD. The initial BiGS GWA study was funded through the Foundation for the National Institutes of Health Genetic Information Association Network (GAIN) initiative (http://www. genome.gov/19518664) and we report the results of this GWA study here. Of note, many investigators have access to and have utilized the DNA samples from individuals with BD that were collected as part of the Bipolar Consortium. Thus, it is the case that a portion of the samples on which we report here are not entirely independent of previously published BD GWA studies15,16 and an ongoing BD GWA study (Scott et al., submitted).",
year = "2009",
month = aug,
doi = "10.1038/mp.2009.43",
language = "English (US)",
volume = "14",
pages = "755--763",
journal = "Molecular psychiatry",
issn = "1359-4184",
publisher = "Nature Publishing Group",
number = "8",
}