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dc.contributor.authorWray, N R
dc.contributor.authorPergadia, M L
dc.contributor.authorBlackwood, D H R
dc.contributor.authorPenninx, B W J H
dc.contributor.authorNyholt, D R
dc.contributor.authorMacIntyre, D J
dc.contributor.authorMcGhee, K A
dc.contributor.authorMaclean, A W
dc.contributor.authorSmit, J H
dc.contributor.authorHottenga, J J
dc.contributor.authorWillemsen, G
dc.contributor.authorMiddeldorp, C M
dc.contributor.authorde Geus, E J C
dc.contributor.authorMcGuffin, P
dc.contributor.authorHickie, I B
dc.contributor.authorvan den Oord, E J C G
dc.contributor.authorMacgregor, S
dc.contributor.authorMcEvoy, B P
dc.contributor.authorMedland, S E
dc.contributor.authorStatham, D J
dc.contributor.authorHenders, A K
dc.contributor.authorMontgomery, G W
dc.contributor.authorBoomsma, D I
dc.contributor.authorMadden, P A F
dc.contributor.authorGordon, S. D.
dc.contributor.authorLewis, C. M.
dc.contributor.authorLiu, J. Z.
dc.contributor.authorByrne, E. M.
dc.contributor.authorHeath, A. C.
dc.contributor.authorMartin, N. G.
dc.contributor.authorSullivan, P. F.
dc.contributor.authorRipke, Stephan
dc.date.accessioned2013-02-15T19:07:21Z
dc.date.issued2012
dc.identifier.citationWray, N.R., M.L. Pergadia, D.H.R. Blackwood, B.W.J.H. Penninx, S.D. Gordon, D.R. Nyholt, S. Ripke, et al. 2012. Genome-wide association study of major depressive disorder: New results, meta-analysis, and lessons learned. Molecular Psychiatry 17(1): 36-48.en_US
dc.identifier.issn1359-4184en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:10304391
dc.description.abstractMajor depressive disorder (MDD) is a common complex disorder with a partly genetic etiology. We conducted a genome-wide association study of the MDD2000+ sample (2431 cases, 3673 screened controls and >1 M imputed single-nucleotide polymorphisms (SNPs)). No SNPs achieved genome-wide significance either in the MDD2000+ study, or in meta-analysis with two other studies totaling 5763 cases and 6901 controls. These results imply that common variants of intermediate or large effect do not have main effects in the genetic architecture of MDD. Suggestive but notable results were (a) gene-based tests suggesting roles for adenylate cyclase 3 (ADCY3, 2p23.3) and galanin (GAL, 11q13.3); published functional evidence relates both of these to MDD and serotonergic signaling; (b) support for the bipolar disorder risk variant SNP rs1006737 in CACNA1C (P=0.020, odds ratio=1.10); and (c) lack of support for rs2251219, a SNP identified in a meta-analysis of affective disorder studies (P=0.51). We estimate that sample sizes 1.8- to 2.4-fold greater are needed for association studies of MDD compared with those for schizophrenia to detect variants that explain the same proportion of total variance in liability. Larger study cohorts characterized for genetic and environmental risk factors accumulated prospectively are likely to be needed to dissect more fully the etiology of MDD.en_US
dc.language.isoen_USen_US
dc.publisherNature Publishing Groupen_US
dc.relation.isversionofdoi:10.1038/mp.2010.109en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3252611/pdf/en_US
dash.licenseLAA
dc.subjectmajor depressive disorderen_US
dc.subjectdepressionen_US
dc.subjectgenome-wide association studyen_US
dc.subjectCACNA1Cen_US
dc.subjectADCY3en_US
dc.subjectGALen_US
dc.titleGenome-Wide Association Study of Major Depressive Disorder: New Results, Meta-Analysis, and Lessons Learneden_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalMolecular Psychiatryen_US
dash.depositing.authorRipke, Stephan
dc.date.available2013-02-15T19:07:21Z
dc.identifier.doi10.1038/mp.2010.109*
dash.authorsorderedfalse
dash.contributor.affiliatedRipke, Stephan


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