DESCRIPTION:

List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Major depressive disorder. The EFO term unipolar depression was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.

LABEL:

GWAS: unipolar depression

SCORE TYPE:

P-Value

DATE ADDED:

2017-05-02

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

NR Wray, ML Pergadia, DH Blackwood, BW Penninx, SD Gordon, DR Nyholt, S Ripke, DJ MacIntyre, KA McGhee, AW Maclean, JH Smit, JJ Hottenga, G Willemsen, CM Middeldorp, EJ de Geus, CM Lewis, P McGuffin, IB Hickie, EJ van den Oord, JZ Liu, S Macgregor, BP McEvoy, EM Byrne, SE Medland, DJ Statham, AK Henders, AC Heath, GW Montgomery, NG Martin, DI Boomsma, PA Madden, PF Sullivan

TITLE:

Genome-wide association study of major depressive disorder: new results, meta-analysis, and lessons learned.

JOURNAL:

Molecular psychiatry Jan 2012, Vol 17, pp. 36-48

ABSTRACT:

Major 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. PUBMED: 21042317
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