Meta-analysis of genome-wide association studies of anxiety disorders.
paper
Cited
Public
- Authors
- Otowa, T; Hek, K; Lee, M; Byrne, E M; Mirza, S S; Nivard, M G; Bigdeli, T; Aggen, S H; Adkins, D; Wolen, A; Fanous, A; Keller, M C; Castelao, E; Kutalik, Z; Van der Auwera, S; Homuth, G; Nauck, M; Teumer, A; Milaneschi, Y; Hottenga, J-J; Direk, N; Hofman, A; Uitterlinden, A; Mulder, C L; Henders, A K; Medland, S E; Gordon, S; Heath, A C; Madden, P A F; Pergadia, M L; van der Most, P J; Nolte, I M; van Oort, F V A; Hartman, C A; Oldehinkel, A J; Preisig, M; Grabe, H J; Middeldorp, C M; Penninx, B W J H; Boomsma, D; Martin, N G; Montgomery, G; Maher, B S; van den Oord, E J; Wray, N R; Tiemeier, H; Hettema, J M
- Year
- 2016
- Journal
- Molecular psychiatry
- PMID
- 26754954
- DOI
- 10.1038/mp.2015.197
- PMCID
- PMC4940340
Anxiety disorders (ADs), namely generalized AD, panic disorder and phobias, are common, etiologically complex conditions with a partially genetic basis. Despite differing on diagnostic definitions based on clinical presentation, ADs likely represent various expressions of an underlying common diathesis of abnormal regulation of basic threat-response systems. We conducted genome-wide association analyses in nine samples of European ancestry from seven large, independent studies. To identify genetic variants contributing to genetic susceptibility shared across interview-generated DSM-based ADs, we applied two phenotypic approaches: (1) comparisons between categorical AD cases and supernormal controls, and (2) quantitative phenotypic factor scores (FS) derived from a multivariate analysis combining information across the clinical phenotypes. We used logistic and linear regression, respectively, to analyze the association between these phenotypes and genome-wide single nucleotide polymorphisms. Meta-analysis for each phenotype combined results across the nine samples for over 18 000 unrelated individuals. Each meta-analysis identified a different genome-wide significant region, with the following markers showing the strongest association: for case-control contrasts, rs1709393 located in an uncharacterized non-coding RNA locus on chromosomal band 3q12.3 (P=1.65 × 10(-8)); for FS, rs1067327 within CAMKMT encoding the calmodulin-lysine N-methyltransferase on chromosomal band 2p21 (P=2.86 × 10(-9)). Independent replication and further exploration of these findings are needed to more fully understand the role of these variants in risk and expression of ADs.
Quantile-quantile plots of meta-analysis results for (a) case-control and (b) factor score phenotypes. Observed association results of −log10P , after LD-pruning at r2 of 0.4, are plotted against the expected distribution under the null hypothesis of no association.
Manhattan plots of meta-analysis results for (a) case-control and (b) factor score phenotypes. Red horizontal line indicates the genome-wide significant p-value 5×10−8; blue line indicates the suggestive p-value=1×10−5.
Regional plots around most significant SNPs in (a) case-control and (b) factor score model.
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