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Genome-wide association study of major recurrent depression in the U.K. population

Lewis, Cathryn M., Ng, Mandy Y., Butler, Amy W., Cohen-Woods, Sarah, Uher, Rudolf, Pirlo, Katrina, Weale, Michael E., Schosser, Alexandra, Paredes, Ursula M, Rivera, Margarita, Craddock, Nicholas John, Owen, Michael John, Jones, Lisa, Jones, Ian Richard, Korszun, Ania, Aitchison, Katherine J., Shi, Jianxin, Quinn, John P., MacKenzie, Alasdair, Vollenweider, Peter, Waeber, Gerard, Heath, Simon, Lathrop, Mark, Muglia, Pierandrea, Barnes, Michael R., Whittaker, John C., Tozzi, Frederica, Holsboer, Florian, Preisig, Martin, Farmer, Anne E., Breen, Gerome, Craig, Ian W. and McGuffin, Peter 2010. Genome-wide association study of major recurrent depression in the U.K. population. American Journal of Psychiatry 167 (8) , pp. 949-957. 10.1176/appi.ajp.2010.09091380

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Abstract

Objective Studies of major depression in twins and families have shown moderate to high heritability, but extensive molecular studies have failed to identify susceptibility genes convincingly. To detect genetic variants contributing to major depression, the authors performed a genome-wide association study using 1,636 cases of depression ascertained in the U.K. and 1,594 comparison subjects screened negative for psychiatric disorders. Method Cases were collected from 1) a case-control study of recurrent depression (the Depression Case Control [DeCC] study; N=1346), 2) an affected sibling pair linkage study of recurrent depression (probands from the Depression Network [DeNT] study; N=332), and 3) a pharmacogenetic study (the Genome-Based Therapeutic Drugs for Depression [GENDEP] study; N=88). Depression cases and comparison subjects were genotyped at Centre National de Génotypage on the Illumina Human610-Quad BeadChip. After applying stringent quality control criteria for missing genotypes, departure from Hardy-Weinberg equilibrium, and low minor allele frequency, the authors tested for association to depression using logistic regression, correcting for population ancestry. Results Single nucleotide polymorphisms (SNPs) in BICC1 achieved suggestive evidence for association, which strengthened after imputation of ungenotyped markers, and in analysis of female depression cases. A meta-analysis of U.K. data with previously published results from studies in Munich and Lausanne showed some evidence for association near neuroligin 1 (NLGN1) on chromosome 3, but did not support findings at BICC1. Conclusions This study identifies several signals for association worthy of further investigation but, as in previous genome-wide studies, suggests that individual gene contributions to depression are likely to have only minor effects, and very large pooled analyses will be required to identify them.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG)
Neuroscience and Mental Health Research Institute (NMHRI)
Subjects: Q Science > QH Natural history > QH426 Genetics
R Medicine > R Medicine (General)
R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Publisher: American Psychiatric Publishing
ISSN: 0002-953X
Last Modified: 04 Jun 2017 03:53
URI: http://orca.cf.ac.uk/id/eprint/28667

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