Journal
BRITISH JOURNAL OF PSYCHIATRY
Volume 195, Issue 1, Pages 30-38Publisher
CAMBRIDGE UNIV PRESS
DOI: 10.1192/bjp.bp.108.062521
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Funding
- GlaxoSmithKline
- Lundbeck
- MRC [G0701003] Funding Source: UKRI
- Medical Research Council [G0701003] Funding Source: researchfish
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Background There have been conflicting reports on whether the length polymorphism in the promoter of the serotonin transporter gene (5-HTTLPR) moderates the antidepressant effects of selective serotonin reuptake inhibitors (SSRIs). We hypothesised that the pharmacogenetic effect of 5-HTTLPR is modulated by gender, age and other variants in the serotonin transporter gene. Aims To test the hypothesis that the 5-HTTLPR differently influences response to escitalopram (an SSRI) compared with nortriptyline (a noradrenaline reuptake inhibitor). Method The 5-HTTLPR and 13 additional markers across the serotonin transporter gene were genotyped in 795 adults with mode rate-to-severe depression treated with escitalopram or nortriptyline in the Genome Based Therapeutic Drugs for Depression (GENDEP) project. Results The 5-HTTLPR moderated the response to escitalopram, with long-allele carriers improving more than short-allele homozygotes. A significant three-way interaction between 5-HTTLPR, drug and gender indicated that the effect was concentrated in males treated with escitalopram. The single-nucleotide polymorphism rs2020933 also influenced outcome. Conclusions The effect of 5-HTTLPR on antidepressant response is SSRI specific conditional on gender and modulated by another polymorphism at the 5' end of the serotonin transporter gene.
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