Institute of Psychiatry, Kings College London, UK
Central Institute of Mental Health, Division of Genetic Epidemiology in Psychiatry, Mannheim, Germany
Croatian Institute for Brain Research, Medical School, University of Zagreb, Croatia
i
, PhD
Institute of Public Health, Ljubljana, Slovenia
Centre for Psychiatric Research, Aarhus University Hospital, Risskov, Denmark
Department of Psychiatry, University of Bonn, Germany
Laboratory of Psychiatric Genetics, Poznan University of Medical Sciences, Poland
Université Libre de Bruxelles, Erasme Academic Hospital, Department of Psychiatry, Brussels, Belgium
Biological Psychiatry Unit and Dual Diagnosis ward IRCCS, Centro San Giovanni di Dio, FBF, Brescia, Italy
Department of Psychiatry, University of Bonn, Germany
Mood Disorders Research Unit, Aarhus University Hospital, Risskov, Denmark
Laboratory of Psychiatric Genetics, Poznan University of Medical Sciences, Poland
Institute of Psychiatry, Kings College London, UK.
Correspondence: Rudolf Uher, P080, Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, 16 De Crespigny Park, London SE5 8AF UK. Email: rudolf.uher{at}iop.kcl.ac.uk
N.H. participated in clinical trials sponsored by pharmaceutical companies including GlaxoSmithKline and Lundbeck. A.F, P.M. and K.J.A have received consultancy fees and honoraria for participating in expert panels from pharmaceutical companies, including Lundbeck and GlaxoSmithKline.
The GENDEP study was funded by a European Commission Framework 6 grant, EC Contract Ref.: LSHB-CT-2003-503428. Lundbeck provided both nortriptyline and escitalopram free of charge for the GENDEP study. GlaxoSmithKline contributed by funding an add-on project in the London centre. The sponsors had no role in the design and conduct of the study, in data collection, analysis, interpretation or writing the report.
* These authors contributed equally to the work.
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 moderate-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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