ORIGINAL PAPER Is 5-HTTLPR linked to the response of selective serotonin reuptake inhibitors in MDD? Ari Illi • Outi Poutanen • Eija Seta ¨la ¨-Soikkeli • Olli Kampman • Merja Viikki • Heini Huhtala • Nina Mononen • Susann Haraldsson • Pasi A. Koivisto • Esa Leinonen • Terho Lehtima ¨ki Received: 19 February 2010 / Accepted: 5 July 2010 / Published online: 17 July 2010 Ó Springer-Verlag 2010 Abstract The role of a functional polymorphism in the transcriptional control region of serotonin transporter gene (5-HTTLPR, SERTPR) has been studied intensively in major depression and in the response to selective sero- tonin inhibitors (SSRIs) in major depression. The findings have been contradictory, although majority of the studies indicate that the short allele is associated with poor response to SSRIs in major depression. In the present study, we evaluated the association of 5-HTTLPR with treatment response to SSRI medication in Finnish Cau- casian MDD patients. A secondary purpose was to study the possible association of this particular polymorphism with major depressive disorder. The aim of the study was to replicate the previous findings in this area. Primary outcomes of the treatment were remission, defined by an exit score of seven or less, and response, defined by a reduction of at least 50% on the MADRS. We had also a control population of 375 healthy blood donors, as a secondary objective was to evaluate the possible associ- ation of this particular polymorphism with major depressive disorder. Twenty-nine of the 85 (34.1%) patients reached the remission and 58.8% achieved the predefined response criteria. The l/l genotype of 5-HTTLPR was presented in 51.7% of those patients who achieved remission vs. 25.0% in the non-remitters (P = 0.03). The result remained statistically significant after adjusting for age, gender, medication and MADRS points at the study entry. However, the small sample size limits the reliability of this result. Keywords Serotonin transporter Á 5-HTTLPR Á MDD Á SSRI Á Drug response A. Illi (&) Á O. Poutanen Á O. Kampman Á M. Viikki Á E. Leinonen Medical School, University of Tampere, 33014 Tampere, Finland e-mail: ari.illi@uta.fi A. Illi Á O. Poutanen Á E. Leinonen Department of Psychiatry, Tampere University Hospital, Tampere, Finland N. Mononen Á T. Lehtima ¨ki Centre for Laboratory Medicine, Tampere University Hospital, Tampere, Finland E. Seta ¨la ¨-Soikkeli Department of Psychiatry, Kanta-Ha ¨me Central Hospital, Ha ¨meenlinna, Finland O. Kampman Department of Psychiatry, Seina ¨joki Hospital District, Seina ¨joki, Finland H. Huhtala School of Public Health, University of Tampere, Tampere, Finland O. Kampman Department of Psychiatry, Pa ¨ija ¨t-Ha ¨me Social and Health Care District, Lahti, Finland S. Haraldsson Á P. A. Koivisto Division of Medical and Clinical Genetics, Department of Medical Biosciences, Umea ˚ University, Umea ˚, Sweden P. A. Koivisto Laboratory of Molecular Genetics, Tampere University Hospital, Tampere, Finland T. Lehtima ¨ki Department of Clinical Chemistry, Medical School, University of Tampere, Tampere, Finland 123 Eur Arch Psychiatry Clin Neurosci (2011) 261:95–102 DOI 10.1007/s00406-010-0126-x