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Psychiatry Journal
Volume 2013 (2013), Article ID 849346, 6 pages
Clinical Study

Association between Neurocognitive Impairment and the Short Allele of the 5-HTT Promoter Polymorphism in Depression: A Pilot Study

1Institute of Behavioural Sciences, University of Helsinki, P.O. Box 9, 00014 University of Helsinki, Finland
2Department of Pharmacology, Drug Development and Therapeutics, University of Turku, 20014 Turku, Finland
3Department of Psychiatry, Helsinki University Central Hospital, P.O. Box 590, 00029 HUS, Finland
4Department of Psychiatry, University of Helsinki, P.O. Box 22, 00014 University of Helsinki, Finland

Received 19 September 2012; Revised 20 November 2012; Accepted 20 November 2012

Academic Editor: José F. Navarro

Copyright © 2013 Hely Kalska et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Depression has been shown to be associated with cognitive deficits in various cognitive domains. However, it is still unclear which factors contribute to cognitive impairment. The objective of this study was to find out whether a functional polymorphism in the promoter region of the serotonin transporter (5-HTTLPR) gene is associated with the impairment of cognitive functioning among depressed patients. In a pilot study, a sample of 19 patients with major depressive disorder (MDD) and 19 healthy controls was investigated with an extensive psychiatric and neuropsychological examination. All participants were genotyped for 5-HTTLPR. Depressed patients with the short allele of the 5-HTT promoter region exhibited inferior cognitive performance compared to patients with the long allele polymorphism. In healthy controls, no association between genotype and cognitive performance was found. The result suggests that in MDD patients with the short allele of the 5-HTTLPR polymorphism the vulnerability to cognitive impairment is increased compared to MDD patients without the short allele inheritance. These preliminary findings need to be confirmed in a larger cohort of MDD patients.