ArticleMolecular biology reports2015
Serotonin transporter polymorphism (5-HTTLPR) in Croatian population.
Article in Molecular biology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Serotonin transporter functional polymorphisms potentially increase risk of schizophrenia separately and as a haplotype.Scientific reports · 2022Article
- INFLUENCE OF THE SEROTONERGIC SYSTEM POLYMORPHISM ON THE EXPRESSION OF DENTAL ANXIETY.Acta clinica Croatica · 2018Article
- Prediction of schizophrenia using MAOA-uVNTR polymorphism: A case-control study.Indian journal of psychiatryArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serotonin transporter polymorphism (5-HTTLPR) is a well-studied polymorphism in psychiatric research. The function of serotonin transporter is to control neural stimulation and maintain homeostasis of serotonin in other cells like platelets and enterochromaffin cells. Considering serotonin function in human behavior, and the role of serotonin transporter, 5-HTTLPR has been associated with depression related disorders, anxiety related personality traits, and adverse response to psychotherapy. However, many studies failed to replicate the association of 5-HTTLPR polymorphism with mentioned disorders. The aim of our study was to assess genotype frequencies in Croatian physically and psychologically healthy population and compare our results with previously published data. Genotype distribution in our research was similar to previous studies on Caucasian population regardless of inclusion criteria. Genotype distribution was as follows: LL 38 %; LS 45 %; SS 17 % and allele frequencies for L and S allele were 61 and 39 %, respectively. Obtained results were in an agreement with the Hardy-Weinberg equilibrium. Comparing inclusion criteria from different studies, we noticed a difference in population selection from one study to another. Increased possibility for selection bias, population stratification and complexity of psychiatric disorders might present a source of possible errors in genetic association studies.
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