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Association study of trauma load and SLC6A4 promoter polymorphism in posttraumatic stress disorder : evidence from survivors of the Rwandan genocide
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 1095040
Author(s) Kolassa, Iris-Tatjana; Ertl, Verena; Eckart, Cindy; Glöckner, Franka; Kolassa, Stephan; Papassotiropoulos, Andreas; de Quervain, Dominique J.-F.; Elbert, Thomas
Author(s) at UniBasel Papassotiropoulos, Andreas
de Quervain, Dominique
Year 2010
Title Association study of trauma load and SLC6A4 promoter polymorphism in posttraumatic stress disorder : evidence from survivors of the Rwandan genocide
Journal The Journal of clinical psychiatry
Volume 71
Number 5
Pages / Article-Number 543-7
Mesh terms Adolescent; Adult; Aged; Female; Genetic Predisposition to Disease, genetics; Genotype; Homicide, psychology; Homozygote; Humans; Male; Middle Aged; Polymorphism, Genetic, genetics; Psychiatric Status Rating Scales; Rwanda; Serotonin Plasma Membrane Transport Proteins, genetics; Stress Disorders, Post-Traumatic, psychology; Stress, Psychological, psychology; Survivors, psychology; Young Adult
Abstract As exposure to different types of traumatic stressors increases, the occurrence of posttraumatic stress disorder (PTSD) increases. However, because some people exhibit either surprising resilience or high vulnerability, further influencing factors have been conjectured, such as gene-environment interactions. The SLC6A4 gene, which encodes serotonin transporter, has been identified as predisposing toward differential emotional processing between genotypes of its promoter polymorphism.; We investigated 408 refugees from the Rwandan genocide and assessed lifetime exposure to traumatic events, PTSD (according to DSM-IV) status, and genotype of the SLC6A4 promoter polymorphism. The study was conducted from March 2006 to February 2007.; The prevalence of PTSD approached 100% when traumatic exposure reached extreme levels. However, persons homozygous for the short allele of the SLC6A4 promoter polymorphism showed no dose-response relationship but were at high risk for developing PTSD after very few traumatic events. This genotype influence vanished with increasing exposure to traumatic stressors.; We find evidence for a gene-environment interplay for PTSD and show that genetic influences lose importance when environmental factors cause an extremely high trauma burden to an individual. In the future, it may be important to determine whether the effectiveness of therapeutic interventions in PTSD is also modulated by the SLC6A4 genotype.
Publisher Physicians Postgraduate Press
ISSN/ISBN 0160-6689
edoc-URL http://edoc.unibas.ch/dok/A5849012
Full Text on edoc No
Digital Object Identifier DOI 10.4088/JCP.08m04787blu
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/20441718
ISI-Number WOS:000277946400005
Document type (ISI) Journal Article
 
   

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