Abstract
The probability to develop posttraumatic stress disorder (PTSD), characterized by vivid, intrusive emotional memories of the encountered traumatic events, depends - among other factors - on the number of previous traumatic experiences (traumatic load) and individual genetic vulnerability. So far, our knowledge regarding the biological underpinnings of PTSD is relatively sparse. Genome-wide association studies (GWAS) followed by independent replication might help to discover novel, so far unknown biological mechanisms associated with the development of traumatic memories. Here, a GWAS was conducted in N = 924 Northern Ugandan rebel war survivors and identified seven suggestively significant single nucleotide polymorphisms (SNPs; p ≤ 1 × 10−5) for lifetime PTSD risk. Of these seven SNPs, the association of rs3852144 on chromosome 5 was replicated in an independent sample of Rwandan genocide survivors (N = 370, p < .01). While PTSD risk increased with accumulating traumatic experiences, the vulnerability was reduced in carriers of the minor G-allele in an additive manner. Correspondingly, memory for aversive pictures decreased with higher number of the minor G-allele in a sample of N = 2698 healthy Swiss individuals. Finally, investigations on N = 90 PTSD patients treated with Narrative Exposure Therapy indicated an additive effect of genotype on PTSD symptom change from pre-treatment to four months after treatment, but not between pre-treatment and the 10-months follow-up. In conclusion, emotional memory formation seems to decline with increasing number of rs3852144 G-alleles, rendering individuals more resilient to PTSD development. However, the impact on therapy outcome remains preliminary and further research is needed to determine how this intronic marker may affect memory processes in detail.
Highlights
Kolassa 1Clinical & Biological Psychology, Ulm University, Ulm, Germany 2Clinical Psychology and Neuropsychology, University of Konstanz, Konstanz, Germany Full list of author information is available at the end of the article. These authors contributed : Sarah Wilker, Anna Schneider, Daniela Conrad. Traumatic experiences such as war, terror, or natural disasters can lead to the development of posttraumatic stress disorder (PTSD), a disorder characterized by extremely vivid emotional memories of the traumatic events experienced
Ugandan therapy sample we investigated whether single nucleotide polymorphisms (SNPs) rs3852144 had an effect on the decrease of PTSD symptoms by exposurebased psychotherapy, including the PDS sum score as outcome variable, a time × genotype interaction as predictor and traumatic load and genotyping-batch as covariates
One might speculate that SNP rs3852144 Gallele is associated with diminished emotional memory formation, which leads to a reduced PTSD vulnerability, but on the other hand complicates memory extinction throughout the therapeutic progress
Summary
Traumatic experiences such as war, terror, or natural disasters can lead to the development of posttraumatic stress disorder (PTSD), a disorder characterized by extremely vivid emotional memories of the traumatic events experienced. The risk of PTSD development increases with. Substantial interindividual differences can be observed at lower levels of traumatic load, which underscores the role of individual risk factors in the aetiology of PTSD. Individuals vary in their response to exposure-based psychotherapies for PTSD. These treatments are considered very effective for PTSD12,13, approximately one third of trauma survivors still present with clinically significant symptoms after therapy. A deeper knowledge about individual predispositions related to PTSD development or lower treatment responsiveness might help to identify individuals at risk early, allocate therapeutic resources and yet importantly, to personalize treatments according to the individual needs of trauma survivors
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