ArticleTranslational psychiatry2014
The role of FKBP5 genotype in moderating long-term effectiveness of exposure-based psychotherapy for posttraumatic stress disorder.
Article in Translational psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 65 citations in OpenAlex.
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- Analysis of the cerebellar molecular stress response led to first evidence of a role for FKBP51 in brain FKBP52 expression in mice and humans.Neurobiology of stress · 2021Article
- Genes and hormones of the hypothalamic-pituitary-adrenal axis in post-traumatic stress disorder. What is their role in symptom expression and treatment response?Journal of neural transmission (Vienna, Austria : 1996) · 2021Review
- FKBP5 polymorphisms induce differential glucocorticoid responsiveness in primary CNS cells - First insights from novel humanized mice.The European journal of neuroscience · 2021Article
- Assessing the Role of Long Noncoding RNA in Nucleus Accumbens in Subjects With Alcohol Dependence.Alcoholism, clinical and experimental research · 2020Article
- The Pathways between Cortisol-Related Regulation Genes and PTSD Psychotherapy.Healthcare (Basel, Switzerland) · 2020Review
- Does cumulative exposure to traumatic stressors predict treatment outcome of community-implemented exposure-based therapy for PTSD?European journal of psychotraumatology · 2020Article
- Trajectories of posttraumatic stress symptoms during and after Narrative Exposure Therapy (NET) in refugees.BMC psychiatry · 2020Article
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- Interaction of both positive and negative daily-life experiences withEuropean psychiatry : the journal of the Association of European Psychiatrists · 2020Article
- Integrated genetic, epigenetic, and gene set enrichment analyses identify NOTCH as a potential mediator for PTSD risk after trauma: Results from two independent African cohorts.Psychophysiology · 2020Article
- A precision medicine approach to pharmacological adjuncts to extinction: a call to broaden research.Psychopharmacology · 2019Review
- Glucocorticoid-induced enhancement of extinction-from animal models to clinical trials.Psychopharmacology · 2019Review
- Borderline personality disorder, trauma, and the hypothalamus-pituitary-adrenal axis.Neuropsychiatric disease and treatment · 2019Article
- Genetic variation is associated with PTSD risk and aversive memory: Evidence from two trauma-Exposed African samples and one healthy European sample.Translational psychiatry · 2018Article
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure-based therapies are considered the state-of-the-art treatment for Posttraumatic Stress Disorder (PTSD). Yet, a substantial number of PTSD patients do not recover after therapy. In the light of the well-known gene × environment interactions on the risk for PTSD, research on individual genetic factors that influence treatment success is warranted. The gene encoding FK506-binding protein 51 (FKBP5), a co-chaperone of the glucocorticoid receptor (GR), has been associated with stress reactivity and PTSD risk. As FKBP5 single-nucleotide polymorphism rs1360780 has a putative functional role in the regulation of FKBP5 expression and GR sensitivity, we hypothesized that this polymorphism influences PTSD treatment success. We investigated the effects of FKBP5 rs1360780 genotype on Narrative Exposure Therapy (NET) outcome, an exposure-based short-term therapy, in a sample of 43 survivors of the rebel war in Northern Uganda. PTSD symptom severity was assessed before and 4 and 10 months after treatment completion. At the 4-month follow-up, there were no genotype-dependent differences in therapy outcome. However, the FKBP5 genotype significantly moderated the long-term effectiveness of exposure-based psychotherapy. At the 10-month follow-up, carriers of the rs1360780 risk (T) allele were at increased risk of symptom relapse, whereas non-carriers showed continuous symptom reduction. This effect was reflected in a weaker treatment effect size (Cohen's D=1.23) in risk allele carriers compared with non-carriers (Cohen's D=3.72). Genetic factors involved in stress response regulation seem to not only influence PTSD risk but also responsiveness to psychotherapy and could hence represent valuable targets for accompanying medication.
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