Background
The most effective treatment for posttraumatic stress disorder (PTSD) is exposure
therapy, which aims to facilitate extinction of conditioned fear. Recent evidence
suggests that brain-derived neurotrophic factor (BDNF) facilitates extinction learning.
This study assessed whether the Met-66 allele of BDNF, which results in lower activity-dependent
secretion, predicts poor response to exposure therapy in PTSD.
Methods
Fifty-five patients with PTSD underwent an 8-week exposure-based cognitive behavior
therapy program and provided mouth swabs or saliva to extract genomic DNA to determine
their BDNF Val66Met genotype (30 patients with the Val/Val BDNF allele, 25 patients
with the Met-66 allele). We examined whether BDNF genotype predicted reduction in
PTSD severity following exposure therapy.
Results
Analyses revealed poorer response to exposure therapy in the PTSD patients with the
Met-66 allele of BDNF compared with patients with the Val/Val allele. Pretreatment
Clinician Administered PTSD Scale severity and BDNF Val66Met polymorphism predicted
response to exposure therapy using hierarchical regression.
Conclusions
This study provides the first evidence that the BDNF Val66Met genotype predicts response
to cognitive behavior therapy in PTSD and is in accord with evidence that BDNF facilitates
extinction learning.
Key Words
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Article info
Publication history
Published online: January 10, 2013
Accepted:
October 16,
2012
Received in revised form:
October 16,
2012
Received:
April 30,
2012
Identification
Copyright
© 2013 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
ScienceDirect
Access this article on ScienceDirectLinked Article
- The First Steps on the Path Toward Genomic Predictors of Behavioral Therapy for Posttraumatic Stress DisorderBiological PsychiatryVol. 73Issue 11
- PreviewNot everyone who has personally experienced, or has been exposed to, severe trauma develops posttraumatic stress disorder (PTSD). The risk-resilience equation is complex and, as we are becoming increasingly aware, includes both genetic predictors and environmental stressors, starting in early childhood. For example, as Binder and colleagues (1) first showed, FKBP5, a gene influencing activity of the hypothalamic-pituitary-adrenal axis, together with exposure to childhood trauma but not adult stressors, predicted the development of PTSD in a low-income, urban African American sample.
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