Related Experiment Video
Updated: May 15, 2026

Rapid Fractionation and Isolation of Whole Blood Components in Samples Obtained from a Community-based Setting
Published on: November 30, 2015
The brain-derived neurotrophic factor Val66Met polymorphism predicts response to exposure therapy in posttraumatic
Kim L Felmingham1, Carol Dobson-Stone, Peter R Schofield
1School of Psychology, University of Tasmania, Hobart, TAS 7005, Australia. Kim.Felmingham@utas.edu.au
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.
Related Concept Videos
Post-traumatic Stress Disorder
Symptoms and Behavioral Manifestations
A spectrum of distressing symptoms characterizes PTSD. Recurrent flashbacks, where individuals involuntarily relive traumatic events, are a...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
