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In human and animal studies of the Val66Met polymorphism in the brain-derived neurotrophic factor gene (BDNF), Met carriers showed reduced activity-dependent BDNF secretion, impaired extinction learning, and reduced activity in the ventromedial prefrontal cortex and rostral anterior cingulate, accompanied by heightened amygdala activity. Presumably, cortical activity reflected lower inhibitory pathways, leading to heightened fear, as manifested in the amygdala. Researchers hypothesized that people who carried the Met allele would respond poorly to exposure therapy for post-traumatic stress disorder (PTSD) because this treatment modality depends upon BDNF activity.
In a test of this hypothesis, 55 participants who completed an 8-week exposure…