Not 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. There is much to be understood
about the etiology of PTSD and equally there is much to be learned about developing
new treatment options and improving the rates of response to the current first-line
treatment for PTSD: cognitive behavioral therapy (CBT).To read this article in full you will need to make a payment
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References
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- Variant brain-derived neurotrophic factor Val66Met endophenotypes: implications for posttraumatic stress disorder.Ann N Y Acad Sci. 2010; 1208: 150-157
- Polymorphisms in FKBP5 are associated with increased recurrence of depressive episodes and rapid response to antidepressant treatment.Nat Genet. 2004; 36: 1319-1325
- Association between serotonin transporter gene promoter-region polymorphism and 4- and 12-week treatment response to sertraline in posttraumatic stress disorder.J Affect Disord. 2012; 136: 955-962
- The brain-derived neurotrophic factor Val66Met polymorphism predicts response to exposure therapy in posttraumatic stress disorder.Biol Psychiatry. 2013; 73: 1059-1063
- Preliminary evidence of the short allele of the serotonin transporter gene predicting poor response to cognitive behavior therapy in posttraumatic stress disorder.Biol Psychiatry. 2010; 67: 1217-1219
- Serotonin transporter polyadenylation polymorphism modulates the retention of fear extinction memory.Proc Natl Acad Sci U S A. 2012; 109: 5493-5498
- The risk of posttraumatic stress disorder after trauma depends on traumatic load and the catechol-o-methyltransferase Val(158)Met polymorphism.Biol Psychiatry. 2010; 67: 304-308
Article info
Publication history
Accepted:
April 9,
2013
Received:
March 28,
2013
Identification
Copyright
Published by Elsevier Inc.
ScienceDirect
Access this article on ScienceDirectLinked Article
- The Brain-Derived Neurotrophic Factor Val66Met Polymorphism Predicts Response to Exposure Therapy in Posttraumatic Stress DisorderBiological PsychiatryVol. 73Issue 11
- PreviewThe 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.
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