Neuropsychiatric Disease and Treatment
Open access peer-reviewed scientific and medical journals.
Dove Medical Press is now a member of the Open Access Initiative
An Author's Guide
A guide to help authors get their paper published.
Support Open Access and Dove Press
Promotional Article Monitoring - further details
Favored Author Program
Real benefits for authors, including fast-track processing of papers.
Higher FKBP5, COMT, CHRNA5, and CRHR1 allele burdens are associated with PTSD and interact with trauma exposure: implications for neuropsychiatric research and treatment
(8383) Total Article Views
Authors: Boscarino JA, Erlich PM, Hoffman SN, Zhang X
Published Date March 2012
Volume 2012:8 Pages 131 - 139
|Received:||26 December 2011|
|Accepted:||11 February 2012|
|Published:||23 March 2012|
1Center for Health Research, Geisinger Clinic, Danville, PA, 2Department of Psychiatry, 3Department of Medicine, Temple University School of Medicine, Philadelphia, PA, 4Department of Neurology, 5Department of Anesthesiology, Geisinger Clinic, Danville, PA, USA
Objective: The study aim was to assess the cumulative burden of polymorphisms located within four genetic loci previously associated with posttraumatic stress disorder (PTSD) among outpatients at risk for PTSD.
Methods: Diagnostic interviews were completed and DNA samples collected among 412 pain patients to determine if FKBP5 (rs9470080), COMT (rs4680), CHRNA5 (rs16969968), and CRHR1 (rs110402) single nucleotide polymorphisms were cumulatively associated with increased risk for PTSD.
Results: In bivariate analyses, it was found that a count of specific PTSD risk alleles located within FKBP5, COMT, CHRNA5, and CRHR1 genetic loci (allele range = 0–6, mean count = 2.92, standard deviation = 1.36) was associated with lifetime (t  = 3.430, P = 0.001) and early onset PTSD (t  = 4.239, P = 0.000028). In logistic regression, controlling for demographic factors, personality traits, and trauma exposures, this risk allele count remained associated with both lifetime (odds ratio = 1.49, P = 0.00158) and early onset PTSD (odds ratio = 2.36, P = 0.000093). Interaction effects were also detected, whereby individuals with higher risk allele counts and higher trauma exposures had an increased risk of lifetime PTSD (allele count × high trauma, P = 0.026) and early onset PTSD (allele count × high trauma, P = 0.016) in these logistic regressions. Those with no or few risk alleles appeared resilient to PTSD, regardless of exposure history.
Conclusion: A cumulative risk allele count involving four single nucleotide polymorphisms located within the FKBP5, COMT, CHRNA5, and CRHR1 genes are associated with PTSD. Level of trauma exposure interacts with risk allele count, such that PTSD is increased in those with higher risk allele counts and higher trauma exposures. Since the single nucleotide polymorphisms studied encompass stress circuitry and addiction biology, these findings may have implications for neuropsychiatric research and treatment.
Keywords: posttraumatic stress disorder, genetic association study, single nucleotide polymorphism, risk alleles, trauma exposure, neuroticism, childhood adversity
Cannotea Citeulike Del.icio.us Facebook LinkedIn Twitter
Other articles by Dr Joseph Boscarino
Readers of this article also read:
"I was impressed at the rapidity of publication from submission to final acceptance." Dr Edwin Thrower, PhD, Yale University.
- MLA'14 -
May 16–21, 2014
- CINP World Congress
22 - 26 June, 2014
- 27th ECNP Congress
18 - 21 October, 2014
- Neuroscience 2014 Annual Meeting
November 15 - 19
- Aggressive behavior, cognitive impairment, and depressive symptoms in elderly subjects
- Critical appraisal of the role of davunetide in the treatment of progressive supranuclear palsy
- Role of nucleus accumbens glutamatergic plasticity in drug addiction
- Long-term treatment of bipolar disorder with a radioelectric asymmetric conveyor