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Author Notes:

Tel.: (404) 727-7739 Fax: (404) 727-8070 Email: kressle@emory.edu

The authors declare no conflict of interest, financial or otherwise.

Subject:

Research Funding:

This work was primarily supported by the National Institutes of Mental Health (MH071537 and MH096764 to K.J.R., MH095456 to N.F., and MH085806 to A.K.S.).

Support was also received from Emory and Grady Memorial Hospital General Clinical Research Centre, NIH National Centres for Research Resources (M01RR00039), and Howard Hughes Medical Institute (K.J.R.)

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Clinical Neurology
  • Neurosciences
  • Pharmacology & Pharmacy
  • Psychiatry
  • Neurosciences & Neurology
  • Anxiety
  • epigenetics
  • neuroimaging
  • psychiatry
  • stress
  • SEROTONIN-TRANSPORTER-GENE
  • CATECHOL-O-METHYLTRANSFERASE
  • BETA-HYDROXYLASE ACTIVITY
  • GENOME-WIDE ASSOCIATION
  • FACTOR VAL66MET POLYMORPHISM
  • TRADE-CENTER ATTACKS
  • EARLY-LIFE ADVERSITY
  • PLATELET MAO-B
  • DOPAMINE TRANSPORTER
  • HIPPOCAMPAL VOLUME

Genetic approaches to understanding post-traumatic stress disorder

Tools:

Journal Title:

International Journal of Neuropsychopharmacology

Volume:

Volume 17, Number 2

Publisher:

, Pages 355-370

Type of Work:

Article | Final Publisher PDF

Abstract:

Post-traumatic stress disorder (PTSD) is increasingly recognized as both a disorder of enormous mental health and societal burden, but also as an anxiety disorder that may be particularly understandable from a scientific perspective. Specifically, PTSD can be conceptualized as a disorder of fear and stress dysregulation, and the neural circuitry underlying these pathways in both animals and humans are becoming increasingly well understood. Furthermore, PTSD is the only disorder in psychiatry in which the initiating factor, the trauma exposure, can be identified. Thus, the pathophysiology of the fear and stress response underlying PTSD can be examined and potentially interrupted. Twin studies have shown that the development of PTSD following a trauma is heritable, and that genetic risk factors may account for up to 30-40% of this heritability. A current goal is to understand the gene pathways that are associated with PTSD, and how those genes act on the fear/stress circuitry to mediate risk vs. resilience for PTSD. This review will examine gene pathways that have recently been analysed, primarily through candidate gene studies (including neuroimaging studies of candidate genes), in addition to genome-wide associations and the epigenetic regulation of PTSD. Future and on-going studies are utilizing larger and collaborative cohorts to identify novel gene candidates through genome-wide association and other powerful genomic approaches. Identification of PTSD biological pathways strengthens the hope of progress in the mechanistic understanding of a model psychiatric disorder and allows for the development of targeted treatments and interventions. © 2013 CINP.

Copyright information:

© CINP 2013

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