Public Release: 

Identification of the first gene in posttraumatic stress disorder

Molecular Psychiatry

Post-traumatic stress disorder (PTSD) is a prevalent anxiety disorder, marked by behavioral, physiological and hormonal alterations. Patients complain of symptoms of intrusive memories of the traumatic event, avoidance of cues reminding of the trauma and constant hyper-arousal. These symptoms may persist for years, and are often associated with significant disability and distress. The lifetime prevalence of PTSD in the general population is estimated to be of 10%, and the incidence of new cases of PTSD among survivors of traumatic events varies between 2% and 49%.

The etiology of PTSD is complex and multifactorial. Importantly, exposure to a traumatic event does not fully explain the occurrence of the disorder. Exposure, in fact, triggers a cascade of biological events that ultimately lead to the occurrence of chronic PTSD. Individuals with prior vulnerability are at higher risk for developing PTSD upon exposure to a trauma. Previous studies found correlates of abnormal biological reactivity of brain endocrine and autonomic nervous system, among PTSD patients, however the molecular basis of such vulnerability is unknown at this stage. A large twin study of Vietnam veterans has shown significant genetic contribution to PTSD. Multiple small effect genes are likely to contribute in concert with environmental exposure to risk for PTSD. Previous studies showing abnormal dopamine reactivity among PTSD patients, and stressed animals, have suggested that stress-induced alterations of brain dopamine reactivity may be genetically dependent and expressed in behavior.

Based on the above, researchers at the department of psychiatry at the Hebrew University in Jerusalem investigated a gene coding for the dopamine transporter (DAT) that is located pre-synaptically on dopaminergic neurons. Reuptake of dopamine released into the synaptic cleft limits the extent and duration of dopamine receptor activation. Researchers found a common mutation in the DAT gene to show an increased frequency among trauma survivors who developed chronic PTSD, and add a small significant contribution to the risk for PTSD. If replicated, results imply that genetically determined variation in dopaminergic neurotransmission may participate in shaping the pathological response to trauma, and, in general, the vulnerability to the effect of stress.

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Citation source: Molecular Psychiatry 2002 Volume 7, number 8, pages 903-907.

AUTHORS: RH Segman, R Cooper-Kazaz, F Macciardi, T Goltser, Y Halfon, T Dobroborski, AY Shalev

Department of Psychiatry, Hadassah Ð Hebrew University Medical Center, Jerusalem, Israel; Center for Addiction and Mental Health, University of Toronto, Canada.

For further information on this work, please contact RH Segman or AY Shalev, Department of Psychiatry, Hadassah University Hospital, PO Box 12000, Ein Karem, Jerusalem 91120, Israel. E-mail: sronen@md2.huji.ac.il, Tel: 972-2-5844317, or ashalev@cc.huji.ac.il, Tel: 972-2-6777184

Molecular Psychiatry is published by the Nature Publishing Group. http://www.nature.com/mp

Editor: Julio Licinio, M.D.; phone: 310-825-7113; FAX: 310-206-6715; e-mail: licinio@ucla.edu

For a copy of this article and accompanying editorial, please contact Aimee Midei, editorial assistant, e-mail: molecularpsychiatry@mednet.ucla.edu.

PLEASE CITE MOLECULAR PSYCHIATRY AS THE SOURCE OF THIS MATERIAL.

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