Response Variation following Trauma: A Translational Neuroscience Approach to Understanding PTSD

Division of Traumatic Stress Studies, Mount Sinai School of Medicine, James J Peters Veteran Affairs, New York, NY 10468, USA.
Neuron (Impact Factor: 15.05). 11/2007; 56(1):19-32. DOI: 10.1016/j.neuron.2007.09.006
Source: PubMed


Exposure to traumatic stress is a requirement for the development of posttraumatic stress disorder (PTSD). However, because the majority of trauma-exposed persons do not develop PTSD, examination of the typical effects of a stressor will not identify the critical components of PTSD risk or pathogenesis. Rather, PTSD represents a specific phenotype associated with a failure to recover from the normal effects of trauma. Thus, research must focus on identifying pre- and posttraumatic risk factors that explain the development of the disorder and the failure to reinstate physiological homeostasis. In this review, we summarize what is known about the clinical and biological characteristics of PTSD and articulate some of the gaps in knowledge that can be addressed by basic neuroscience research. We emphasize how knowledge about individual differences related to genetic and epigenetic factors in behavioral and brain responses to stress offers the hope of a deeper understanding of PTSD.

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Available from: Rachel Yehuda, Mar 18, 2014
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    • "DNA methylation patterns are maintained after cell division and are consequently passed from parent to daughter cells (Taylor & Jones 1985; Turner 2002; Razin 1998). Dysregulation of methylation can lead to aberrant transcriptional control and subsequent alterations in gene expression (Yehuda & LeDoux 2007). Another essential role of DNA methylation is the repression of retrotransposons and other foreign elements (Sasaki & Matsui 2008). "

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    • "Findings have indicated polymorphisms (phenotypical aberrations) within two genes, FKBP5 and CRHR1 (Binder et al., 2008) that regulate HPA axis function when the child is also exposed to child maltreatment (Klengel et al., 2013). Significant associations were also found with a variable number tandem repeat (VNTR) polymorphism (Segman & Shalev, 2003; Yehuda & LeDoux, 2007). Other genes, such as the PRKCA were found to lead to improved memory, and therefore also to increased risk of PTSD (de Quervain et al., 2012). "
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    DESCRIPTION: Abstract Transgenerational transmission of trauma (TTT) renders some children of survivors vulnerable to stress while others become more resilient. TTT was previously assumed to be caused primarily by environmental factors, such as the parents’ child-rearing behavior. Recent research findings, reviewed in this paper, suggest that it may also be inherited through epigenetic mechanisms. New data indicate that the glucocorticoid receptor gene may cause the stress hormones of the child to become allostatic rather than resilient. Six clinical case anecdotes on suicidality, depression and PTSD, as well as on certain olfactory, cardiac and pulmonary problems, are presented to illustrate such possible epigenetic transgenerational transmission of Holocaust trauma. Further studies may justify the introduction of a new diagnostic entity -- transgenerational stress disorder -- with immediate relevance for the assessment, prevention, and treatment of the offspring of many kinds of trauma survivors.
    Full-text · Research · Nov 2015
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    • "In the present study, we advanced our prior work by evaluating PTSD symptom severity among service members who report experiencing traumatic events, using measures that allow direct comparisons of the association between anger and PTSD symptom severity to the extant psychological literature. PTSD symptom severity captures important and distinct information from PTSD diagnosis (Yehuda & LeDoux, 2007) and research has shown that individuals who do not meet diagnostic criteria for PTSD may experience a similar level of functional "
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    ABSTRACT: Studies have found a stronger association between anger and posttraumatic stress disorder (PTSD) severity in military populations than in nonmilitary populations. Two hypotheses have been proposed to explain this difference: Military populations are more prone to anger than nonmilitary populations, and traumas experienced on deployment create more anger than nondeployment traumas. To examine these hypotheses, we evaluated the association between anger and PTSD severity among never-deployed military service members with nondeployment traumas (n = 226) and deployed service members with deployment traumas (n = 594) using linear regression. We further examined these associations stratified by gender. Bivariate associations between anger and PTSD severity were similar for nondeployment and deployment events; however, gender modified this association. For men, the association for deployment events was stronger than for nondeployment events (β = .18, r = .53 vs. β = .16, r = .37, respectively), whereas the reverse was true for women (deployment: β = .20, r = .42 vs. nondeployment: β = .25, r = .65). Among men, findings supported the hypothesis that deployment traumas produce stronger associations between PTSD and anger and are inconsistent with hypothesized population differences. In women, however, there was not a clear fit with either hypothesis.
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