| Sumario: | Epidemiological evidence supports a role for gene-environmental interactions in post-traumatic stress disorder (PTSD). Because environmental exposure to trauma is an etiological factor necessary for the development of PTSD, understanding the molecular mechanisms by which genes respond to traumatic stress may provide insight into the development and life-long persistence of PTSD symptoms. Emerging evidence suggests that DNA methylation, histone modifications, noncoding RNA regulation, and alternative splicing of mRNA provide an epigenetic means by which chronic stress and traumatic experiences alter gene expression to produce long-term changes in neuroanatomy, physiology and behavior. This research topic will focus on epigenetic components of PTSD, and highlight translational research including common measures and outcomes of stress and trauma found in animal, civilian and military research. We will also consider observational and epidemiologic studies that support epigenetic transmission of stress-related phenotypes. We aim to provide a forum for experts in the field to present novel research findings, methodology, opinions, hypotheses and critical reviews that address how traumatic stress interacts with the genome.
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