摘要：Posttraumatic stress disorder (PTSD) and other deployment-related outcomes originate from a complex interplay between constellations of changes in DNA, environmental traumatic exposures, and other biological risk factors. These factors affect not only individual genes or bio-molecules but also the entire biological networks that in turn increase or decrease the risk of illness or affect illness severity. This review focuses on recent developments in the field of systems biology which use multidimensional data to discover biological networks affected by combat exposure and post-deployment disease states. By integrating large-scale, high-dimensional molecular, physiological, clinical, and behavioral data, the molecular networks that directly respond to perturbations that can lead to PTSD can be identified and causally associated with PTSD, providing a path to identify key drivers. Reprogrammed neural progenitor cells from fibroblasts from PTSD patients could be established as an in vitro assay for high throughput screening of approved drugs to determine which drugs reverse the abnormal expression of the pathogenic biomarkers or neuronal properties.Keywords: PTSD; genomics; gene expression; proteomics; Computational Biology; risk factorsResponsible Editors: Alexander McFarlane, The University of Adelaide, Australia; Eric Vermetten, Central Military Hospital, University Medical Center Utrecht, Netherlands.This paper is part of the Special Issue: PTSD in the military: prevalence, pathophysiology, treatment. More papers from this issue can be found at http://www.eurojnlofpsychotraumatol.net(Published: 14 August 2014)Citation: European Journal of Psychotraumatology 2014, 5: 23938 - http://dx.doi.org/10.3402/ejpt.v5.23938
