Diagnostic Biomarkers for Posttraumatic Stress Disorder: Promising Horizons from Translational Neuroscience Research

Abstract

Posttraumatic stress disorder (PTSD) is a heterogeneous disorder that affects individuals exposed to trauma (e.g., combat, interpersonal violence, and natural disasters). Although its diagnostic features have been recently reclassified with the emergence of the Diagnostic and Statistical Manual for Mental Disorders, Fifth Edition, the disorder remains characterized by hyperarousal, intrusive reminders of the trauma, avoidance of trauma-related cues, and negative cognition and mood. This heterogeneity indicates the presence of multiple neurobiological mechanisms underlying the etiology and maintenance of PTSD. Translational research spanning the past few decades has revealed several potential avenues for the identification of diagnostic biomarkers for PTSD. These include, but are not limited to, monoaminergic transmitter systems, the hypothalamic-pituitary-adrenal axis, metabolic hormonal pathways, inflammatory mechanisms, psychophysiological reactivity, and neural circuits. The current review provides an update to the literature with regard to the most promising putative PTSD biomarkers, with specific emphasis on the interaction between neurobiological influences on disease risk and symptom progression. Such biomarkers will most likely be identified by multi-dimensional models derived from comprehensive descriptions of molecular, neurobiological, behavioral, and clinical phenotypes.

Keywords: Biomarkers; Inflammation; Neuroendocrinology; Neuroimaging; PTSD; Psychophysiology.

Copyright © 2015 Society of Biological Psychiatry. All rights reserved.

Figures

Figure 1

A summary of key biomarkers that are associated with PTSD, highlighting the interactions between different biological systems that influence and complicate biological phenotypes within PTSD. Gonadal steroid hormones and the HPA axis modulate neurotransmitter and neuropeptide systems (146), influence amygdala activity (147, 148), and influence inflammatory responses (93). HPA activity, via cortisol and CRH, alters sensitivity to gonadal hormones (149). Inflammation alters HPA activity and has adverse effects on cardiovascular function (150). Taken together, these data indicate that as a field we must begin to study these physiological systems in concert with one another to begin to characterize comprehensive biological phenotypes of PTSD.