title: Traumatic stress, oxidative stress and post-traumatic stress disorder: neurodegeneration and the accelerated-aging hypothesis.
abstract: Post-traumatic stress disorder (PTSD) is associated with elevated risk for a variety of age-related diseases and neurodegeneration. In this paper, we review evidence relevant to the hypothesis that chronic PTSD constitutes a form of persistent life stress that potentiates oxidative stress (OXS) and accelerates cellular aging. We provide an overview of empirical studies that have examined the effects of psychological stress on OXS, discuss the stress-perpetuating characteristics of PTSD, and then identify mechanisms by which PTSD might promote OXS and accelerated aging. We review studies on OXS-related genes and the role that they may have in moderating the effects of PTSD on neural integrity and conclude with a discussion of directions for future research on antioxidant treatments and biomarkers of accelerated aging in PTSD.
authors.affiliation: Department of Psychiatry, National Center for PTSD, VA Boston Healthcare System and Boston University School of Medicine, Boston, MA, USA.
authors.forename: M W
authors.initials: MW
authors.lastname: Miller
authors.affiliation: Department of Psychiatry, National Center for PTSD, VA Boston Healthcare System and Boston University School of Medicine, Boston, MA, USA.
authors.forename: N
authors.initials: N
authors.lastname: Sadeh
mesh_terms: D000375:Aging / Q000235:genetics / Q000502:physiology*; D000818:Animals; D002908:Chronic Disease; D006801:Humans; D009410:Nerve Degeneration / Q000235:genetics / Q000503:physiopathology*; D018384:Oxidative Stress / Q000235:genetics / Q000502:physiology*; D013313:Stress Disorders, Post-Traumatic / Q000235:genetics / Q000503:physiopathology*; D013315:Stress, Psychological / Q000235:genetics / Q000503:physiopathology*