Oxidative Stress, Inflammation, and Neuroprogression in Chronic PTSD.
Oxidative Stress, Inflammation, and Neuroprogression in Chronic PTSD.
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DOI：
10.1097/hrp.0000000000000167
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发表时间：
2018
影响因子：
3.8
通讯作者：
Miller DR
中科院分区：
文献类型：
--
作者：
Miller MW;Lin AP;Wolf EJ;Miller DR
创伤后应激障碍是一种严重的，往往致残的综合征，发展在应对创伤事件。许多最初患上这种疾病的人会经历一种慢性形式的疾病，在某些情况下可能持续多年。在这些患者中，精神和医学共病很常见，包括早发性年龄相关疾病，如慢性疼痛、心脏代谢疾病、神经认知障碍和痴呆。创伤后应激的标志性症状-创伤的反复感觉记忆再体验-与伴随的威胁和应激相关神经生物学通路的激活相关，这些通路在睡眠障碍和增强的生理唤醒的紧张背景下发生。新出现的证据表明，这种压力持续综合征的分子后果包括氧化应激和炎症的全身水平升高。在本文中，我们回顾了氧化应激和炎症参与慢性PTSD的证据，以及这些过程的神经生物学后果，包括加速细胞衰老和神经进展。我们的目的是更新和扩展以前的评论，这一快速发展的文献和讨论磁共振波谱成像技术非常适合测量体内氧化应激和炎症标志物。最后，我们强调了未来的研究方向和途径，为开发新的治疗方法，靶向OXS和炎症的PTSD患者。
Posttraumatic stress disorder is a serious and often disabling syndrome that develops in response to a traumatic event. Many individuals who initially develop the disorder go on to experience a chronic form of the condition that in some cases can last for many years. Among these patients, psychiatric and medical comorbidities are common including early onset of age-related conditions such as chronic pain, cardiometabolic disease, neurocognitive disorders, and dementia. The hallmark symptoms of posttraumatic stress—recurrent sensory-memory reexperiencing of the trauma(s)—are associated with concomitant activations of threat- and stress-related neurobiological pathways that occur against a tonic backdrop of sleep disturbance and heightened physiological arousal. Emerging evidence suggests that the molecular consequences of this stress-perpetuating syndrome include elevated systemic levels of oxidative stress and inflammation. In this paper, we review evidence for the involvement of oxidative stress and inflammation in chronic PTSD and the neurobiological consequences of these processes including accelerated cellular aging and neuroprogression. Our aim was to update and expand upon previous reviews of this rapidly-developing literature and discuss magnetic resonance spectroscopy as an imaging technology uniquely-suited to measuring oxidative stress and inflammatory markers in vivo. Finally, we highlight future directions for research and avenues for the development of novel therapeutics targeting OXS and inflammation in patients with PTSD.