Compelling evidence from animal and human research suggest a strong link between inflammation and posttraumatic stress disorder (PTSD). Furthermore, recent findings support compromised neurocognitive function as a key feature of PTSD, particularly with deficits in attention and processing speed, executive function, and memory. These cognitive domains are supported by brain structures and neural pathways that are disrupted in PTSD and which are implicated in fear learning and extinction processes. The disruption of these supporting structures potentially results from their interaction with inflammation. Thus, the converging evidence supports a model of inflammatory dysregulation and cognitive dysfunction as combined mechanisms underpinning PTSD symptomatology. In this review, we summarize evidence of dysregulated inflammation in PTSD and further explore how the neurobiological underpinnings of PTSD, in the context of fear learning and extinction acquisition and recall, may interact with inflammation. We then present evidence for cognitive dysfunction in PTSD, highlighting findings from human work. Potential therapeutic approaches utilizing novel pharmacological and behavioral interventions that target inflammation and cognition also are discussed.

来自动物和人类研究的令人信服的证据表明炎症与创伤后应激障碍 (PTSD) 之间存在密切联系。此外，最近的研究结果支持受损的神经认知功能是 PTSD 的一个关键特征，尤其是注意力和处理速度、执行功能和记忆力的缺陷。这些认知领域得到了 PTSD 中被破坏的大脑结构和神经通路的支持，这些结构和神经通路与恐惧学习和灭绝过程有关。这些支撑结构的破坏可能是由于它们与炎症的相互作用造成的。因此，汇聚证据支持炎症失调和认知功能障碍模型作为支持 PTSD 症状的联合机制。在这次审查中，我们总结了 PTSD 中炎症失调的证据，并进一步探讨了 PTSD 的神经生物学基础，在恐惧学习和灭绝获得和回忆的背景下，如何与炎症相互作用。然后，我们提供了 PTSD 中认知功能障碍的证据，突出了人类工作的发现。还讨论了利用针对炎症和认知的新型药理学和行为干预的潜在治疗方法。