Citation

Quinones MM, Gallegos AM, Lin FV, Heffner K. Cogn. Affect. Behav. Neurosci. 2020; ePub(ePub): ePub.

Affiliation

Division of Geriatrics & Aging, Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA.

Copyright

(Copyright © 2020, Holtzbrinck Springer Nature Publishing Group)

DOI

10.3758/s13415-020-00782-9

PMID

32170605

Abstract

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.

Language: en

Keywords

Cognition; Inflammation; Intervention; Neurobiology; Posttraumatic stress disorder