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The centrality of fear extinction in linking risk factors to PTSD: A narrative review

•Impaired fear extinction is considered a key mechanism of PTSD.•Impaired fear extinction and PTSD symptoms share neural brain networks.•PTSD risk factors include genetics, hormones, cognition, and sleep disturbances.•Fear extinction is involved in all risk factors associated with PTSD.•Fear extinct...

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Bibliographic Details
Published in:Neuroscience and biobehavioral reviews 2016-10, Vol.69, p.15-35
Main Authors: Zuj, Daniel V., Palmer, Matthew A., Lommen, Miriam J.J., Felmingham, Kim L.
Format: Article
Language:English
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Summary:•Impaired fear extinction is considered a key mechanism of PTSD.•Impaired fear extinction and PTSD symptoms share neural brain networks.•PTSD risk factors include genetics, hormones, cognition, and sleep disturbances.•Fear extinction is involved in all risk factors associated with PTSD.•Fear extinction may be the central mechanism linking risk factors to PTSD. Recent prospective studies in emergency services have identified impaired fear extinction learning and memory to be a significant predictor of Posttraumatic Stress Disorder (PTSD), complementing a wealth of cross-sectional evidence of extinction deficits associated with the disorder. Additional fields of research show specific risk factors and biomarkers of the disorder, including candidate genotypes, stress and sex hormones, cognitive factors, and sleep disturbances. Studies in mostly nonclinical populations also reveal that the aforementioned factors are involved in fear extinction learning and memory. Here, we provide a comprehensive narrative review of the literature linking PTSD to these risk factors, and linking these risk factors to impaired fear extinction. On balance, the evidence suggests that fear extinction may play a role in the relationship between risk factors and PTSD. Should this notion hold true, this review carries important implications for the improvement of exposure-based treatments, as well as strategies for the implementation of treatment.
ISSN:0149-7634
1873-7528
DOI:10.1016/j.neubiorev.2016.07.014