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This review aims to systematically assess the current literature about prenatal epigenetic markers that lead to post-traumatic stress disorder susceptibility across the lifespan. Studies included in this review met several research criteria: Studies included (1) participants with a PTSD diagnosis according to the DSM-5, (2) prenatal epigenetic marker data that could be analyzed, and (3) explicit references to postnatal PTSD susceptibility. Our study sample fit within a timeframe of 2002 (the earliest recorded studies of prenatal susceptibility to post-traumatic stress disorder in the databases used) and February 2021 when the literature search for this review was terminated. Studies for this review were collated from PubMed, MEDLINE, Science Direct, and Boston College School of Social Work Library databases. A systematic search was conducted in these databases using basic keyword terms, such as "PSTD resilience" and "PTSD vulnerability," and then adding clarifying terms to refine specific searches, such as "epigenetics," "genetics," "epigenetic markers," "haplotypes," and "mRNA methylation." Based on these criteria and research methods, 33 studies remained for inclusion in the review sample. This review suggests that BDNF Val66-Met, a polymorphism of FKBP5, and an altered messenger ribonucleic acid methylation marker in NR3C1 present most often in cases of PTSD. These epigenetic markers might be implicated in central neurological processes related to post-traumatic stress disorder symptomatology.

This review presents the current state of understanding of trauma-informed modalities in light of current research in neuroscience, analyzing which brain structures and processes are impacted by these modalities. Studies included in the present review met the inclusion criteria of 1) addressing post-traumatic stress disorder (PTSD) in a specific population, 2) treatment of PTSD using any of the evidence-based trauma-informed modalities considered in this review, and 3) presenting functional magnetic resonance imagery (fMRI) data, derived from BOLD signals and voxel-compression maps, of brain structures impacted by these trauma-informed modalities. Articles for this review were collated through PubMed and MEDLINE, using key terms in descending order, such as 'childhood trauma', 'adolescent trauma', and 'adulthood trauma', to 'PTSD', 'fMRI', and so on, depending on the modality in question. Based on these criteria and research methods, 37 studies remained for inclusion in the present review. Among a number of critical findings, this review demonstrates that eye movement desensitization and reprocessing (EMDR) and mindfulness therapy effectively deactivate hindbrain regions implicated in the downregulation of autonomic nervous system (ANS) hyperarousal. This review also shows that trauma-focused cognitive behavioral therapy (TF-CBT) and EMDR activate the hippocampus, anterior cingulate cortex (ACC), medial prefrontal cortex (mPFC), and orbitofrontal cortex (OFC)-areas that are implicated in crucial cognitive, affective, and behavioral processes that aid trauma survivors in navigating their challenges.