The epigenetic machinery in the brain is both complex and intertwined and it’s difficult to disentangle brain-region and cell-type specific epigenetic codes in a given environmental condition (Graff, Kim, Dobbin, & Tsai, 2011). Chronic stress may cause smaller hippocampal volume, deficits in declarative (conscious) memory and some amnesia (Baker et al., 2005; Bremner et al., 1995; Samuelson, 2011). Stress hormones triggered by way of the HPA-axis are encoded by the basolateral area of the Amygdala (BLA). This makes the person respond emotionally to anything that unconsciously is associated with the event (Bokkon et al., 2014; LaBar & Cabeza, 2006; McGaugh, 2000). Functioning independently of the hippocampus, the BLA thus conserved the emotional…show more content… Specifically, epigenetic changes have been found in different gene locations involved in the regulation of the HPA axis (Voisey, Young, Lawford, & Morris, 2014). The glucocorticoid receptor (GR) gene in the hippocampus was found to be critical for negative feedback in the stress response (Champagne, 2013) and for increased corticotropin-releasing hormone (CRH). Findings have indicated polymorphisms (phenotypical aberrations) within two genes, FKBP5 and CRHR1 (Binder et al., 2008) that regulate HPA axis function when the child is also exposed to child maltreatment (Klengel et al., 2013). Significant associations were also found with a variable number tandem repeat (VNTR) polymorphism (Segman & Shalev, 2003; Yehuda & LeDoux, 2007). Other genes, such as the PRKCA were found to lead to improved memory, and therefore also to increased risk of PTSD (de Quervain et al., 2012). In addition, increased DNA methylation at the NGFI-A binding site of the NR3C1 promoter was associated with reduced PTSD risks in male survivors of the Rwandan genocide (Vukojevic et al.,