INTRODUCTIONPost‐traumatic stress disorder (PTSD) is an anxiety disorder developed after exposures to severe traumatic events that threaten physical injury or death (Zoladz & Diamond, ). Although pathophysiological mechanism of this disorder has not been elucidate yet, gene‐environment interactions are considered to result in the development of PTSD (Liberzon et al., ; Tian et al., ). Genetic factors contribute approximately 32–35% of the variance of PTSD symptoms (Afifi, Asmundson, Taylor, & Jang, ; Xian et al., ). A number of single nucleotide polymorphisms (SNPs) have been found to be linked to the susceptibility of PTSD (Ryan, Chaudieu, Ancelin, & Saffery, ; Stein et al., ), and some of which may interact with environment to increase the risk of PTSD (Smoller, ; Tian et al., ).Indirect evidences suggest associations of estrogen receptor alpha (ESR1) with PTSD. ESR1 is expressed in hippocampus, amygdala, and medial prefrontal cortex (Osterlund & Hurd, ), indicating its roles in affective, emotional, and motivational behaviors (McEwen, ; Osterlund & Hurd, ; Ostlund, Keller, & Hurd, ; Westberg & Eriksson, ). In addition, PTSD patients had lower hippocampal volume than healthy controls in men and women (Bremner et al., ; Zandieh et al., ), diminished right basolateral amygdala
American Journal of Medical Genetics – Wiley
Published: Jan 1, 2018
Keywords: ; ; ; ;
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