“…At present, the neurobiological mechanism of PTSD has not been confirmed, and the research directions mainly include four aspects: (1) Genes involved with monoamine and the hypothalamic-pituitary-adrenal (HPA) axis function have been examined extensively in epigenetic and genetic studies of PTSD risk and separately in studies of disease risk and response to treatments for mood disorders ( Kato and Serretti, 2010 ; Domschke et al, 2014 ; Zannas et al, 2015 ; Smoller, 2016 ). Two of the most commonly characterized genes in this regard are the serotonin transporter (SLC6A4) and FK506 binding protein 5 (FKBP5) ( Bishop et al, 2021 ); (2) neuroendocrine dysfunction, such as the increased secretion of catecholamines ( Olson et al, 2011 ) and decreased secretion of 5-hydroxytryptamine (5-HT) hormones ( Liu et al, 2018 ) and corticosterone ( Geracioti et al, 2008 ); (3) changes in the neural structure and circuitry. Basic and clinical studies have demonstrated that structural and functional abnormalities in the hippocampus, prefrontal cortex (PFC), amygdala, and other brain areas were observed in both animal models and individuals with PTSD ( Rauch et al, 2006 ; Hayes et al, 2012 ; Disner et al, 2018 ).…”