Abstract
Post-traumatic stress disorder (PTSD) is a well-known psychiatric disorder that affects millions of people worldwide. Pharmacodynamic and cognitive-behavioral therapies (CBT) have been used to treat patients with PTSD. However, it remains unclear whether there are concurrent changes in psychopathological and neurophysiological factors associated with PTSD patients. Past reports described those PTSD patients with efficient fatty acid metabolism, neurogenesis, mitochondrial energy balance could improve ability to cope against the conditioned fear responses and traumatic memories. Furthermore, cognitive, behavioral, cellular, and molecular evidence can be combined to create personalized therapies for PTSD sufferers either with or without comorbidities such as depression or memory impairment. Unfortunately, there is still evidence lacking to establish a full understanding of the underlying neurophysiological and psychopathological aspects associated with PTSD. This review has extensively discussed the single nucleotide polymorphism (SNPs) of genetic factors to cause PTSD, the implications of inflammation, neurotransmitter genomics, metabolic alterations, neuroendocrine disturbance (hypothalamus-pituitary-adrenal (HPA) axis), mitochondrial dynamics, neurogenesis, and premature aging related to PTSD-induced psychopathology and neurophysiology. In addition, the review delineated the importance of CBT and several pharmacodynamic therapies to mitigate symptomatology of PTSD.
Highlights
Post-traumatic stress disorder (PTSD) comprises a set of alterations in cognition and mood [1]
This study reported that the synthetic glucocorticoid dexamethasone enhanced p11 expression through glucocorticoid response elements (GREs) in the p11 promoter, which has implications in psychopathology during PTSD [66]
Special attention has been paid to RD2, DRD4, SLC6A3 (DAT1 transporter), SLC6A4, HTR2, FKBP5 (FK506 binding protein 5), brain-derived neurotrophic factor (BDNF), neuropeptide Y (NPY), GCCR, DBH, CNR1, GABRA2 (GABAA receptor), COMT (Catechol-O-methyltransferase), Apo-E (Apolipoprotein E), and RGS2 (Regulator of G-protein signaling 2)
Summary
Post-traumatic stress disorder (PTSD) comprises a set of alterations in cognition and mood [1]. Brain tissue recovery is enhanced for PTSD patients who interact socially to gain new learning skills, engage in regular exercise, avoid potential threats and negative thoughts, and enthusiastically develop skills to execute challenging tasks [1,3]. Such healthy lifestyles are complemented by nutrition and weight management, good sleep patterns, and regular medical supervision. Brain imaging studies have reported that individuals with PTSD have a hyperactive prefrontal cortex (PFC) and an underactive amygdala when compared to controls [24] These findings suggest that inhibitory neuronal signaling loops mediating fear management are disrupted in PTSD patients experiencing traumatic memories [25].
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