TY - JOUR
T1 - The role of suboptimal mitochondrial function in vulnerability to post-traumatic stress disorder
AU - Preston, Graeme
AU - Kirdar, Faisal
AU - Kozicz, Tamas
N1 - Publisher Copyright:
© 2018, SSIEM.
PY - 2018/7/1
Y1 - 2018/7/1
N2 - Abstract: Post-traumatic stress disorder remains the most significant psychiatric condition associated with exposure to a traumatic event, though rates of traumatic event exposure far outstrip incidence of PTSD. Mitochondrial dysfunction and suboptimal mitochondrial function have been increasingly implicated in several psychopathologies, and recent genetic studies have similarly suggested a pathogenic role of mitochondria in PTSD. Mitochondria play a central role in several physiologic processes underlying PTSD symptomatology, including abnormal fear learning, brain network activation, synaptic plasticity, steroidogenesis, and inflammation. Here we outline several potential mechanisms by which inherited (genetic) or acquired (environmental) mitochondrial dysfunction or suboptimal mitochondrial function, may contribute to PTSD symptomatology and increase susceptibility to PTSD. The proposed pathogenic role of mitochondria in the pathophysiology of PTSD has important implications for prevention and therapy, as antidepressants commonly prescribed for patients with PTSD have been shown to inhibit mitochondrial function, while alternative therapies shown to improve mitochondrial function may prove more efficacious.
AB - Abstract: Post-traumatic stress disorder remains the most significant psychiatric condition associated with exposure to a traumatic event, though rates of traumatic event exposure far outstrip incidence of PTSD. Mitochondrial dysfunction and suboptimal mitochondrial function have been increasingly implicated in several psychopathologies, and recent genetic studies have similarly suggested a pathogenic role of mitochondria in PTSD. Mitochondria play a central role in several physiologic processes underlying PTSD symptomatology, including abnormal fear learning, brain network activation, synaptic plasticity, steroidogenesis, and inflammation. Here we outline several potential mechanisms by which inherited (genetic) or acquired (environmental) mitochondrial dysfunction or suboptimal mitochondrial function, may contribute to PTSD symptomatology and increase susceptibility to PTSD. The proposed pathogenic role of mitochondria in the pathophysiology of PTSD has important implications for prevention and therapy, as antidepressants commonly prescribed for patients with PTSD have been shown to inhibit mitochondrial function, while alternative therapies shown to improve mitochondrial function may prove more efficacious.
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U2 - 10.1007/s10545-018-0168-1
DO - 10.1007/s10545-018-0168-1
M3 - Review article
C2 - 29594645
AN - SCOPUS:85044468079
SN - 0141-8955
VL - 41
SP - 585
EP - 596
JO - Journal of inherited metabolic disease
JF - Journal of inherited metabolic disease
IS - 4
ER -