AbstractHIV-associated neurocognitive disorders (HAND) are increasingly prevalent despite the use of antiretroviral therapies. Previous research suggests that individual host factors play an important role in determining susceptibility to HAND. In… Click to show full abstract
AbstractHIV-associated neurocognitive disorders (HAND) are increasingly prevalent despite the use of antiretroviral therapies. Previous research suggests that individual host factors play an important role in determining susceptibility to HAND. In this review, we propose that childhood trauma (CT) and HAND share several common aetiological mechanisms, namely hypothalamic-pituitary-adrenal axis dysregulation, neuroinflammation and oxidative stress. These convergent and consequent mechanisms may translate into an increased risk of developing HAND in individuals who have experienced early life stress. We provide an overview of basic and clinical research relating to these pathophysiological mechanisms and suggest that further research examine brain-derived neurotrophic factor and telomere length as common mediating factors and potential therapeutic targets for HAND and CT. Graphical abstractBoth childhood trauma and HIV-associated neurocognitive disorders are associated with HPA axis dysregulation, inflammation and oxidative stress
               
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