Citation

Womersley JS, Seedat S, Hemmings SMJ. Metab. Brain Dis. 2017; 32(5): 1717-1733.

Affiliation

Department of Psychiatry, Faculty of Medicine and Health Sciences, Stellenbosch University, Francie van Zijl Drive, Tygerberg, 7505, South Africa. smjh@sun.ac.za.

Copyright

(Copyright © 2017, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s11011-017-0062-9

PMID

28681198

Abstract

HIV-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 abstract Both childhood trauma and HIV-associated neurocognitive disorders are associated with HPA axis dysregulation, inflammation and oxidative stress.

Language: en

Keywords

Childhood trauma; HIV-associated neurocognitive disorders; hypothalamic-pituitary-adrenal axis; inflammation; oxidative stress