Author:
Clark Uraina S.,Cohen Ronald A.,Sweet Lawrence H.,Gongvatana Assawin,Devlin Kathryn N.,Hana George N.,Westbrook Michelle L.,Mulligan Richard C.,Jerskey Beth A.,White Tara L.,Navia Bradford,Tashima Karen T.
Abstract
AbstractBoth HIV infection and high levels of early life stress (ELS) have been related to abnormalities in frontal-subcortical structures, yet the combined effects of HIV and ELS on brain structure and function have not been previously investigated. In this study we assessed 49 non-demented HIV-seropositive (HIV+) and 47 age-matched HIV-seronegative healthy control (HC) adults. Levels of ELS exposure were quantified and used to define four HIV-ELS groups: HC Low-ELS (N= 20); HC High-ELS (N= 27); HIV+ Low-ELS (N= 24); HIV+ High-ELS (N= 25). An automated segmentation tool measured volumes of brain structures known to show HIV-related or ELS-related effects; a brief neurocognitive battery was administered. A significant HIV-ELS interaction was observed for amygdala volumes, which was driven by enlargements in HIV+ High-ELS participants. The HIV+ High-ELS group also demonstrated significant reductions in psychomotor/processing speed compared with HC Low-ELS. Regression analyses in the HIV+ group revealed that amygdala enlargements were associated with higher ELS, lower nadir CD4 counts, and reduced psychomotor/processing speed. Our results suggest that HIV infection and high ELS interact to increase amygdala volume, which is associated with neurocognitive dysfunction in HIV+ patients. These findings highlight the lasting neuropathological influence of ELS and suggest that high ELS may be a significant risk factor for neurocognitive impairment in HIV-infected individuals. (JINS, 2012,19, 1–12)
Publisher
Cambridge University Press (CUP)
Subject
Psychiatry and Mental health,Neurology (clinical),Clinical Psychology,General Neuroscience
Cited by
35 articles.
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