Abstract
This study used converging methods to examine the neural substrates of cognitive ability in middle-aged and older men with well-controlled HIV infection. Seventy-six HIV+ men on antiretroviral treatment completed an auditory oddball task and an inhibitory control (Simon) task while time-locked high-density EEG was acquired; 66 had usable EEG data from one or both tasks; structural MRI was available for 43. We investigated relationships between task-evoked EEG responses, cognitive ability and immunocompromise. We also explored the structural correlates of these EEG markers in the sub-sample with complete EEG and MRI data (N = 27). EEG activity was associated with cognitive ability at later (P300) but not earlier stages of both tasks. Only the oddball task P300 was reliably associated with HIV severity (nadir CD4). Source localization confirmed that the tasks engaged partially distinct circuits. Thalamus volume correlated with oddball task P300 amplitude, while globus pallidus volume was related to the P300 in both tasks. This is the first study to use task-evoked EEG to identify neural correlates of individual differences in cognition in men living with well-controlled HIV infection, and to explore the structural basis of the EEG markers. We found that EEG responses evoked by the oddball task are more reliably related to cognitive performance than those evoked by the Simon task. We also provide preliminary evidence for a subcortical contribution to the effects of HIV infection severity on P300 amplitudes. These results suggest brain mechanisms and candidate biomarkers for individual differences in cognition in HIV.
Highlights
Despite effective viral suppression, cognitive impairment is a frequent concern in persons living with HIV, as they grow older
Thalamus volume correlated with oddball task P300 amplitude, while globus pallidus volume was related to the P300 in both tasks
We provide preliminary evidence for a subcortical contribution to the effects of HIV infection severity on P300 amplitudes
Summary
Cognitive impairment is a frequent concern in persons living with HIV, as they grow older. Prevalence estimates are as high as 30 to 50%. [1, 2], these may be over-estimates due to selection bias [3]. Attention, and processing speed are commonly affected in those with cognitive impairment [4, 5]. While typically mild in people taking combined antiretroviral therapy (cART), impairment can limit occupational function, quality of life, and medication adherence [6,7,8,9], as well as the costs of medical care [10]. The causes and underlying neural mechanisms of cognitive impairment remain unclear. Candidate mechanisms include direct effects of HIV infection on the brain, especially prior to cART, cerebrovascular injury due to metabolic complications of chronic HIV, amongst others. There is no consensus on optimal neuroimaging markers or intervention targets
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