Neurofunctional characteristics of executive control in older people with HIV infection: a comparison with Parkinson’s disease

Springer Science and Business Media LLC - Tập 16 - Trang 1776-1793 - 2022
Eva M. Müller-Oehring1,2,3, Jui-Yang Hong1, Kathleen L. Poston3,4, Helen M. Brontë-Stewart3,4, Edith V. Sullivan2, Lawrence McGlynn2, Tilman Schulte1,5
1Neuroscience Program, Center for Health Sciences, Biosciences Division, SRI International, Menlo Park, USA
2Department of Psychiatry & Behavioral Sciences, Stanford University School of Medicine, Stanford, USA
3Department of Neurology & Neurological Sciences, Stanford University School of Medicine, Stanford, USA
4Department of Neurosurgery, Stanford University School of Medicine, Stanford, USA
5Department of Psychology, Palo Alto University, Palo Alto, USA

Tóm tắt

Expression of executive dysfunctions is marked by substantial heterogeneity in people living with HIV infection (PLWH) and attributed to neuropathological degradation of frontostriatal circuitry with age and disease. We compared the neurophysiology of executive function in older PLWH and Parkinson’s disease (PD), both affecting frontostriatal systems. Thirty-one older PLWH, 35 individuals with PD, and 28 older healthy controls underwent executive task-activated fMRI, neuropsychological testing, and a clinical motor exam. fMRI task conditions distinguished cognitive control operations, invoking a lateral frontoparietal network, and motor control operations, activating a cerebellar-precentral-medial prefrontal network. HIV-specific findings denoted a prominent sensorimotor hypoactivation during cognitive control and striatal hypoactivation during motor control related to CD4+ T cell count and HIV disease duration. Activation deficits overlapped for PLWH and PD, relative to controls, in dorsolateral frontal, medial frontal, and middle cingulate cortices for cognitive control, and in limbic, frontal, parietal, and cerebellar regions for motor control. Thus, despite well-controlled HIV infection, frontostriatal and sensorimotor activation deficits occurred during executive control in older PLWH. Overlapping activation deficits in posterior cingulate and hippocampal regions point toward similarities in mesocorticolimbic system aberrations among older PLWH and PD. The extent of pathophysiology in PLWH was associated with variations in immune system health, neural signature consistent with subclinical parkinsonism, and mild neurocognitive impairment. The failure to adequately engage these pathways could be an early sign for cognitive and motor functional decline in the aging population of PLWH.

Tài liệu tham khảo

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