Benedetta Milanini1, Victor Valcour2. 1. Memory and Aging Center, Department of Neurology, University of California, San Francisco, CA, USA. Benedetta.Milanini@ucsf.edu. 2. Memory and Aging Center, Department of Neurology, University of California, San Francisco, CA, USA.
Abstract
PURPOSE OF REVIEW: The purpose of this review was to examine characteristics that may distinguish HIV-associated neurocognitive disorder (HAND) from early Alzheimer's disease (AD). RECENT FINDINGS: Cerebrospinal fluid (CSF) AD biomarkers are perturbed in HIV, yet these alterations may be limited to settings of advanced dementia or unsuppressed plasma HIV RNA. Neuropsychological testing will require extensive batteries to maximize utility. Structural imaging is limited for early AD detection in the setting of HIV, but proper studies are absent. While positron-emission tomography (PET) amyloid imaging has altered the landscape of differential diagnosis for age-associated neurodegenerative disorders, costs are prohibitive. Risk for delayed AD diagnosis in the aging HIV-infected population is now among the most pressing issues in geriatric neuroHIV. While clinical, imaging, and biomarker characterizations of AD are extensively defined, fewer data define characteristics of HIV-associated neurocognitive disorder in the setting of suppressed plasma HIV RNA. Data needed to inform the phenotype of AD in the setting of HIV are equally few.
PURPOSE OF REVIEW: The purpose of this review was to examine characteristics that may distinguish HIV-associated neurocognitive disorder (HAND) from early Alzheimer's disease (AD). RECENT FINDINGS:Cerebrospinal fluid (CSF)AD biomarkers are perturbed in HIV, yet these alterations may be limited to settings of advanced dementia or unsuppressed plasma HIV RNA. Neuropsychological testing will require extensive batteries to maximize utility. Structural imaging is limited for early AD detection in the setting of HIV, but proper studies are absent. While positron-emission tomography (PET) amyloid imaging has altered the landscape of differential diagnosis for age-associated neurodegenerative disorders, costs are prohibitive. Risk for delayed AD diagnosis in the aging HIV-infected population is now among the most pressing issues in geriatric neuroHIV. While clinical, imaging, and biomarker characterizations of AD are extensively defined, fewer data define characteristics of HIV-associated neurocognitive disorder in the setting of suppressed plasma HIV RNA. Data needed to inform the phenotype of AD in the setting of HIV are equally few.
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