Distinguishing Amnestic Mild Cognitive Impairment From HIV-Associated Neurocognitive Disorders
Erin E. Sundermann, Mark W. Bondi, Laura M. Campbell, Ben Gouaux, Raeanne C. Moore, Virawudh Soontornniyomkij, David J. Moore
Abstract
BACKGROUND: Memory impairment occurs in human immunodeficiency virus (HIV)-associated neurocognitive disorders (HAND) and amnestic mild cognitive impairment (aMCI), the precursor to Alzheimer disease (AD). Methods are needed to distinguish aMCI-associated from HAND-associated impairment in people with HIV (PWH). We developed a neuropsychological method of identifying aMCI in PWH and tested this by relating AD neuropathology (β-amyloid, phospho-Tau) to aMCI versus HAND classification. METHODS: Seventy-four HIV-positive cases (aged 50-68 years) from the National NeuroAIDS Tissue Consortium had neurocognitive data within 1 year of death and data on β-amyloid and phospho-Tau pathology in frontal brain tissue. High aMCI risk was defined as impairment (<1.0 SD below normative mean) on 2 of 4 delayed recall or recognition outcomes from a verbal and nonverbal memory test (at least 1 recognition impairment required). Differences in β-amyloid and phospho-Tau by aMCI and HAND classification were examined. RESULTS: High aMCI risk was more common in HAND (69.0%) versus no HAND (37.5%) group. β-amyloid pathology was 4.75 times more likely in high versus low aMCI risk group. Phospho-Tau pathology did not differ between aMCI groups. Neither neuropathological feature differed by HAND status. CONCLUSIONS: Amnestic mild cognitive impairment criteria that include recognition impairment may help to detect AD-like cognitive/biomarker profiles among PWH.