11C-PiB imaging of human immunodeficiency virus-associated neurocognitive disorder.

OBJECTIVE: To evaluate whether the amyloid-binding agent carbon 11-labeled Pittsburgh Compound B ((11)C-PiB) could differentiate Alzheimer disease (AD) from human immunodeficiency virus (HIV)-associated neurocognitive disorder (HAND) in middle-aged HIV-positive participants. DESIGN: (11)C-PiB scanning, clinical assessment, and cerebrospinal fluid (CSF) analysis were performed. Both χ(2) and t tests assessed differences in clinical and demographic variables between HIV-positive participants and community-living individuals observed at the Knight Alzheimer's Disease Research Center (ADRC). Analysis of variance assessed for regional differences in amyloid-ß protein 1-42 (Aß42) using (11)C-PiB. SETTING: An ADRC and HIV clinic. PARTICIPANTS: Sixteen HIV-positive participants (11 cognitively normal and 5 with HAND) and 19 ADRC participants (8 cognitively normal and 11 with symptomatic AD). MAIN OUTCOME MEASURES: Mean and regional (11)C-PiB binding potentials. RESULTS: Participants with symptomatic AD were older (P < .001), had lower CSF Aß42 levels (P < .001), and had higher CSF tau levels (P < .001) than other groups. Regardless of degree of impairment, HIV-positive participants did not have increased (11)C-PiB levels. Mean and regional binding potentials were elevated for symptomatic AD participants (P < .001). CONCLUSIONS: Middle-aged HIV-positive participants, even with HAND, do not exhibit increased (11)C-PiB levels, whereas symptomatic AD individuals have increased fibrillar Aß42 deposition in cortical and subcortical regions. Observed dissimilarities between HAND and AD may reflect differences in Aß42 metabolism. (11)C-PiB may provide a diagnostic biomarker for distinguishing symptomatic AD from HAND in middle-aged HIV-positive participants. Future cross-sectional and longitudinal studies are required to assess the utility of (11)C-PiB in older individuals with HAND.

Neurological evaluation of untreated human immunodeficiency virus infected adults in Ethiopia.

Human immunodeficiency virus (HIV) has been implicated in neurological complications in developed countries. Developing countries have different viral clades and potentially different genetic and social risks for these complications. Baseline neurological performance measures associated with HIV infection have rarely been available from developing countries. The authors carried our a cross-sectional neurological evaluation of a cohort of community-dwelling treatment-naïve HIV-infected patients and similar control subjects from the same communities in Ethiopia. Blinded evaluation using standardized structured questionnaires and a neurological examination was performed by neurologists and treating physicians trained by an HIV neurology specialist. Quantitative performance measures for cognitive and motor function were employed. Data were analyzed with descriptive statistical methods, standard contingency table methods, and nonparametric methods. HIV-positive and control groups were similar by age, gender, and job site. Participants included 73 HIV-positive and 87 HIV-negative controls. Fingertapping speed in the dominant hand was more poorly performed in HIV positives than negatives (P = .01) and was significantly associated with HIV viral load levels (P = .03). Other quantitative neuropsychiatric tests including timed gait, grooved pegboard, task learning, and animal naming did not show significant differences between the two groups. The overall prevalence of central nervous system (CNS) and/or peripheral nervous system (PNS) disease did not significantly differ in the two populations. HIV patients had slowed fingertapping speed correlating with viral load. Other measures of CNS and/or peripheral nervous performance did not differ from controls. The unanticipated minor evidence of HIV-associated neurocognitive and peripheral nerve deficits in this untreated HIV-positive population invite further investigation.