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Original Contributions
Jan 2012

11C-PiB Imaging of Human Immunodeficiency Virus–Associated Neurocognitive Disorder

Author Affiliations

Author Affiliations: Department of Neurology (Drs Ances, Teshome, Fagan, Holtzman, Morris, and Clifford, Ms Thomas, and Mr Venkat), Knight Alzheimer's Disease Research Center (Drs Ances, Benzinger, Fagan, Holtzman, Morris, and Clifford, Mr Christensen, and Ms Aldea), Hope Center for Neurological Disorders (Drs Ances, Fagan, Holtzman, and Morris), and Department of Radiology (Dr Benzinger and Ms Aldea), Washington University School of Medicine, St Louis, Missouri.

Arch Neurol. 2012;69(1):72-77. doi:10.1001/archneurol.2011.761
Abstract

Objective To evaluate whether the amyloid-binding agent carbon 11–labeled Pittsburgh Compound B (11C-PiB) could differentiate Alzheimer disease (AD) from human immunodeficiency virus (HIV)–associated neurocognitive disorder (HAND) in middle-aged HIV-positive participants.

Design 11C-PiB scanning, clinical assessment, and cerebrospinal fluid (CSF) analysis were performed. Both χ2 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-β protein 1-42 (Aβ42) using 11C-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 11C-PiB binding potentials.

Results Participants with symptomatic AD were older (P < .001), had lower CSF Aβ42 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 11C-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 11C-PiB levels, whereas symptomatic AD individuals have increased fibrillar Aβ42 deposition in cortical and subcortical regions. Observed dissimilarities between HAND and AD may reflect differences in Aβ42 metabolism. 11C-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 11C-PiB in older individuals with HAND.

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