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Original Contributions |

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

Beau M. Ances, MD, PhD; Tammie L. Benzinger, MD, PhD; Jon J. Christensen, BS; Jewell Thomas, BA; Rohit Venkat, BA; Mengesha Teshome, MD; Patricia Aldea, BS; Anne M. Fagan, PhD; David M. Holtzman, MD; John C. Morris, MD; David B. Clifford, MD
Arch Neurol. 2012;69(1):72-77. doi:10.1001/archneurol.2011.761.
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Published online

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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Figure 1. Magnetic resonance imaging (MRI) and carbon 11–labeled Pittsburgh Compound B (11C-PiB) imaging in 4 representative study participants. Representative structural MRIs and 11C-PiB images for a cognitively normal human immunodeficiency virus (HIV)–positive participant (A), an HIV-positive participant with HIV-associated neurocognitive disorder (HAND) (B), a cognitively normal Alzheimer’s Disease Research Center (ADRC) participant (C), and ADRC participant with symptomatic Alzheimer disease (AD) (D). Only the symptomatic AD participants had increased fibrillar amyloid deposition using 11C-PiB.

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Figure 2. Mean cortical binding potential (MCBP) and regional binding potential for the 4 clinical groups. A, MCBP. A 2 × 2 matrix is created using cerebrospinal fluid (CSF) amyloid-β protein 1-42 (Aβ42) (<500 pg/mL) and MCBP (>0.18 arbitrary units). All human immunodeficiency virus (HIV)–positive participants, regardless of their degree of cognitive impairment, had normal carbon 11–labeled Pittsburgh Compound B imaging results (<0.18 arbitrary units). B, Regional cortical binding potential. For each region, symptomatic Alzheimer’s Disease Research Center (ADRC) participants had higher binding potentials. AD indicates Alzheimer disease; HAND, human immunodeficiency virus–associated neurocognitive disorder; and asterisk, P < .001.

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