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. 2012 Jan;69(1):72-7.
doi: 10.1001/archneurol.2011.761.

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

Beau M Ances  1 , Tammie L Benzinger, Jon J Christensen, Jewell Thomas, Rohit Venkat, Mengesha Teshome, Patricia Aldea, Anne M Fagan, David M Holtzman, John C Morris, David B Clifford
Affiliations

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

Beau M Ances et al. Arch Neurol. 2012 Jan.

Abstract

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-β protein 1-42 (Aβ42) 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 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 (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 Aβ42 deposition in cortical and subcortical regions. Observed dissimilarities between HAND and AD may reflect differences in Aβ42 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.

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Figures

Figure 1
Figure 1. MRI and 11C-PiB in four representative participants
Representative structural magnetic resonance image (MRI) and amyloid binding agent-N-methyl-[11C]2-(4-methylaminophenyl)-6-hydroxybenzothiazole (or 11C-PiB) images for (A) a cognitively normal HIV infected (HIV+) participant; (B) a HIV+ participant with HIV associated neurocognitive disorder (HAND); (C) a cognitively normal Alzheimer’s Disease Research Center (ADRC) participant; (D) ADRC participant with symptomatic Alzheimer disease (AD). Only the symptomatic AD participants had increased fibrillar amyloid deposition using 11C-PiB.
Figure 2
Figure 2. MCBP and regional BP (pg/mL) for the four clinical groups
A. Mean cortical binding potential (MCBP) for the four clinical groups. A two by two matrix is created using CSF Aβ42 (<500 pg/ml) and MCBP (>0.18 arbitrary units). All HIV+ participants, regardless of their degree of cognitive impairment, had normal 11C-PiB (< 0.18 arbitrary units).B. Regional cortical binding potential for the four clinical groups. For each region symptomatic ADRC participants had higher binding potentials. *= p < 0.001.
See this image and copyright information in PMC

References

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