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  Vol. 69 No. 1, January 2012 TABLE OF CONTENTS
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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

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 {chi}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 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.


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.



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