Cognitively unimpaired HIV-positive subjects do not have increased 11C-PiB A case-control study

Objectives: Diagnostic challenges exist for differentiating HIV dementia from Alzheimer disease (AD) in older HIV-infected (HIV+) individuals. Similar abnormalities in brain amyloid-beta 42 (A beta 42) metabolism may be involved in HIV-associated neuropathology and AD. We evaluated the amyloid-binding agent C-11-Pittsburgh compound B (C-11-PiB), a biomarker for A beta 42 deposition, in cognitively unimpaired HIV+ (n = 10) participants and matched community controls without dementia (n = 20). Methods: In this case-control study, all participants had an C-11-PiB scan within 2 years of concomitant CSF studies and neuropsychometric testing. Statistical differences between HIV+ and community controls for demographic and clinical values were assessed by chi(2) tests. Participants were further divided into either low (<500 pg/mL) or normal (>= 500 pg/mL) CSF A beta 42 groups with Student t tests performed to determine if regional differences in fibrillar amyloid plaque deposition varied with CSF A beta 42. Results: Regardless of CSF A beta 42 level, none of the HIV+ participants had fibrillar amyloid plaques as assessed by increased C-11-PiB mean cortical binding potential (MCBP) or binding potential within 4 cortical regions. In contrast, some community controls with low CSF A beta 42 (<500 pg/mL) had high C-11-PiB MCBP with elevated binding potentials (>0.18 arbitrary units) within cortical regions. Conclusions: Cognitively unimpaired HIV+ participants, even with low CSF A beta 42 (<500 pg/mL), do not have C-11-PiB parameters suggesting brain fibrillar amyloid deposition. The dissimilarity between unimpaired HIV+ and preclinical AD may reflect differences in A beta 42 production and/or formation of diffuse plaques. Future longitudinal studies of HIV+ participants with low CSF A beta 42 and normal C-11-PiB are required. Neurology(R) 2010;75:111-115