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

摘要: Objectives: Diagnostic challenges exist for differentiating HIV dementia from Alzheimer disease (AD) in older HIV-infected (HIV+) individuals. Similar abnormalities brain amyloid-β42 (Αβ42) metabolism may be involved HIV-associated neuropathology and AD. We evaluated the amyloid-binding agent 11 C-Pittsburgh compound B ( C-PiB), a biomarker Αβ42 deposition, cognitively unimpaired HIV+ (n = 10) participants matched community controls without 20). Methods: In this case-control study, all had an C-PiB scan within 2 years of concomitant CSF studies neuropsychometric testing. Statistical differences between demographic clinical values were assessed by χ tests. Participants further divided into either low t tests performed to determine if regional fibrillar amyloid plaque deposition varied with Αβ42. Results: Regardless level, none plaques as increased mean cortical binding potential (MCBP) or 4 regions. contrast, some MCBP elevated potentials (>0.18 arbitrary units) Conclusions: Cognitively participants, even parameters suggesting deposition. The dissimilarity preclinical AD reflect Aβ42 production and/or formation diffuse plaques. Future longitudinal normal are required.