Cognitive Decline and Brain Volume Loss as Signatures of Cerebral Amyloid-β Peptide Deposition Identified With Pittsburgh Compound B

Abstract

Amyloid imaging with positron emission tomography (PET) and the benzothiazole tracer labeled with carbon 11 (¹¹C), Pittsburgh compound B (PiB), is a noninvasive method to assess cerebral amyloid-β peptide (Aβ) levels in the brains of living people¹ and serves as an important new tool in the study of Alzheimer disease (AD). The compound binds to fibrillar amyloid plaques and to amyloid angiopathy in human postmortem specimens,² and PiB uptake corresponds to postmortem assessment of parenchymal Aβ plaques.^3,4 Previous reports^5-7 indicate that some older adults without cognitive impairment at death have brain amyloid plaque levels, 1 of the histopathologic hallmarks of AD, comparable to those measured in individuals with AD. Similarly, some older people without cognitive impairment have elevated Aβ levels as assessed in vivo with [¹¹C]PiB.^8,9