[18F]FDG PET may differentiate cerebral amyloid angiopathy from Alzheimer’s disease

Abstract

Cerebral amyloid angiopathy (CAA) is a frequent cause of both intracerebral hemorrhage (ICH) and cognitive impairment in the elderly. Diagnosis relies on the Boston criteria, which use magnetic resonance imaging markers including ≥2 exclusively lobar cerebral microbleeds (lCMBs). Although amyloid positron emission tomography (PET) may provide molecular diagnosis, its specificity relative to Alzheimer s disease (AD) is limited due to the prevalence of positive amyloid PET in cognitively normal elderly. Using early‐phase 11C‐Pittsburgh compound B as surrogate for tissue perfusion, a significantly lower occipital/posterior cingulate (O/PC) tracer uptake ratio in probable CAA relative to AD was recently reported, consistent with histopathological lesion distribution. We tested whether this finding could be reproduced using [18F]fluorodeoxyglucose (FDG)‐PET, a widely available modality that correlates well with early‐phase amyloid PET in both healthy subjects and AD.