11 CPIB in a nondemented population

BACKGROUND: Beta-amyloid (Abeta) plaques are the hallmark of Alzheimer disease (AD). A PET imaging tracer that binds to Abeta plaques in vivo, N-methyl-(11)C2-(4'-methylaminophenyl)-6-hydroxybenzothiazole (or (11)CPIB for "Pittsburgh Compound-B"), has significantly higher binding in subjects diagnosed with dementia of the Alzheimer type (DAT) compared to nondemented controls. The authors used this imaging technique to investigate whether abnormal binding occurs in clinically normal individuals, prior to the development of cognitive changes. METHODS: Forty-one nondemented subjects (age range 20 to 86 years) and 10 patients with DAT (age range 66 to 86 years) underwent (11)CPIB PET scanning. Regions of interest were drawn on the MRI over the cerebellar, prefrontal, lateral temporal, occipital, gyrus rectus, precuneus, and striatal cortex. Binding potential values (BPs), proportional to the density of (11)CPIB-Abeta binding sites, were calculated using the Logan graphical analysis and the cerebellar cortex for a reference tissue. RESULTS: Patients with DAT had elevated BP values vs nondemented subjects (p < 0.0001). Four of the 41 nondemented subjects had elevated cortical BP values and their BP values as a group were not significantly different from the DAT subjects' BP values. Two of these four nondemented subjects had (11)CPIB uptake, both visually and quantitatively, that was indistinguishable from the DAT subjects. CONCLUSIONS: Elevated (11)CPIB binding in nondemented subjects suggests that (11)CPIB amyloid imaging may be sensitive for detection of a preclinical Alzheimer disease state. Longitudinal studies will be required to determine the association of elevated (11)CPIB binding and risk of developing dementia of the Alzheimer type.