Amyloid β deposition and glucose metabolism on the long-term progression of preclinical Alzheimer's disease.

Abstract

Aim:Longitudinal changes in beta amyloid (Aβ) deposition and glucose metabolism over a long-term progression of preclinical Alzheimer's disease (AD) were evaluated.Methods:22 preclinical AD subjects with amyloid-positive scans underwent [11C]-labeled Pittsburgh Compound-B (PIB) positron emission tomography (PET) and [18F]-fluorodeoxyglucose (FDG) PET imaging over 6.0 ± 1.8 years. A quantitative analysis of [11C]-PIB and [18F]-FDG was used with a standardized uptake value ratio (SUVR) in the same regions.Results:In preclinical AD subjects, the cortical PIB SUVR was higher at baseline and increased at follow-up. 12 of the preclinical AD subjects progressed to mild cognitive impairment, six of whom had reduced glucose metabolism. The annual change in PIB SUVR was not related to that in FDG SUVR.Conclusion:Increases in Aβ deposition lead to the progression to mild cognitive impairment, but decreases in glucose metabolism do not contribute to progression.