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.
Highlights
over the long term if preclinical Alzheimer’s disease (AD) is defined by amyloid positron emission tomography imaging
In preclinical AD subjects who progressed to mild cognitive impairment (MCI)
• A reduction in cerebral glucose metabolism is not correlated with a progression to MCI
Summary
Longitudinal changes in beta amyloid (Aβ) deposition and glucose metabolism over a long-term progression of preclinical Alzheimer’s disease (AD) were evaluated
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