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

Longitudinal changes in beta amyloid (Aβ) deposition and glucose metabolism over a long-term progression of preclinical Alzheimer's disease (AD) were evaluated. 22 preclinical AD subjects with amyloid-positive scans underwent [ C]-labeled Pittsburgh Compound-B (PIB) positron emission tomography (PET) and [ F]-fluorodeoxyglucose (FDG) PET imaging over 6.0 ± 1.8 years. A quantitative analysis of [ C]-PIB and [ F]-FDG was used with a standardized uptake value ratio (SUVR) in the same regions. 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. Increases in Aβ deposition lead to the progression to mild cognitive impairment, but decreases in glucose metabolism do not contribute to progression. Longitudinal changes in Aβ deposition and glucose metabolism were clarified over a long-term progression of preclinical AD using [ C]-PIB PET and [ F]-FDG PET imaging. 73% of the preclinical AD subjects progressed to mild cognitive impairment during 6 years of a long follow-up period. The increases in Aβ deposition lead to the progression to mild cognitive impairment but decreases in glucose metabolism do not contribute to progression.