Wirth M, Oh H, Mormino E, Markley C, Landau S, Jagust W.
A-Beta Deposition in Normal Elderly Is Related to Longitudinal Cognitive Decline.
Human Amyloid Imaging Abstract. 2012 Jan 1;
Objective: There is indication that validated Alzheimer’s disease biomarkers of beta-amyloid (Abeta) accumulation and neurodegenerative pathology are related to preclinical cognitive decline. The present study therefore contrasted effects of Abeta deposition and posterior cortical metabolism to longitudinal cognitive change in cognitively normal elderly.
Methods: Thirty-eight older people completed at least three consecutive annual neuropsychological examinations. Using Positron Emission Tomography (PET), Abeta-plague burden was traced with [11C] labeled Pittsburgh Compound B and posterior glucose metabolism with [18F] Fluorodeoxyglucose (FDG) PET. In a series of multiple regression analyses, biomarkers were related to cognitive composite trajectories. PIB retention was dichotomized into PIB positive (n=13) and PIB negative (n=25) status using a global PIB uptake cutoff; FDG PET values were treated as continuous variable.
Results: An elevated PIB binding status was associated with concurrent intra-individual decline in memory and global cognition (see figure, category slope, red circles indicate PIB positivity). Non-memory decline was related to low FDG uptake, selectively within PIB positive individuals. There were no main effects of glucose metabolism on cognitive change in the total sample.
Conclusion: Our findings provide evidence that longitudinal cognitive decline is related to Abeta deposition in normal elderly individuals. They further support assumptions that the occurrence of posterior cortical hypometabolism contributes to the early preclinical changes in cognitive trajectories within PIB positive individuals.