Amyloid-β and Glucose Metabolism in Alzheimer's Disease

This study used PET with the amyloid-beta (A beta) imaging agent (11) C Pittsburgh Compound-B (PIB) and the glucose metabolic tracer F-18-fluorodeoxyglucose (FDG) to map the relationship of A beta deposition to regional glucose metabolism in Alzheimer's disease (AD). Comparison of 13 AD patients' FDG scans with 11 healthy controls confirmed a typical temporoparietal hypometabolic pattern in AD. In contrast, PIB distribution-volume-ratios showed a distinct pattern of specific tracer retention in fronto-temporo-parietal regions and striatum in AD with peaks in left frontal cortex, precuneus, temporal cortex, striatum and right posterior cingulate. There were no region-to-region or within region correlations between FDG and PIB uptake in PIB positive AD patients but when the impact of A beta load on glucose metabolism was assessed via probabilistic maps, increased amyloid burden was coupled with decreased metabolism in temporo-parietal regions and the posterior cingulate. However, importantly, severe A beta burden was not associated with comparable metabolic decreases in large parts of the frontal lobes, the striatum and the thalamus.