Affiliations: [a] War Related Illness and Injury Study Center, VA Palo Alto Health Care System, Palo Alto, CA, USA | [b] Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA, USA | [c] Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA | [d] University of California at Davis, School of Medicine, Davis, CA, USA
Correspondence:
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Correspondence to: Dr. Ansgar Furst, War Related Illness and Injury Study Center, VA Palo Alto Health Care System, 3801 Miranda Ave, Mailcode 151Y, Palo Alto, CA 94304-1290, USA. Tel.: +650 493 5000 1 1, x68652; E-mail: [email protected].
Abstract: This study used PET with the amyloid-β (Aβ) imaging agent 11 C Pittsburgh Compound-B (PIB) and the glucose metabolic tracer 18F-fluorodeoxyglucose (FDG) to map the relationship of Aβ deposition to regional glucose metabolism in Alzheimer's disease (AD). Comparison of 13 AD patients' FDG scans with 11 healthy controls confirmed a typical temporo-parietal 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 Aβ 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 Aβ burden was not associated with comparable metabolic decreases in large parts of the frontal lobes, the striatum and the thalamus.
