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Neurobiol Aging. 2012 Feb;33(2):215-25. doi: 10.1016/j.neurobiolaging.2010.03.011. Epub 2010 Apr 24.

Cognition, glucose metabolism and amyloid burden in Alzheimer's disease.

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Helen Wills Neuroscience Institute, 132 Barker Hall, University of California, Berkeley, Berkeley, CA 94720, USA.


The authors investigated relationships between glucose metabolism, amyloid load, and measures of cognitive and functional impairment in Alzheimer's disease (AD). Patients meeting criteria for probable AD underwent (11)C-labeled Pittsburgh Compound-B ([(11)C]PIB) and 18F-fluorodeoxyglucose ([(18)F]FDG) positron emission tomography (PET) imaging and were assessed on a set of clinical measures. The Pittsburgh Compound-B (PIB) Distribution volume ratios and fluorodeoxyglucose (FDG) scans were spatially normalized and average PIB counts from regions-of-interest (ROI) were used to compute a measure of global PIB uptake. Separate voxel-wise regressions explored local and global relationships between metabolism, amyloid burden, and clinical measures. Regressions reflected cognitive domains assessed by individual measures, with visuospatial tests associated with more posterior metabolism, and language tests associated with metabolism in the left hemisphere. Correlating regional FDG uptake with these measures confirmed these findings. In contrast, no correlations were found between either voxel-wise or regional PIB uptake and any of the clinical measures. Finally, there were no associations between regional PIB and FDG uptake. We conclude that regional and global amyloid burden does not correlate with clinical status or glucose metabolism in AD.

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