Amyloid, hypometabolism, and cognition in Alzheimer disease

OBJECTIVE: To investigate the association between brain amyloid load in Alzheimer disease (AD) measured by 11CPIB-PET, regional cerebral glucose metabolism (rCMRGlc) measured by 18FFDG-PET, and cognition. METHODS: Nineteen subjects with AD and 14 controls had 11CPIB-PET and underwent a battery of psychometric tests. Twelve of those subjects with AD and eight controls had 18FFDG-PET. Parametric images of 11CPIB binding and rCMRGlc were interrogated with a region-of-interest atlas and statistical parametric mapping. 11CPIB binding and rCMRGlc were correlated with scores on psychometric tests. RESULTS: AD subjects showed twofold increases in mean 11CPIB binding in cingulate, frontal, temporal, parietal, and occipital cortical areas. Higher cortical amyloid load correlated with lower scores on facial and word recognition tests. Two patients fulfilling the clinical criteria for AD had normal 11CPIB at baseline. Over 20 months this remained normal in one but increased in the cingulate of the other. Mean levels of temporal and parietal rCMRGlc were reduced by 20% in AD and these correlated with mini mental scores, immediate recall, and recognition memory test for words. Higher 11CPIB uptake correlated with lower rCMRGlc in temporal and parietal cortices. CONCLUSION: 11CPIB-PET detected an increased amyloid plaque load in 89% of patients with clinically probable Alzheimer disease (AD). The high frontal amyloid load detected by 11CPIB-PET in AD in the face of spared glucose metabolism is of interest and suggests that amyloid plaque formation may not be directly responsible for neuronal dysfunction in this disorder.