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© 1989 American Academy of Neurology Regional cerebral glucose transport and utilization in Alzheimer's diseaseFrom Donner Laboratory, Lawrence Berkeley Laboratory (Drs. Friedland, Jagust, Huesman, Mathis, Mazoyer, and Budinger, and B. Knittel), University of California, Berkeley; Department of Neurology (Drs. Friedland, Jagust, and Koss), Veterans Administration Medical Center, Martinez, and University of California, Davis; and Veterans Administration Medical Center (Dr. Ober), Livermore, CA. We performed dynamic positron emission tomographic (PET) studies of glucose utilization, using (18F) 2-fluoro-2-deoxy-D-glucose (FDG), in patients with probable Alzheimer's disease (AD) and healthy age-matched controls, to evaluate blood-brain-barrier glucose transport and glucose utilization rates in the disease. We found no significant differences in rate constants for glucose transport (k1 and k2) and phosphorylation (k3), nor for the vascular fraction (fv), between the 2 groups, although k3 and fv were relatively depressed in temporal cortex in AD. Absolute rates of glucose use were depressed in temporal and parietal cortex, and relative rCMRglc rates were lower in frontal, temporal, parietal, and occipital cortices. These data suggest that in AD bidirectional glucose transport is intact, and that temporal-parietal hypometabolism is present upon a background of widespread cortical metabolic impairment. Address correspondence and reprint requests to Dr. Friedland, Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Building 10, Room 6C414, Bethesda, MD 20892. Supported by National Institutes of Health grants AG05890, AG07793, HL25840, and CA38086, by the Medical Research service of the US Veterans Administration, and by the Director, Office of Energy Research, Office of Health and Environmental Research at the US Department of Energy, under contract DE-AC03765F00098. Received July 21, 1988. Accepted for publication in final form May 8, 1989.
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