UNLABELLED: In an effort to better understand the metabolic basis for the reported decreases in regional cerebral cortex glucose metabolism in patients with Alzheimer's disease, glucose utilization oxygen consumption and regional cerebral blood flow were examined. METHODS: Nine patients with Alzheimer's disease and nine age-matched normal controls were imaged using 18F-labeled deoxyglucose and 15O-labeled gases. RESULTS: Regional analysis of the cerebral metabolic rate of glucose (CMRglu), cerebral metabolic rate of oxygen (CMRO2) and cerebral blood flow (CBF) revealed that these values were significantly low in the frontal, parietal and temporal regions. The parietotemporal region had an abnormally high metabolic ratio (CMRO2/CMRglu), while the frontal, sensorimotor and occipital visual cortices had a metabolic ratio similar to that of the normal controls. CONCLUSIONS: These findings suggest that the abnormal parietotemporal metabolism in Alzheimer's disease involves a metabolic shift from glycolytic to oxidative metabolism. This impairment of glucose degradation may be the basis for synoptic dysfunction underlying the impairment observed in Alzheimer's disease.
UNLABELLED: In an effort to better understand the metabolic basis for the reported decreases in regional cerebral cortex glucose metabolism in patients with Alzheimer's disease, glucose utilization oxygen consumption and regional cerebral blood flow were examined. METHODS: Nine patients with Alzheimer's disease and nine age-matched normal controls were imaged using 18F-labeled deoxyglucose and 15O-labeled gases. RESULTS: Regional analysis of the cerebral metabolic rate of glucose (CMRglu), cerebral metabolic rate of oxygen (CMRO2) and cerebral blood flow (CBF) revealed that these values were significantly low in the frontal, parietal and temporal regions. The parietotemporal region had an abnormally high metabolic ratio (CMRO2/CMRglu), while the frontal, sensorimotor and occipital visual cortices had a metabolic ratio similar to that of the normal controls. CONCLUSIONS: These findings suggest that the abnormal parietotemporal metabolism in Alzheimer's disease involves a metabolic shift from glycolytic to oxidative metabolism. This impairment of glucose degradation may be the basis for synoptic dysfunction underlying the impairment observed in Alzheimer's disease.