Altered cerebral energy metabolism in Alzheimer's disease: a PET study.

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.

[1]  R. Nitsch,et al.  Predominant abnormality in cerebral glucose utilization in late-onset dementia of the Alzheimer type: A cross-sectional comparison against advanced late-onset and incipient early-onset cases , 1991, Journal of neural transmission. Parkinson's disease and dementia section.

[2]  Richard S. J. Frackowiak,et al.  The cerebral metabolism of glucose and oxygen measured with positron tomography in patients with mitochondrial diseases. , 1988, Brain : a journal of neurology.

[3]  M E Phelps,et al.  Quantitation in Positron Emission Tomography: 8. Effects of Nonlinear Parameter Estimation on Functional Images , 1987, Journal of computer assisted tomography.

[4]  E. Masliah,et al.  Increased immunoreactivity of brain spectrin in Alzheimer disease: a marker for synapse loss? , 1990, Brain Research.

[5]  S. Baldwin,et al.  Anatomical mapping of glucose transporter protein and pyruvate dehydrogenase in rat brain: an immunogold study , 1989, Brain Research.

[6]  K Torizuka,et al.  Performance characteristics of Positologica III: a whole-body positron emission tomograph. , 1985, Journal of computer assisted tomography.

[7]  Arne Brun,et al.  PATHOLOGICAL AND POSITRON EMISSION TOMOGRAPHIC CORRELATIONS IN ALZHEIMER'S DISEASE , 1985, The Lancet.

[8]  J. Haxby,et al.  Clinical history, brain metabolism, and neuropsychological function in Alzheimer's disease , 1985, Annals of neurology.

[9]  T Jones,et al.  Regional cerebral oxygen supply and utilization in dementia. A clinical and physiological study with oxygen-15 and positron tomography. , 1981, Brain : a journal of neurology.

[10]  N. Allen.  Oxidative metabolism of brain tumors. , 1972, Progress in experimental tumor research.

[11]  E. Hoffman,et al.  TOMOGRAPHIC MEASUREMENT OF LOCAL CEREBRAL GLUCOSE METABOLIC RATE IN HUMANS WITH (F‐18)2‐FLUORO-2‐DEOXY-D‐GLUCOSE: VALIDATION OF METHOD , 1980, Annals of neurology.

[12]  H. Handa,et al.  Thalamic tumours invading the brain stem produce crossed cerebellar diaschisis demonstrated by PET. , 1986, Journal of neurology, neurosurgery, and psychiatry.

[13]  W. Jagust,et al.  Diminished Glucose Transport in Alzheimer's Disease: Dynamic PET Studies , 1991, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[14]  A. Brun,et al.  Regional pattern of degeneration in Alzheimer's disease: neuronal loss and histopathological grading , 1981, Histopathology.