UNLABELLED: Using dynamic [18F]fluorodeoxyglucose (FDG) and PET, kinetic rate constants that describe influx (K1) and efflux (k2) of FDG as well as phosphorylation (k3) and dephosphorylation (k4) were determined in patients with probable Alzheimer's disease and similarly aged normal controls. METHODS: The regional cerebral metabolic rate for glucose (CMRglu) was calculated from individually fitted rate constants in frontal, temporal, parietal and occipital cerebral cortex, caudate nucleus, putamen, thalamus and cerebellar cortex. Dynamic PET scans were obtained in normal controls (n = 10, mean age = 67) and Alzheimer's disease patients (n = 8, mean age = 67) for 60 min following injection of 10 mCi of FDG. RESULTS: The Alzheimer's disease group was characterized by decreases of the CMRglu ranging from 13.3% in the frontal to 40.9% in the parietal cortex, which achieved significance in all regions except the thalamus. K1 was significantly reduced in the parietal (p < 0.01) and temporal cortices (p < 0.05). Significant declines in k3 were found in the parietal (p < 0.005), temporal and occipital cortex, and in the putamen and cerebellum (p < 0.05). The rate constants k2 and k4 were unchanged in the Alzheimer's disease group. CONCLUSION: These data suggest that hypometabolism in Alzheimer's disease is related to reduced glucose phosphorylation activity as well as diminished glucose transport, particularly in the most metabolically affected areas of the brain, the parietal and temporal cortex.
UNLABELLED: Using dynamic [18F]fluorodeoxyglucose (FDG) and PET, kinetic rate constants that describe influx (K1) and efflux (k2) of FDG as well as phosphorylation (k3) and dephosphorylation (k4) were determined in patients with probable Alzheimer's disease and similarly aged normal controls. METHODS: The regional cerebral metabolic rate for glucose (CMRglu) was calculated from individually fitted rate constants in frontal, temporal, parietal and occipital cerebral cortex, caudate nucleus, putamen, thalamus and cerebellar cortex. Dynamic PET scans were obtained in normal controls (n = 10, mean age = 67) and Alzheimer's diseasepatients (n = 8, mean age = 67) for 60 min following injection of 10 mCi of FDG. RESULTS: The Alzheimer's disease group was characterized by decreases of the CMRglu ranging from 13.3% in the frontal to 40.9% in the parietal cortex, which achieved significance in all regions except the thalamus. K1 was significantly reduced in the parietal (p < 0.01) and temporal cortices (p < 0.05). Significant declines in k3 were found in the parietal (p < 0.005), temporal and occipital cortex, and in the putamen and cerebellum (p < 0.05). The rate constants k2 and k4 were unchanged in the Alzheimer's disease group. CONCLUSION: These data suggest that hypometabolism in Alzheimer's disease is related to reduced glucose phosphorylation activity as well as diminished glucose transport, particularly in the most metabolically affected areas of the brain, the parietal and temporal cortex.
Authors: Lisa Mosconi; Wai H Tsui; Henry Rusinek; Susan De Santi; Yi Li; Gene-Jack Wang; Alberto Pupi; Joanna Fowler; Mony J de Leon Journal: Eur J Nucl Med Mol Imaging Date: 2007-04-04 Impact factor: 9.236
Authors: Winnie S Liang; Eric M Reiman; Jon Valla; Travis Dunckley; Thomas G Beach; Andrew Grover; Tracey L Niedzielko; Lonnie E Schneider; Diego Mastroeni; Richard Caselli; Walter Kukull; John C Morris; Christine M Hulette; Donald Schmechel; Joseph Rogers; Dietrich A Stephan Journal: Proc Natl Acad Sci U S A Date: 2008-03-10 Impact factor: 11.205
Authors: Eric M Reiman; Kewei Chen; Gene E Alexander; Richard J Caselli; Daniel Bandy; David Osborne; Ann M Saunders; John Hardy Journal: Proc Natl Acad Sci U S A Date: 2003-12-19 Impact factor: 11.205