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Kinsmen Laboratory of Neurological Research (Dre McGeer, Kamo, and KG. McGeer), the Departments of Medicine (Dr. Martin), Psychiatry (Dre. P.L. McGeer, Kamo, and E.G. McGeer), and Radiology (Dr. Li), Faculty of Pharmaceutical Sciences (Dr. Pate), and the UBC/TRIUMF Program on Positron Emission Tomography (Drs. Harrop, Martin, and Pate), University of British Columbia, Vancouver; and the School of Computing Science (Dr. Harrop), Simon Fraser University, Burnaby, BC, Canada.
Positron emission tomography (PET) with fluorodeoxyglucose (FDG), magnetic resonance imaging (MRI), and CT were carried out in a patient with Alzheimer's disease 16 months before he died. At autopsy, the gross appearance of the brain correlated with MRI and CT, which showed some regional atrophy. These were much less revealing than PET, which correlated with microscopic findings of neuronal loss and proliferation of glia. In areas of moderately impaired local cerebral metabolic rate of glucose, as revealed by reduced FDG uptake, there was some gliosis, primarily around the numerous senile plaques. In areas of severe metabolic impairment, there was a profound loss of neurons, extensive gliosis, and a diminished appearance of plaques. PET-FDG is a better measure of the severity of Alzheimer's disease than MRI or CT, because it reflects the degree of neuronal pathology.
Address correspondence and reprint requests to Dr. P.L. McGeer, University of British Columbia, Kinsmen Laboratory of Neurological Research, 2255 Wesbrook Mall, Vancouver, BC, Canada V6T 1W5.
Supported by grants from the Medical Research Council of Canada, the Mr. and Mrs. P. A. Woodward's Foundation, the B.C. Medical Services Foundation, and the Alzheimer's Support Association of B.C.
Accepted for publication March 24, 1986.
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