Positron emission tomography and the possible origins of cytopathology in Alzheimer's disease.
The local cerebral metabolic rate for glucose (LCMRgl), as determined by positron emission tomography (PET), declines in the cerebral cortex in Alzheimer's disease; the severity of the decline parallels the severity of the dementia and correlates with regional cortical neuronal loss and glial proliferation. The cholinergic cells of the medial basal forebrain show a pathological dropout in Alzheimer's disease which accounts for the decline in choline acetyltransferase in the cerebral cortex and hippocampus. It is proposed that these cholinergic cells serve both as an acquisition and readout device for memory; reconstruction of real time events can thus be created in the areas of neocortex where consciousness resides. Alzheimer's disease may have a toxic, genetic or infectious origin; electron microscopic evidence is presented for the possible presence of viral particles of the double stranded DNA type in Alzheimer's brain tissue.
D000544:Alzheimer Disease / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D001921:Brain / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D003071:Cognition; D005947:Glucose / Q000378:metabolism; D006801:Humans; D008568:Memory; D010275:Parasympathetic Nervous System / Q000502:physiology; D014055:Tomography, Emission-Computed; D014780:Viruses / Q000302:isolation & purification
D005947:Glucose