Abnormal brain glucose metabolism in Alzheimer's disease, as measured by position emission tomography.

Resting glucose metabolism in the association neocortices, measured with positron emission tomography (PET), is disturbed early and throughout the course of Alzheimer's disease (AD), whereas resting metabolism in the primary sensory and motor neocortices is relatively spared. Neocortical metabolic asymmetries precede and predict appropriate deficits in neocortically-mediated cognitive functions in the initial course of disease, indicating that PET can be used for the early diagnosis and characterization of AD. Metabolic abnormalities of the neocortices in late-stage AD correlate with regional densities of neurofibrillary tangles but not of senile plaques post mortem, suggesting that tangle formation is important in disease pathogenesis. Despite demonstrating reduced resting glucose metabolism, visual association areas demonstrate equivalent (as percent baseline) blood flow responses in mildly-moderately demented AD patients and controls who are performing a face matching task. Thus, viability and integrity of this cortical circuitry is retained into the intermediate stages of the disease, and glucose delivery to the AD brain can be increased.