Abstract
Reductions in cerebral metabolism sufficient to impair cognition in normal individuals also occur in Alzheimer's disease (AD). FDG PET studies have shown that decreased glucose metabolism in AD precedes clinical diagnosis and the degree of clinical disability in AD correlates closely to the magnitude of the reduction in brain metabolism. This suggests that the clinical deterioration and metabolic impairment in AD are related closely. Diminished metabolism can lead to the hyperphosphorylation of tau and increased production of amyloid beta peptide, hallmarks of AD. These observations suggest also that early mitochondrially therapeutic interventions may be an important target in delaying AD progression in elderly individuals and in treating AD patients.
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