To the Editor: Pharmacologic attempts to reverse symptoms of Alzheimer's dementia have thus far lacked conspicuous success. Most recent therapeutic strategies have been designed to correct a cholinergic loss arising from degeneration of acetylcholine-containing neuronal projections to the cerebral cortex. However, the widespread distribution of cholinergic depletion in Alzheimer's dementia1 does not correlate with the focal distribution of functional brain abnormalities in this disorder, as determined by positron emission tomography with fluorodeoxyglucose (PET/FDG).2 Thus, there is reason to suspect that stimulation of cholinergic transmission might not reverse a functionally relevant defect in the dementia. Imaging studies with PET/FDG suggest a.
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