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Challenging the Cholinergic Hypothesis in Alzheimer Disease
Peter Davies, PhD
JAMA. 1999;281:1433-1434.
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The idea that some of the symptoms of Alzheimer disease are due to a deficiency of the neurotransmitter acetylcholine in the brain first surfaced in 1976 and 1977.1-3 Several groups of investigators reported that the activity of enzymes involved in the synthesis (choline acetyltransferase [ChAT]) and degradation (acetylcholinesterase [AChE]) of acetylcholine were markedly reduced in activity in autopsy brain tissue from patients with end-stage Alzheimer disease, and many subsequent studies have confirmed these findings. A few groups have reported deficits in ChAT activity or acetylcholine release in biopsy tissue from living patients with Alzheimer disease4 and several reports have shown that the extent of the deficits in autopsy brain tissue correlate with the severity of the disease (as determined by the density of neuritic plaques, neurofibrillary tangles, or both). The cholinergic hypothesis5 of Alzheimer disease that evolved from these studies simply postulates that at least some of . . . [Full Text of this Article]
Author Affiliation: Albert Einstein College of Medicine, Bronx, NY.
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JAMA. 1999;281(15):1401-1406.
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