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To the Editor: It has been nearly 20 years since the inception and integration of the cholinergic hypothesis,¹ the only approach that has so far produced drugs approved for treating Alzheimer disease (AD). The study by Dr Davis and colleagues² is the first attempt to explore the temporal relationship between progressive declines in key cholinergic markers and memory in AD. The authors report that choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities remain normal until the late stages of AD and suggest that the link between cholinergic dysfunction and the onset of the characteristic symptoms is therefore weak. However, caution must be exercised when interpreting data using ChAT and AChE as markers of cholinergic function.

Neither ChAT nor AChE is rate-limiting, and therefore they do not reflect cholinergic function.³ In fact, ChAT can be inhibited up to 90% with no measurable effects on acetylcholine synthesis or release. At the same time, . . . [Full Text of this Article]

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