Commentary on William Summers Paper on Tacrine March 6, 2000.

The cholinergic dysfunction in AD is not necessarily predominant (1,4,5) and responsivity to a cholinesterase inhibitor is not diagnostic for Alzheimer’s disease. Normal young people have improved on psychometric measures in memory and attention after physostigmine challenge (3). Additionally, postmortem neurochemical measures of cholinergic function in AD patients do not correlate with ante mortem measures of cognitive dysfunction as measured with CDR (2) suggesting that patients who have responded to cholinesterase inhibitors in clinical trials (with mild to moderate AD) may have a limited cholinergic deficit. The argument of using acetylcholinesterase inhibitors as a diagnostic challenge in AD is tautological. AD patients may respond to cholinesterase inbibitors and there is a cholinergic deficit in AD. However, a response to cholinesterase inbibitors does not reliably diagnose AD.