By Dwaine F. Emerich, Reginald L. Dean III, Paul R. Sanberg
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Extra info for Central Nervous System Diseases
4,32,34,140). Yet, variations between the two clinica profiles should surprise no one, for many functional differences exist between block ing postsynaptic receptors, versus the constellation of cholinergic deficits and noncholinergic deficits that likely exist in normal aging and especially AD. For this reason, the issue should not be how exactly one situation matches the other, but rathe whether sufficient similarities exist to support a plausible cause-effect relationship fo some of the important cognitive symptoms.
However, several muscarinic agonist have been tested in AD clinical trials, and although some preliminary reports of effi of these compounds seem cacy weregenerated (9), further development work on many to have been terminated (miscellaneous press releases; Table 4). Thus, either the thera peutic effects were not sufficient and/or the cholinergic side effects induced were too severe. , serious side effects). Only time andadditional research wil provide the answer. The likelihood that cholinergic side effects can be sufficiently reduced remain uncertain.
Figs. 1 and 2) demonstrated that the classic centrally acting cholinergic blocking drugs, scopolamine and atropine, were able to produce an amnestic effect in young monkeys that were remarkably similar to the most sensitive deficit in aged monkeys (78). This scopolamine deficit in recent episodic memory in young monkeys was also shown to be dose-related, with higher doses of scopolamine producing even greater memory impairments (78) (Fig. 3). Finally, it appeared to be somewhat selective to CNS cholinergic neurons, in that it was attenuated by the cholinomimetic, physostigmine, but not the CNS stimulant methyphenidate (Ritalin) (127).