Many cognitive skills decline with age, including short and long-term memory (Smith 1996; Zornetzer, et al. 1982). In rats, these deficits appear to be associated with neurochemical changes in the brain such as reduced levels of acetylcholine (Perry et al.
1992) and a decrease in the number of nicotine receptors (Court and Clementi, 1995). Deficits similar to these have been reported in patients suffering from Alzheimer's disease (Coyle et al., 1983) and suggesting that drug treatments that increase the levels of acetylcholine in the brain (cholinergic agonists) may be an effective treatment for this disease. The two cholinergic agonists currently approved by the FDA (Donepezil and Tacrine) have a limited positive effect on memory and have serious side effects (Sahakian and Coull, 1993). There is a need for the development of new drug treatments that are effective in counering the effects of aging on memory.

One possible cholinergic agonist with promising effect is nicotine. Nicotine agonists produce memory deficits in rats (Levin et al. 1997) and impair the neurological functioning of healthy humans in ways that mimic the early stages of Alzheimer's disease (Newhouse et al., 1992). The evidence in supprt of nicotine as a treatment for memory deficits is mixed. Some studies have found improvements in short-term memory but not
long-term memory in rats(Levin et al., 1993), while other have found the opposite (Arendash et al. 1995).

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