Abstract
Receptor binding studies have uniform-ly found a significant reduction in the density of neuronal nicotinic cholinergic receptors in postmortem tissue obtained from Alzheimer's Disease (AD) pa-tients. Nicotine is widely recognized as an pharma-cological agent that facilitates cognitive performance in human smokers as well as preclinical models utilizing rodents or non-human primates. Furthermore, epidemiological studies have consistently shown that the incidence of neurodegenerative diseases such as AD and Parkinson's Disease is lower in cigarette smokers than age-matched controls. These findings have prompted speculation that brain nicotinic receptors could be important therapeutic targets for Alzheimer's Disease. However, many questions remain with regard to the specificity and significance of the findings that have been reported with brain nicotinic receptors and AD. Few studies have controlled for the potential influence of cigarette smoking, which increases the density of nicotinic receptors in human smokers. Questions also remain concerning alterations in individual nicotinic receptors subtypes as well as the regional variability of the deficits previously reported in AD. Therefore, although the findings related to nicotinic receptors and AD to this date are intriguing, they appear to have raised more questions than they have answered.