Elevated amyloid-beta peptide (Abeta) and loss of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's disease (AD). Since the discovery of an Abeta-nAChR interaction, much effort has been expended to understand how this interaction may contribute to normal physiological processes as well as AD. Several researchers have expanded on the initial observation of an Abeta-nAChR interaction to characterize the pertinent factors that confer Abeta sensitivity to nAChRs. Some of which include the following: 1. receptor subunit composition; 2. receptor subunit stoichiometry; 3. regional distribution; 4. presynaptic versus somatic distribution; 5. neuron versus glia expression; 6. in vitro expression system. These aspects of nAChR composition and expression appear to confer the specific functional consequences of Abeta interaction which range from blockade of receptor activation to stimulation of second messenger cascades that provide neuroprotection from Abeta toxicity. This review will discuss the extant literature on the subject in terms of clarifying this apparent dichotomy regarding the consequences of Abeta-nAChR interaction during health and disease.