Alzheimer’s disease (AD) is the leading cause of dementia in the elderly. Neuropathological hallmarks of AD are amyloid plaques composed of amyloid-β (Aβ), neurofibrillary tangles originating from hyperphosphorylated tau protein and neuronal loss preferentially affecting cholinergic neurons. Mutations in the amyloid precursor protein (APP), presenilin 1, or presenilin 2 genes are autosomal dominant causes of familial AD (FAD); the ε4 allele of the apolipoprotein E gene represents a strong genetic risk factor. Various animal models have been developed, replicating signs, lesions, and causes of AD to a varying degree. Nicotinic acetylcholine receptors (nAChRs), particularly the α7 subtype, are highly expressed in brain regions relevant to cognitive and memory functions and involved in the processing of sensory information. There is strong evidence for the participation of α7-nAChRs in the pathogenesis of AD. In the brains of AD patients, α7-nAChR binding sites are reduced as well as α7-nAChR protein levels. Aβ binds to α7-nAChRs and modulates their function. Co-localization of α7-nAChRs, Aβ and amyloid plaques also indicates that these receptors play a role in the pathogenesis of AD. α7-nAChRs are also located on nonneuronal structures affected by AD, such as microglia, astrocytes, and vascular smooth muscle cells, and are involved in neuroinfl ammation. Functional modulation of α7-nAChRs in these structures has also been shown to contribute to the pathogenesis of AD. Epidemiological evidence suggests an increased risk of AD in cigarette smokers. Based on the importance of α7-nAChRs in AD pathogenesis, modulators of this receptor have been suggested for the therapy of AD.