Amyloid plaques, derived from aggregates of amyloid β (Aβ), are closely linked to the pathogenesis of Alzheimer’s disease (AD). Another neuropathological hallmark is the loss of cholinergic markers, associated with a reduction in the α7 subunit of the nicotinic acetylcholine receptor (nAChR) in the brains of AD patients. The α7-nAChR plays an important role in circuits involved in learning and memory, and may be a promising target for the treatment of AD. Numerous studies indicate that binding to α7-nAChRs is neuroprotective. However, Aβ has also been shown to induce tau phosphorylation via α7-nAChR activation. In addition, picomolar to nanomolar concentrations of Aβ stimulate presynaptic α7-nAChRs, evoking an increase in presynaptic Ca2+ levels. There is evidence that Aβ infl uences hippocampus-dependent cognitive functions and synaptic plasticity such as long-term potentiation by modulating the function of α7-nAChRs. In line with the roles of α7-nAChRs in AD pathogenesis, allosteric modulators of α7-nAChRs have been proposed as novel therapeutical agents in the treatment of this disease.