We have previously demonstrated that the AChE-peptide is increased in AD brains (Garcia-Ratés et al., 2016) and its interaction with the α7-nAChR can elicit neurodegenerative-like events, such as reduction of neuronal activity monitored in real-time (Badin et al., 2016) and alteration of protein levels, including the nicotinic receptor itself, Aβ, APP, p-Tau, and GSK3 (Garcia-Ratés et al., 2016; Brai et al., 2017), thus compromising cell viability (Garcia-Ratés et al., 2016). Here, ACHE is linked to Alzheimer disease.