Interestingly Tropea et al. showed that α7nAChRs KO mice develop an AD-like phenotype with aging, showing increased Aβ and phospho-tau and cognitive impairment, suggesting that the lack of a physiological target of Aβ, i.e., α7nAChRs, may lead to a compensatory Aβ overproduction that induces neurotoxicity and AD-like symptoms (Tropea et al. (2021) [58]). The gene discussed is CHRNA7; the disease is Alzheimer disease.