Conversely, the activation of α7 nAChR with Aβ was shown to produce tau phosphorylation (Hu et al., 2008), and the deletion of this receptor gene improved memory impairments, reduced gliosis and preserved long-term potentiation in aged mice modeling the key pathological features of AD (Dziewczapolski et al., 2009). The gene discussed is CHRNA7; the disease is Alzheimer disease.