Surprisingly, stimulation of α3β4 nAChRs with α7 nAChRs, α4β2 nAChRs, or both failed to restore AMPAR surface expression following Aβ1–42 treatment, suggesting that these receptor subtypes may activate distinct and interactive downstream pathways and that highly selective stimulation is required for therapeutic effects on AD, such as cognitive enhancement [56] (Table 1). The gene discussed is CHRNA7; the disease is Alzheimer disease.