Observations in an AD transgenic mouse model overexpressing APP, presenilin-1, and tau (3xTg-ADmice) (Oddo et al., 2003; Billings et al., 2005; Kitazawa et al., 2005) were consistent with the aforementioned in vitro conclusions for human AD, demonstrating an age dependent reduction of α7 nAChR, as higher Aβ may eventually block remaining α7 nAChRs (Hernandez et al., 2010). The gene discussed is CHRNA7; the disease is Alzheimer disease.