A recent study reported that early tau pathology in the triple Tg AD mouse model resulted in a reduction in theta oscillations and overall excitability in the CA1 region of the hippocampus; perhaps as a compensatory mechanism for the prevention of Aβ-induced NMDA-mediated overexcitation (Mondragón-Rodríguez et al., 2018). The gene discussed is MAPT; the disease is Alzheimer disease.