Using this AD mouse model, we showed, for the first time, that sustained optogenetic activation of SST and PV interneurons could selectively restore the power of hippocampal theta and gamma oscillations impaired by AβO pathology in vivo, respectively, (Figs. 1, 2) without affecting other frequencies such as delta and beta oscillations (Online resource Fig. 2), and resynchronize the CA1 PC spike phases relative to both theta and gamma oscillations to the level observed in the control mice (Fig. 3). This evidence concerns the gene SST and Alzheimer disease.