SCN1A and Alzheimer disease: Searching for other possible channel defects in AD, in the report by Verret et al. [158] using human amyloid precursor protein (hAPP) transgenic mice (which show key features of human AD), network hypersynchrony was present, associated with impaired PV cell function and decreased levels of the PV interneuron‐specific voltage‐gated sodium channel subunit Nav1.1.