Increased SCN2B (encode gene of Navβ2) expression in the hippocampus was associated with cognitive deficits in the senescence-accelerated P8 mice [32], while Navβ2 knockdown reversed the APP/PS1 mutation-induced deficiency in amyloid β (Aβ) degradation by regulating NEP in APP/PS1 mouse-derived neurons [47], preserved neurons, redressed Nav1.1α distributions, and improved spatial cognition by partially decreasing pathological amyloidogenic APP processing in aged APP/PS1 mice [38]. This evidence concerns the gene SCN2B and Cognitive impairment.