The expression of BACE1 is reportedly increased in AD pathology, resulting in abnormal VGSC beta subunit cleavage, which has been shown to result in reduced levels of functional Nav1.1 channels on the surface of GABAergic interneurons, leading to network disinhibition and higher susceptibility to seizures in mouse models of AD (Kim et al., 2007; Kim et al., 2011; Corbett et al., 2013). This evidence concerns the gene BACE1 and Alzheimer disease.