This study utilized APPNL−G−F AD model mice, which incorporate Swedish (KM670/671 NL) and Beyreuther/Iberian (I716 F) mutations into the endogenous App gene [24], thereby avoiding the overexpression issues seen in traditional transgenic mice, accurately reflecting the formation and distribution of Aβ plaques characteristic of human AD pathology. This evidence concerns the gene APP and Alzheimer disease.