These findings provide insight into the roles of NSAIDs in inhibiting secretion of the Aβ1-42 peptide in cultured cells and mouse models of AD (Weggen et al., 2003), the suppressive effects of NSAIDs on the γ-secretase activity in D385TG mice that accumulated Aβ1–42, and the induced potentiation of AP formation caused by COX-2 expression in APP(swe)/PS1/COX-2 mice (Xiang et al., 2002). This evidence concerns the gene APP and Alzheimer disease.