Numerous studies have shown that the protective effects of PPARα and PPARγ on AD model were associated with the reduction of Aβ levels, where PPARα stimulated APP degradation by up-regulating the transcription of α-secretase (ADAM10) to produce sAPPα and decrease Aβ production, while PPARγ modulated the clearance of Aβ through the inhibition of β-secretase (BACE1) transcription (Zhang et al., 2014; Yan et al., 2017). The gene discussed is BACE1; the disease is Alzheimer disease.