In AD brains, both the activation of JNK signaling cascade [54–56] and the elevation of BACE1 and PS1 expression/activity have been detected [57–59]; thus, it is possible that the increased oxidative stress in AD brains may initiate the activation of a cascade of redox-sensitive cell signal pathways including JNK, which promotes the expression of BACE1 and PS1, eventually enhancing the production of Abeta and the deterioration of cognitive function. This evidence concerns the gene BACE1 and Alzheimer disease.