“…In addition to Aβ aggregation and tau protein hyperphosphorylation, OS contributes significantly to exacerbate AD pathology. The OS induces Aβ deposition and apoptosis, contributing to loss of neurons, brain mass, memory loss, and cognitive impairment [ [73] , [74] , [75] , [76] ]. In physiological conditions, Nrf2 is negatively regulated by Keap1 in the cytoplasm, but in the stressful conditions, Nrf2 is released from Keap1, enters into the nucleus and binds to antioxidant response elements and stimulates transcription of antioxidants to fight against excessive ROS [ 35 ].…”