The restoration of the pathway of nuclear factor erythroid-derived 2-related factor 2 (NRF2) in Alzheimer’s disease (AD) models that are treated with phytochemicals. Phytochemicals scavenge reactive oxygen species (ROS) and free radicals reducing oxidative stress in the brain. They also upregulate NRF2, restoring its nuclear translocation that is inhibited in AD, thus upregulating antioxidant genes and downregulating pro-oxidant and pro-inflammatory genes. GSK-3β (glycogen synthase kinase-3β) has also been shown to be inhibited by certain phytochemicals, reducing the phosphorylation and subsequent aggregation of tau protein, along with the other AD pathological findings. Aβ, amyloid beta; Keap1, Kelch-like ECH-associated protein 1; sMafs, small musculoaponeurotic fibrosarcoma proteins; ARE, antioxidant response element; HO-1, heme oxygenase-1; NQO1, NAD(P)H quinone oxidoreductase 1; GPx, glutathione peroxidase; GCLC, glutamate-cysteine ligase catalytic subunit; GCLM, glutamate-cysteine ligase regulatory subunit; NOS2, nitric oxide synthase 2; IL-6, interleukin-6; COX-2, cyclooxygenase 2; NF-κB, nuclear factor kappa beta; TNF-a, tumor necrosis factor-a; NFTs, neurofibrillary tangles.