Although the role of PF in the treatment of AD through GSK-3β and NF-κB pathway is not completely clear, current studies have shown that PF is likely to inhibit the activation of GSK-3β and NF-κB pathway [49], which suppressed the production of IL-6, IL-1β, and tumor necrosis factor-alpha (TNF-α) [32]. This evidence concerns the gene NFKB1 and Alzheimer disease.