It was found that the survival rate of neural cells increased, the expression of inflammatory factors decreased, ABACE1 expression was inhibited, and the Wnt/β-catenin pathway was activated, reducing the aggregation of Aβ amyloid protein and NF-κB levels, effectively inhibiting cell apoptosis and inflammatory response in the brain of AD mice [108–111]. This evidence concerns the gene NFKB1 and Alzheimer disease.