Moreover, AG downregulated the levels of MDA, TNF-α, IL-1β, IL-6, Notch1, HES-1, RBP-Jκ, and NF-κB, upregulated T-SOD, T-AOC, CAT, GSH-Px, IL-10, and APP, and reduced the expressions of GFAP+ and IBA1+ signals, indicating that suppressing the Notch/HES-1-NF-κB signaling pathway and attenuating microglia activation might account for the therapeutic effect of AG in cognitive impairment (Hu et al., 2022). The gene discussed is NFKB1; the disease is Cognitive impairment.