Specifically, in experiments conducted on 5xFAD mice and LPS-induced AD models using BV2 cells, AS-IV was found to effectively suppress the activation of the NF-κB pathway and decrease the expression of proinflammatory mediators such as IL-1β, COX-2, iNOS, and TNF-α [148]. Here, NFKB1 is linked to Alzheimer disease.