The AD-like skin lesions, such as large ulcers, ear swelling, and hyperkeratosis, the thickness of the epidermis and dermis, and inflammatory cell infiltration, are inhibited by treatment with ZC-EO through the downregulation of NF-κB and the phosphorylated MAPK pathway in a DNCB-induced AD mouse model [114]. Here, NFKB1 is linked to Alzheimer disease.