Ameliorated the cognition processes and histopathological damages due to atopic dermatitis (AD) in rats by decreasing the deposition of Aβ1-42 and downregulating the expression of NF-κB, TNF-α, and IL-6 and modulated changes in the diversity and composition of intestinal microbiota to suppress the relative abundance of inflammation-associated microbiota. The gene discussed is NFKB1; the disease is Alzheimer disease.