This study found that in the AD model group, the expression of SOCS1 in the ear skin tissue was decreased, the expression of its downstream JAK-STAT3 pathway and T lymphoid activation related promoters IL-6 and IL-17 were increased, and the AD-like pathological damage of skin was aggravated, suggesting that the decreased expression of SOCS1 and the continued activation of JAK-STAT3 might be one of the reasons for aggravation of skin inflammatory damage mediated the activation of T lymphocytes in AD mice. This evidence concerns the gene STAT3 and Alzheimer disease.