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To explore the protective effect of exogenous adiponectin on neurological function of Alzheimer's disease mice by affecting nucleotide-binding oligomerization domain receptor/nuclear factor-kappa B/tumor necrosis factor signal pathway. 60 healthy male mice with C57BL/6J were divided into 5 groups; control (group A) (n=12), sham operation (group B) (n=12), model (group C) (n=12) and high (group D) and low dose adiponectin groups (group E) (n=12). Normal saline was given to the group A, B, C, D and E group, once a day. Adiponectin high and low dose group was given adiponectin (10 mg/kg and 2.5 mg/kg) intragastric administration. The Morris water maze test of mice in each group was analyzed, the expressions of nucleotide-binding oligomerization domain 2, nuclear factor-kappa B, toll-like receptor-4, tumor necrosis factor-alpha and interleukin-1 beta in each group were compared, and the expressions of caspase-3, c-caspase-3 and B-cell lymphoma 2 proteins in each group were studied. Compared with the group C, the latent period of the experiment was decreased and the number of diving was increased in the high and low dose groups of adiponectin. Compared with the group C, the nucleotide-binding oligomerization domain 2, nuclear factor-kappa B and toll-like receptor-4 in group D and E were lower. Compared with the group C, the levels of the above factors in the group D and E decreased. Compared with the group C, the caspase-3 and cleaved caspase-3 in the group D and E decreased, while the B-cell lymphoma 2 increased. Exogenous adiponectin can enhance the learning and memory ability of patients with Alzheimer's disease, affect the expression of nucleotide-binding oligomerization domain 2, nuclear factorkappa B, toll-like receptor-4 and other pathways, and reduce the levels of tumor necrosis factor-alpha and interleukin-1 beta, so as to inhibit the inflammatory response of nerves in the brain, reduce the damage to nerve function, and provide new therapeutic ideas for the prevention and treatment of Alzheimer's disease. [ABSTRACT FROM AUTHOR]