BAI triggered the TLR4/myeloid differentiation protein 88 (MyD88)/caspase-3 pathway to reduce neurodegeneration in the hippocampal CA3 area, while decreasing the levels of TLR4, NF-κB p65, iNOS, and COX-2 proteins and suppressing the secretion of TNF-α and IL-1β, which resulted in a protective effect on the nervous system (Tu et al., 2011; Yang et al., 2021). The gene discussed is TLR4; the disease is body adiposity index.