Their research demonstrated that Aβ enhances RANKL-induced osteoclasts activation through the degradation of IκB-α, ERK phosphorylation, and calcium oscillation signaling pathways.113 Additionally, Xia and colleagues demonstrated that APP can inhibit the differentiation of osteogenic lineage cells, which could be a significant reason for bone loss in AD patients.114 In addition to its direct effects on bone resorption and formation, Aβ deposition also impacts the Wnt/β-catenin signaling pathway in AD patients. Here, TNFSF11 is linked to Alzheimer disease.