SLC40A1 and Alzheimer disease: Hepcidin treatment increases intracellular iron and promotes osteoclast differentiation of RAW264.7 cells.34 Iron overload, which is coupled with overexpression of hepcidin by the liver, contributes to unloading-induced bone loss.35 Studies have also shown that FPN in myeloid osteoclast precursors has an important role in regulating intracellular iron levels, osteoclastogenesis, and skeletal homeostasis in mice.36 However, little is known regarding the contribution of hepcidin to AD or AD-associated osteoporosis.