It is speculated that both the disorders share a common etiology; abnormally expressed amyloid depositions in the brain can cause AD, whereas when deposited in the bone, they interfere with the receptor activator of nuclear factor-kappa-Β ligand (RANKL) signaling cascade leading to an increase in osteoclastic activity thereby, decreasing the BMD and leading to the development of osteoporosis [12]. The gene discussed is TNFSF11; the disease is osteoporosis.