Interestingly, in patients with Alzheimer’s disease, who have a high risk of osteoporotic hip fracture, amyloid beta peptide, one of the pathological hallmarks of Alzheimer’s disease that is abnormally deposited in bone tissues [36], was shown to enhance RANKL-induced ERK and NF-κB activation and to promote osteoclastic bone resorption [37]. This evidence concerns the gene NFKB1 and Alzheimer disease.