Animal studies elucidated that elevated secretion of sclerostin could cross the blood-brain barrier, inhibit Wnt-β-catenin signaling in the brain, and impair cognitive function in mice.28 Clinical studies also showed that elevated plasma sclerostin was associated with high amyloid-β load in the human brain.31 The underlying mechanisms mediating the complex bone-brain interorgan connections need to be further unraveled, which may have untapped potential in early detection or therapeutic target identification for dementia. This evidence concerns the gene SOST and dementia.