Sclerostin: A Potential Link between Osteoporosis and Alzheimer's Disease.

Abstract

Osteoporosis and Alzheimer's disease (AD) are age-related health conditions that significantly impact patients and society. Sclerostin, a glycoprotein secreted by osteocytes, regulates bone metabolism by inhibiting the Wnt/β-catenin signaling pathway, which controls bone formation. Elevated sclerostin levels in osteoporosis contribute to increased bone resorption and reduced osteoblast activity. Recent studies suggest that sclerostin also affects the central nervous system, where its expression in brain tissues may impair synaptic function and accelerate cognitive decline in AD. Both osteoporosis and AD share common risk factors, such as aging, neuroinflammation, and oxidative stress, which exacerbate disease progression. Targeting sclerostin with therapies like Romosozumab, a monoclonal antibody that inhibits sclerostin activity, has shown promise in treating osteoporosis by promoting bone formation. Given the potential connection between sclerostin and AD, there is growing interest in exploring sclerostin modulation as a therapeutic strategy for AD, though challenges such as crossing the blood-brain barrier remain. This review discusses the emerging relationship between osteoporosis and AD, emphasizing the shared molecular pathways and the potential for sclerostin-targeted therapies to benefit both conditions. Further research is needed to understand the causal links between sclerostin, osteoporosis, and AD, and to assess the effectiveness of sclerostin modulation in managing both diseases simultaneously.