Research Projects

Alzheimer's disease is often linked to fractures and declines in bone mineral density, even in early stages of the disease. The link between bone loss and AD pathogenesis is unclear, but the presence of Amyloid β peptide (Aβ)42 in bone and a transgenic mouse model over-expressing mutant APP suggests that Aβ 42 could be a causative factor. However, studies on the effects of Aβ 42 on osteoblast and osteoclasts are contradictory. Clinical data suggest that Aβ-42 might involve in osteoporosis, but the effects on osteoblast, osteoclast differentiation, activity, and bone remodeling remain unclear. Using age-dependent serum proteomics, metabolomics, microRNA, and lipidomics approaches, researchers aim to study common factors responsible for early phage of pathogenesis in AD and osteoporosis mouse models. The study will also correlate findings with human cohorts to understand the driving mechanisms involved in comorbid conditions like Alzheimer's disease and osteoporosis. Bone mass, regulated by exercise-related loading and mechanical strain, fluctuates to maintain a target mechanical strain level. Osteocytes, the principal bone cells, are key components of the registration network, integrating stimuli generated by mechanical loading and communicating with surface osteoblasts and osteoclasts to regulate bone mass. The presence of β-amyloid deposits in Alzheimer's patients may lead to increased incidence of osteoporosis due to functional disruption of mechanically adaptive bone modeling.