Recent research published in Nature Aging has uncovered a significant link between Alzheimer’s-related protein aggregates, senescent cells, and osteoporosis.

Studies indicate that individuals with Alzheimer’s are more prone to experience bone loss even before their diagnosis, with accelerated bone loss observed in Alzheimer’s model mice compared to their wild-type counterparts.

In the bones of Alzheimer’s mice, researchers found senescent fat cells exhibiting markers of cellular senescence, suggesting a connection between these cells and bone loss.

The primary factor implicated in this bone loss is SAP/PTX2, which is localized to senescent fat cells and has been shown to promote amyloid aggregation.

Additionally, antibodies against amyloid beta (Aβ) were discovered in the bones of Alzheimer’s mice, indicating that Alzheimer’s may contribute to premature bone aging.

In exploring potential therapies, the compound CPHPC, which targets SAP, demonstrated effectiveness in reducing both Aβ deposition and the prevalence of osteoclasts, opening new therapeutic avenues for addressing amyloid-related osteoporosis.

Further promising results were observed with treatments such as dasatinib and quercetin or ruxolitinib, which, when administered to Alzheimer’s mice, reduced SAP levels and showed potential in mitigating both bone loss and Aβ deposition.

However, further research is essential to determine the effectiveness of these therapies in humans and their implications for other amyloid-related conditions.

It's also noteworthy that amyloid tangles, typically associated with Alzheimer’s, can occur in other organs and are linked to aging, contributing to systemic amyloidosis, a potentially fatal condition.