New Research Suggests Link Between Amyloid Deposits in Brain and Bone Marrow Aging

Recent experimental studies conducted by researchers at Johns Hopkins University School of Medicine have provided groundbreaking evidence indicating that amyloid beta proteins—commonly associated with Alzheimer's disease—can accumulate in the bone marrow of aging mice. Unlike the dense amyloid plaques characteristic of Alzheimer’s in the human brain, these deposits in bone marrow are of a different form but still significant in their potential impact.

The study highlights that amyloid buildup occurs in organs outside the brain, such as the heart and kidneys, though the presence of amyloid in bone tissue remained largely unexplored until now. Dr. Mei Wan, a lead author of the study, emphasizes that understanding amyloid presence in the skeleton might be crucial, especially since Alzheimer’s disease and osteoporosis— a condition of low bone density—are both prevalent in aging populations.

The research specifically focuses on the role of fat cells within the bone marrow, called bone marrow adipocytes (BMAds), which release a protein known as SAP/PTX2. This protein appears to be a key player in triggering amyloid fiber formation. The accumulation of these fibers impairs osteoblast activity (bone formation) while activating osteoclasts (bone resorption), leading to bone loss.

In the experiments, mice aged from 4 to 24 months were treated with a compound called CPHPC (also known as Miridesap), which is designed to eliminate amyloid deposits. The mice received the drug via drinking water, and researchers observed that it reduced amyloid fibril buildup and reversed bone deterioration, suggesting a promising approach for osteoporosis treatment.

High-resolution imaging revealed that aged mice and those with Alzheimer’s played a role in the formation of ring-like amyloid fibril structures around BMAds. These deposits were associated with increased bone loss, but intervention with CPHPC successfully depleted these fibers,
pointing to a potential therapeutic target.

Dr. Wan notes that this is among the first studies to demonstrate harmful amyloid fiber buildup in the bone marrow of aged organisms. The findings suggest that fat cells in bone marrow secrete SAP/PTX2, which promotes amyloid formation, damaging bone health and possibly connecting to dementia risk. This research opens avenues for new treatments that could prevent or treat osteoporosis and potentially impact Alzheimer’s disease by focusing on eliminating age-related fat cell changes and amyloid-promoting proteins.

These insights offer a fresh perspective on the biological links between bone aging and neurodegenerative conditions, highlighting the importance of exploring bone health as a factor in cognitive decline and dementia prevention.