Research suggests that Alzheimer’s disease may be influenced by immune system aging and dysfunction, particularly in microglia, the brain’s innate immune cells. Inflammation in the brain can stem from both systemic and local factors, with senescent cells in the body producing inflammatory signals that impact all tissues. Addressing immune system changes in the bone marrow, such as through young bone marrow transplantation, can reduce inflammation and improve clearance of Alzheimer’s-related amyloid-β. This approach highlights the potential of immune rejuvenation as a therapeutic strategy for Alzheimer’s disease.
In a recent study, young bone marrow transplantation in aged Alzheimer’s model mice led to a decrease in inflammation, improved amyloid-β clearance by circulating monocytes, and reduced amyloid-β burden in the brain. The findings support the notion that restoring a more youthful immune cell production can mitigate Alzheimer’s pathology and behavioral deficits. By targeting immunosenescence, or age-related immune changes, researchers are exploring promising avenues for treating Alzheimer’s disease and related conditions.
Rejuvenation of peripheral immune cells attenuates Alzheimer’s disease-like pathologies and behavioral deficits in a mouse model
The aging immune system experiences alterations in immune cell production, diversity, and function, collectively termed immunosenescence. These changes not only contribute to systemic aging but also increase susceptibility to age-related diseases like Alzheimer’s. To address this, researchers investigated immune rejuvenation through young bone marrow transplantation in aged Alzheimer’s model mice. The procedure restored gene expression, reduced senescence-related proteins, and improved amyloid-β clearance, ultimately alleviating Alzheimer’s pathology. This study highlights the potential of immune system rejuvenation as a therapeutic approach for Alzheimer’s disease.
