A new study suggests that aging may be driven in part by a breakdown in communication between two key immune cells. Researchers found that aging macrophages become less effective at clearing worn-out neutrophils, allowing chronic inflammation to build up and accelerate organ decline. In mice, blocking a single inflammatory receptor called EP2 restored this cleanup process, preserving brain, heart, liver, kidney, muscle, and memory function while reducing frailty and inflammation. Although the findings are still preclinical, they reveal a promising target for future anti-aging therapies aimed at extending healthy lifespan rather than simply increasing longevity.
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