Neuroinflammation And Cellular Senescence In Brain Aging And Neurodegeneration
Our brains, like the rest of our bodies, undergo changes as we age. A key factor in how our brains age, and how some people develop conditions like Alzheimer’s and Parkinson’s, is a process called “neuroinflammation,” which is a complex, ongoing immune response within the brain. Normally, our brain’s immune cells, such as microglia and astrocytes, protect us. However, with age, these cells can become dysfunctional, shifting from protective roles to promoting inflammation. This chronic inflammation is further fueled by “cellular senescence,” a state where cells stop dividing but remain active, releasing a mix of inflammatory signals and harmful substances known as the senescence-associated secretory phenotype (SASP). These senescent cells accumulate in the aging brain, creating a toxic environment. This persistent inflammation involves various molecular pathways, which are constantly active, contributing to a vicious cycle of damage. This cycle can also involve issues with the blood-brain barrier, allowing harmful substances to enter the brain, and the accumulation of abnormal proteins, like those seen in Alzheimer’s. Understanding these mechanisms opens new doors for potential treatments. Researchers are exploring strategies to modulate the function of these brain immune cells, inhibit the core inflammatory pathways, and even use “senolytics”—drugs designed to clear out those problematic senescent cells. Other approaches include boosting the brain’s natural anti-inflammatory defenses and repurposing existing drugs. By targeting this chronic brain inflammation, there is significant promise in developing ways to slow down brain aging and prevent or treat neurodegenerative diseases.
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