Zombified cells may drive aging, and scientists are devising new ways to get rid of them
Immune cells that clear old and dying cells get sluggish with age. Scientists think that rejuvenating these cells could help combat aging.
Aging may be driven by "zombie" cells that fail to die off properly, according to researchers. These damaged cells continue releasing harmful substances rather than being cleared by the immune system. Scientists are exploring ways to eliminate these senescent cells directly, but another approach could be to strengthen the body's cleanup system.
When cells die, they display proteins on their surface that signal immune cells called macrophages to engulf and destroy them. However, some cells refuse to die and become senescent, lingering in tissues for years and releasing chemicals that cause inflammation and damage. Factors such as DNA damage from oxidative stress, radiation, or normal cell division can lead to senescence. As people age, the number of senescent cells increases and is associated with various age-related conditions like heart disease and dementia.
Researchers have developed drugs called senolytics that force senescent cells to enter programmed cell death, reducing inflammation and improving tissue function. However, it's unclear why the immune system fails to eliminate senescent cells in the first place.
One study found that old macrophages have more EP2 receptors, which disrupt their ability to eat senescent cells effectively. EP2 is a receptor on macrophages that, when activated by PGE2, a molecule involved in inflammation, impairs macrophage function. In a 2001 study, researchers discovered a link between EP2-blocking drugs and a reduced risk of Alzheimer's disease in older adults.
A recent study by Stanford University neurologist Dr. Katrin Andreasson revealed that aging macrophages have higher EP2 receptor levels, leading to disrupted energy use and impaired cell function. This energy issue makes it difficult for macrophages to perform their role in consuming and eliminating senescent cells. Blocking the EP2 receptor in old mice restored normal energy use, reduced inflammation, and improved cognitive function.
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