--- title: "New Approach Emerges in Fight Against Aging" url: https://newscentral.site/new-approach-emerges-in-fight-against-aging/ language: en publisher: "News Central Site" section: "Science" published: 2026-10-07T10:00:00.000Z updated: 2026-10-07T18:36:52.668Z id: 404ba8b2-fc33-4ac7-a7d5-bac8da404bd7 source: "Live Science https://www.livescience.com/health/aging/zombified-cells-may-drive-aging-and-scientists-are-devising-new-ways-to-get-rid-of-them" attribution: "Link to https://newscentral.site/new-approach-emerges-in-fight-against-aging/ and name News Central Site when you quote or summarize this story." --- # New Approach Emerges in Fight Against Aging Scientists are exploring ways to revitalize the body's natural cleaning mechanism to eliminate "zombie cells" that accumulate with age. A new approach in the fight against aging is gaining momentum as scientists explore ways to revitalize the body's natural cleaning mechanism and eliminate "zombie cells that accumulate with age. These damaged cells, known as senescent cells, refuse to die and instead release chemicals that drive inflammation and damage surrounding tissues. The buildup of such cells has been linked to various age-related diseases, making it a prime target for emerging treatments aimed at reversing or stalling the signs of aging. According to Roel de Maeyer, an immunologist at the University of Oxford, rejuvenating the immune system could potentially rectify many problems associated with aging. He notes that hospitals are often filled with older individuals suffering from infections that younger people rarely need medical attention for. The main goal of these rejuvenating therapies is to enable people to live healthier and longer lives. By boosting the body's natural defenses, scientists hope to prevent age-related diseases from taking hold in the first place. The immune system plays a crucial role in maintaining tissue health by constantly removing old, dysfunctional, or dead cells. This process involves macrophages, which engulf and destroy damaged cells displaying eat me signals on their surfaces. However, as people age, this cleanup mechanism becomes less effective, allowing senescent cells to linger in tissues for years. These zombified cells can cause a significant amount of damage by releasing chemicals that drive inflammation and promote disease. The formation of senescent cells is often the result of DNA damage caused by oxidative stress, radiation, or even normal cell division. According to de Maeyer, cells have intricate mechanisms to decide when it becomes too dangerous to continue dividing. If a cell can no longer divide, it typically undergoes programmed cell death or becomes senescent. As researchers delve deeper into the biology of aging, they are beginning to explore new ways to target and eliminate senescent cells. This could potentially pave the way for novel treatments aimed at reversing or stalling the signs of aging in the human body. The accumulation of senescent cells in the body has been linked to various age-related conditions, including heart disease and dementia. As a result, researchers are exploring ways to eliminate these zombie cells, which can cause damaging inflammation and impaired organ function. While an excess of senescent cells is generally considered a bad sign, some tissues may benefit from their presence in limited quantities. For instance, senescence can aid in wound healing by promoting the repair of damaged tissue. However, this beneficial aspect of senescence is overshadowed by its detrimental effects when it occurs on a larger scale. Studies have shown that using drugs to eliminate senescent cells can lead to significant improvements in inflammation and cellular aging in mice. These medications, known as senolytics, induce senescent cells to undergo programmed cell death, effectively reducing their numbers. This reduction has been linked to improved tissue function and reduced inflammation. However, researchers are still trying to understand why the immune system fails to eliminate senescent cells naturally. To address this question, scientists have turned their attention to macrophages, a type of cell responsible for devouring dying cells. By studying these cells, researchers hope to uncover the underlying mechanisms that allow senescent cells to persist. One key discovery in this area has been the identification of a receptor on macrophages called EP2. Research suggests that old macrophages have an increased number of these receptors, which impede their ability to consume senescent cells effectively. This deficiency in macrophage function may contribute to the accumulation of senescent cells over time. The removal of the EP2 receptor from lab mice has been found to restore the macrophages' functionality and reduce the number of senescent cells. As a result, these genetically modified mice displayed improved health metrics compared to their unaltered counterparts of the same age, with some even showing performance comparable to younger mice on certain tasks. A key player in the aging process has been identified as a molecule called PGE2, which interacts with the EP2 receptor to trigger cellular stress and inflammation. Research has shown that prostaglandins like PGE2 play a crucial role in cell communication during times of injury or stress, contributing to fever, pain, and swelling. Drugs such as ibuprofen have been found to reduce inflammation by blocking prostaglandin production, leading scientists to investigate the connection between these medications and age-related diseases. A large study published in 2001 discovered a significant link between long-term use of prostaglandin-blocking drugs and a lower risk of developing Alzheimer's disease in individuals aged 55 and older. The study's findings sparked interest among researchers, including Dr. Katrin Andreasson, a neurologist at Stanford University, who began exploring the relationship between EP2 activity and aging. Her team made an important breakthrough in 2021 by identifying that macrophages from older adults had higher levels of the EP2 receptor. Increased EP2 activity was found to disrupt energy production in these cells, causing them to store glucose rather than burning it for fuel like their younger counterparts do. As a result, the cells were unable to perform their functions effectively, including gobbling up damaged or dead cells, which requires a significant amount of energy. Dr. Andreasson explained that blocking the EP2 receptor restored normal energy use in macrophages from older mice, leading to reduced inflammation and improved cognitive function compared to those with high EP2 activity. This breakthrough has significant implications for understanding the aging process and developing new treatments to combat age-related diseases. Further research is needed to fully understand the mechanisms behind EP2 activity and its role in aging, but these findings offer a promising starting point for investigating potential therapeutic strategies to target this molecule and alleviate age-related health issues. The study by Andreasson's team has revealed another consequence of aging: old mice accumulate many senescent neutrophils, a type of short-lived immune cell that acts as the first line of defense against germs. Neutrophils are typically very short-lived and die within days, but with age they become more prone to senescence and accumulate in the body. This is an unusual phenomenon because neutrophils are inherently inflammatory, making it valuable to clear them from tissues. Andreasson's team found that old mice have too much EP2 activity in their macrophages, which prevents them from getting rid of these accumulated neutrophils. This may explain why deleting EP2 appears to have anti-aging effects in multiple organs. Another factor contributing to the accumulation of senescent cells is the don't eat me signal used by zombie cells. These cells employ a protein called CD47, which signals that they are healthy and alive and should not be destroyed by macrophages. This don't eat me signal gets amplified in senescent cells, impairing macrophages' ability to function properly when interacting with these cells. As a result, macrophages lose the ability to engulf dying, nonsenescent cells, leading to an accumulation of cellular debris. Reducing the don't eat me signal used by senescent cells could be beneficial in targeting therapeutic strategies against aging. However, CD47 is found on all living cells, making it challenging to deplete its numbers across the body. A potential solution to weakening the don't eat me signal on senescent cells has been identified through research involving a specific enzyme called EP2. This enzyme modifies CD47 on these cells, and blocking it helped spare macrophages from its effects in lab mice. Blocking the enzyme EP2 could be a more selective approach to targeting senescent cells, but experts caution that translating this concept into effective anti-aging treatments for humans is fraught with challenges. The success of EP2-blocking experiments in lab mice may not translate directly to human biology due to inherent variability and environmental factors. Genetically identical rodents bred in controlled environments are fundamentally different from the complex biological systems found in humans, introducing confounding variables that must be addressed. While some research has explored EP2-blocking drugs as cancer treatments, their potential application in aging remains underexplored. Further investigation is needed to determine whether these compounds can effectively target senescent cells and promote healthy aging. Drugs targeting CD47 are still in an early stage of development. Researchers have used both human and mouse macrophages in experiments, but the approach has yet to be tested as an anti-aging treatment in living mice or humans. A different strategy for rejuvenating immune cells was investigated by de Maeyer's team in 2020. They blocked a protein called p38, which is highly active in older adults' macrophages, and found that this helped restore their ability to recognize and consume dying cells in specific tests. As researchers continue to explore the relationship between aging and the presence of zombie cells," they are making progress in finding ways to eliminate these problematic cells. In their latest study, a team led by Dr. Andreasson successfully blocked the EP2 receptor without causing any adverse effects in mice. The next step for this research would be to determine how to safely inhibit the EP2 receptor in humans. This involves further investigation and confirmation of the findings in human subjects. The goal is to develop a method that can effectively eliminate these zombie cells without posing any health risks. By finding ways to get rid of these dysfunctional cells, scientists may be able to slow down or even reverse the aging process. However, more research is needed before this becomes a reality. --- Source: [Live Science](https://www.livescience.com/health/aging/zombified-cells-may-drive-aging-and-scientists-are-devising-new-ways-to-get-rid-of-them) Published by News Central Site: https://newscentral.site/new-approach-emerges-in-fight-against-aging/