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As mammals age, inflammation levels increase. I’m not talking about painful reactions to injury or infection, but rather more subdued, squeaky background inflammation, which becomes more and more intense as we live. This growing inflammation has been linked to diabetes, high blood pressure, frailty, cancer, and almost every chronic health problem that we tend to see in old age. This also includes cognitive decline and, at least in this case, scientists believe it can be reversed by managing inflammation in the brain, as studies in mice have shown.
Researchers at the University of Brighton in the UK have found that microglia – a specialized population of macrophage-like cells in the central nervous system, which act as immune cells that defend the brain and spinal cord from foreign invaders – are very vulnerable to changes in the levels of inflammation, in particular to a molecule called prostaglandin E2 (PGE2).
When this molecule was in large quantities, the microglia found it difficult to carry out its normal cellular processes, and the associated cells did not produce energy as well as they could.
PGE2 levels naturally increase with age in our cells and those of other mammals due to the increasing number of senescent cells. These dysfunctional cells can no longer divide and their presence causes the release of PGE2, as well as other inflammatory molecules.
But there is a way to reverse this process. Write in the journal Nature, scientists described how PGE2 exerts its effects on cells by interacting with the EP2 receptor on macrophages, another important type of white blood cell.
When these white blood cells were treated in the lab with drugs that turned off this receptor, the cells recovered. Moving away from the Petri dish, the researchers replicated the experiment on mice.
The researchers genetically modified rodents that lacked the EP2 receptor and simply waited until they got old (the average lifespan of a mouse kept in captivity is two years). They then tested the cognitive abilities of these elderly mice by subjecting them to a barrage of tests, including navigating mazes and “object locating” tasks.
Strikingly, the researchers found that old, genetically engineered mice could learn and remember things just as well as their younger counterparts. The same effects were reproduced in old normal mice that were not genetically modified but were given drugs that turn the EP2 receptor on or off.
Essentially, this series of experiments shows that suppression of the PGE2 receptor may represent an important target for treating and possibly even reversing age-related cognitive impairment. Or at least, it seems to be the case in mice. Future clinical trials in humans may shed more light.
Meanwhile, research has shown that foods such as blueberries, strawberries, and spinach improve cognition in older mice and humans. These foods are high in fisetin, quercetin, and resveratrol, which are known to clear senescent cells from the body. One possible mechanism by which they can achieve this is by blocking PGE2 at the cellular level. So, until more research can offer simpler answers, stock up on spinach.
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