As mammals age, inflammation levels increase. I’m not talking about painful reactions to wounds or infections, but rather a more discrete and painful background inflammation that gets more and more intense as we live. This growing inflammation has been linked to diabetes, high blood pressure, fragility, cancer and almost all of the chronic health problems that we often see in old age. This also includes cognitive decline and, at least in this case, scientists believe it can be reversed by controlling inflammation in the brain, as studies in mice have shown.
Researchers at the University of Brighton, UK, found that microglia – a specialized population of macrophage-like cells in the central nervous system, that act as immune cells that defend the brain and spinal cord from foreign invaders – are very vulnerable to changes in inflammation levels, particularly for a molecule called prostaglandin E2 (PGE2).
When this molecule was in large quantities, the microglia had problems carrying out their normal cellular processes and the related cells did not generate 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. Writing in the newspaper Nature, the scientists described how PGE2 exerts its effects on cells, interacting with the EP2 receptor on macrophages, another important type of white blood cell.
When these white blood cells were treated in the laboratory with drugs that turned off this receptor, the cells recovered. Moving away from the Petri dish, the researchers replicated the experiment on rats.
The researchers genetically modified rodents that lacked the EP2 receptor and simply waited for them to age (the average life of a mouse kept in captivity is two years). They then tested the cognitive abilities of these elderly rats, subjecting them to a series of tests, including navigating mazes and “object location” tasks.
Surprisingly, the researchers found that the old genetically modified mice could learn and remember things as well as their younger colleagues. The same effects have been replicated in old, normal mice that have not been genetically modified, but have received drugs that activate or deactivate the EP2 receptor.
Essentially, this series of experiments shows that suppression of the PGE2 receptor can represent an important target for treatment and perhaps even reverse age-related cognitive disorders. Or at least it seems to be the case with mice. Future clinical trials in humans may shed more light.
In the meantime, research has shown that foods like blueberries, strawberries and spinach improve cognition in mice and older people. These foods are rich in fisetin, quercetin and resveratrol, which are known to release senescent cells in 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 more direct answers, stock up on that spinach.
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