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French Media AgencyJanuary 21, 2021 5:03:00 PM IST
The passage of time can be cruel to the human body, but new research points to a cause, and a possible solution, for some of the ailments and decline that often come with age. Scientists have long known that cognitive decline as we age and specific age-related diseases, including Alzheimer’s, are linked to inflammation, but they are still discovering precisely why and how this is the case. Research published in the journal Nature points to the role of a messenger hormone found at much higher levels in older people and mice than their younger counterparts. When the hormone was blocked in older mice, they were able to perform as well as younger rodents on tests of their memory and navigation.
The study gave mice two experimental compounds that can block the EP2 receptor and found that they reversed the metabolic problems seen in older macrophages, restoring their more youthful behavior and preventing destructive inflammatory activity.
The researchers found that higher levels of the hormone affected the metabolism of immune cells called macrophages, prompting them to store energy rather than consume it.
That effectively starved the cells, sending them into a damaging inflammatory hyperdrive associated with age-related cognitive decline and various age-related diseases.
The hormone, prostaglandin E2 (PGE2), “is an important regulator of all types of inflammation, both good and bad, and its effect depends on the receptor that is activated,” said study lead author Katrin Andreasson. AFP.
“In this study, we identified the EP2 receptor … as the receptor that leads to energy depletion and maladaptive inflammation,” added Andreasson, a professor of neurology at Stanford University.
After isolating the role played by PGE2, Andreasson and his team set out to see if there was a way to counter its negative effects.
They gave mice two experimental compounds that can block the EP2 receptor and found that it reversed metabolic problems seen in older macrophages, restoring their more youthful behavior and preventing destructive inflammatory activity.
They found similar effects in mice that were genetically modified with deletions of the EP2 receptor.
Very excited
Older mice that received the compounds or had the receptor deleted from their genes performed just as well as young mice when subjected to spatial memory and navigation tests, both of which deteriorate with aging and diseases like Alzheimer’s.
“Our study suggests that the development of maladaptive inflammation and cognitive decline in aging may not be a static or permanent condition, but can be reversed,” the study says.
Andreasson said the findings, while still preliminary, could have implications for a wide range of conditions.
“This would apply to most age-related inflammatory diseases,” such as Alzheimer’s, atherosclerosis and arthritis, she told AFP, saying she was “very excited” about the possible applications.
But the investigation is still in its early stages and there are several unanswered questions. It is not yet clear how much PGE2 is too much and how it builds up throughout life.
And none of the experimental compounds have been tested in humans, so it’s unclear whether they could be toxic, although no harmful side effects were seen in the mice tested.
Andreasson said his team is now working on several questions raised by the research, including a more complete understanding of the mechanisms that produce cognitive decline and investigating the role of cellular metabolic functions in aging.
“While intriguing, this is early-stage research conducted in mice,” said Susan Kohlhaas, research director at Alzheimer’s Research UK, who was not involved in the study.
“While the results deserve further follow-up, there are many steps to go before we know if this is likely to be a successful strategy for treating dementia,” he added.
“We need to see experiments in environments that closely mirror the human brain.”
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