New research provides a possible way to stop age-related decline, including memory loss and other illnesses.
TOKYO: The rise of time can be unfriendly to the human body, but new research suggests a cause – and possible solution – for some of the ailments and deteriorations 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 exactly why and how this is the case.
Research published in the journal Nature determines the role of a messenger hormone that is much higher in older people and mice than their younger counterparts.
When the hormone was blocked in older mice, they were able to outperform both younger rodents in their memory and navigation.
The researchers found that higher levels of the hormone affected the metabolism of immune cells, called macrophages, and led them to store energy rather than consume it.
It effectively starved the cells and sent them to a harmful 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,” senior author Katrin Andreasson told AFP.
“In this study, we identified the EP2 receptor … as the receptor leading to energy depletion and maladaptation,” added Andreasson, a professor of neurology at Stanford University.
Andreasson and her team isolated the role played by PGE2 and went on to see if there was a way to counteract its negative consequences.
They administered two experimental compounds that could block the EP2 receptor to mice and found that it reversed the metabolic problems seen in older macrophages, restoring their youthful behavior and preventing destructive inflammatory activity.
They found similar effects in mice genetically modified with the removal of the EP2 receptor.
– ‘Very excited’ –
Older mice that received the compounds or had the receptor removed from their genes, as well as young mice were tested for navigation and spatial memory, both of which weaken with aging and diseases such as 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 that it can be reversed,” the study says.
Andreasson said the findings, while still preliminary, could have implications for a wide range of conditions.
“This applies to most age-associated inflammatory diseases,” including Alzheimer’s, atherosclerosis and arthritis, she told AFP, saying she was “very excited” about the possible applications.
But the research is still at an early stage, and there are several questions that have not been answered. It is not yet clear how much PGE2 is too much and how it accumulates over a lifetime.
And none of the experimental compounds have been tested in humans, so it is unclear whether they can be toxic, although no harmful side effects have been seen in the mice tested.
Andreasson said her team is now working on several questions raised by the research, including better understanding the mechanisms that cause cognitive decline and examining the role of cell metabolism functions in aging.
“While intriguing, it is research in mice that was conducted in the early stages,” remarked Susan Kohlhaas, director of research at Alzheimer’s Research UK, who was not involved in the study.
“Although the results deserve further follow-up, there are still many steps to be taken to know if this is likely to be a successful strategy for treating dementia,” she added.
“We need to see experiments in environments that accurately reflect the human brain.”