Study suggests way to stop decline with age

TOKYO: Time walking can be unpleasant for the human body, but new research suggests a cause – and a possible solution – for some of the ailments and decline that often accompany aging.

Scientists have long known that cognitive decline as we age and that certain age-related diseases, including Alzheimer’s disease, are linked to inflammation, but they are still discovering precisely why and how it is. the case.

Research published in the journal Nature highlights 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 in memory and navigation tests.

The researchers found that higher levels of the hormone affected the metabolism of immune cells called macrophages, causing them to store energy rather than consume it.

This effectively starved the cells, sending them into a damaging inflammatory hyperdrive associated with age-related cognitive decline and several age-related diseases.

The hormone, prostaglandin E2 (PGE2), “is a major regulator of all types of inflammation, good and bad, and its effect depends on which receptor is activated,” senior author Katrin Andreasson told AFP. of the study.

“In this study, we identified the EP2 receptor … as the receptor that leads to energy depletion and maladaptive inflammation,” added Andreasson, professor of neurology at Stanford University.

Having isolated the role played by PGE2, Andreasson and his team then set out to see if there was a way to counter its negative effects.

They gave mice two experimental compounds capable of blocking the EP2 receptor and found that it reversed the metabolic problems seen in older macrophages – restoring their younger behavior and preventing destructive inflammatory activity.

They found similar effects in genetically engineered mice with deletions of the EP2 receptor.

– ‘Very excited’ –

Older mice that received the compounds or had the receptor removed from their genes performed as well as younger mice in tests of navigation and spatial memory, which deteriorate with aging and diseases like Dyssey’s disease. Alzheimer’s.

“Our study suggests that the development of maladaptive inflammation and cognitive decline during aging may not be a static or permanent condition, but rather that it can be reversed,” the study says.

Andreasson said the results, while still preliminary, could have implications for a wide range of conditions.

“This would apply to most inflammatory diseases related to age,” including Alzheimer’s disease, atherosclerosis and arthritis, she told AFP, saying she was “very excited” by the possible applications.

But the research is still in its early stages and several questions remain unanswered. 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’s unclear whether they could be toxic, although no harmful side effects were seen in the mice tested.

Andreasson said his team is currently working on several research questions, including further understanding of the mechanisms that produce cognitive decline and studying the role of cellular metabolic functions in aging.

“Although intriguing, this is early-stage research conducted in mice,” noted Susan Kohlhaas, research director 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 take before we know whether this strategy is likely to be successful for the treatment of dementia,” she added.

“We have to see experiences in environments that closely mirror the human brain.”