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Study hints at cause, possible solution to halt decline due to ageing

A study published in the journal Nature points to the role of a messenger hormone called prostaglandin E2 (PGE2), which is found in much higher levels in older men and mice than in their younger counterparts.

Scientists have long known that dementia as we grow older and age-related diseases including Alzheimer’s are linked to inflammation, but they are still discovering why and how this happens.

A study published in the journal Nature points out the role of messenger hormones in higher levels in older adults and mice than in their younger counterparts.

When the hormone was blocked in older mice, they were able to perform with many younger mice in testing their memory and mobility.

Researchers have found that high levels of hormones that affect the body’s immune system are called macrophages, causing them to store energy rather than use it.

That starve cells to death, exposing them to the dangerous hyperdrive of inflammation associated with age-related dementia and several age-related diseases.

The hormone, prostaglandin E2 (PGE2), “is a major regulator of all forms of inflammation, good and bad, and your effect depends on the active receptor,” the study’s lead author Katrin Andreasson told AFP.

“In this study, we identified the EP2 receptor … as a receptor that leads to the elimination of energy and inflammation that are malignant,” adds Andreasson, a professor of neurology at Stanford University.

They gave the mice two experimental chemicals that could block the EP2 receptor and found it to restore metabolic problems detected in older macrophages – restoring their youthful character and preventing destructive inflammatory activities.

They found similar effects in mice genetically modified by the removal of the EP2 receptor.

‘I am very happy’

Older mice get a chemical or receptor removed from their genes and younger mice when tested for roaming and local memory, both of which are damaged by aging and diseases such as Alzheimer’s.

Andreasson said the findings, although still in its infancy, could affect many different situations.

“This will be especially helpful in age-related inflammatory diseases,” including Alzheimer’s, atherosclerosis and arthritis, he told AFP, saying he was “very happy” about the potential applications.

It is not yet clear how much PGE2 is, and how it accumulates over a lifetime.

And none of the experimental compounds have been tested in humans, so it is not clear whether they can be toxic, although no adverse effects were observed in the tested rats.

Andreasson said his team is now working on a number of questions raised by research, including a full understanding of the mechanisms that produce dementia and investigating the role of cell metabolism functions in aging.

“Although interesting, this is a first-line study performed on mice,” notes Susan Kohlhaas, research director at Alzheimer’s Research UK, who was not involved in the study.

“While the results deserve to be followed, there is still a lot to be done before we will know if this strategy will be successful in treating dementia,” he added.

“We need to see experiments in areas that focus on the human brain.”

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