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The Development That Reverses Aging
We know that time progresses aging for the human body, but new research points to a reason 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 certain age-related diseases, including Alzheimer's, are linked to inflammation, but they still uncover exactly why and how this happened.
Research published Wednesday in the journal Nature reveals the role of a messenger hormone in older humans and mice at much higher levels than their young counterparts.
When the hormone was inhibited in older mice, they were able to perform better as well as younger rodents in memory and navigation tests.
Researchers found that higher hormone levels affect the metabolism of immune cells called macrophages, encouraging them to store energy rather than consume it.
This effectively starves cells and sends them to a damaging inflammatory hyperdrive that contributes to age-related cognitive decline and various age-related diseases.
The hormone prostaglandin E2 (PGE2) is "the main regulator of all kinds of inflammation, both good and bad, and its effect depends on the receptor that is activated," Katrin Andreasson, senior author of the study, told AFP.
"In this study, we identified the EP2 receptor as the receptor that causes energy depletion and incompatible inflammation," added Andreasson, a professor of neurology at Stanford University.
Very exciting
Having isolated the role played by PGE2, Andreasson and his team then set out to see if there was a way to prevent its negative effects.
They administered two experimental compounds to mice that could block 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 mice genetically modified by deletion of the EP2 receptor.
As well as older mice that receive the compounds or delete the receptor from their genes, young mice when tested for navigation and spatial memory were also impaired with diseases such as aging and Alzheimer's.
"Our study suggests that maladaptive development of inflammation and cognitive decline in aging are not static or permanent, but can be reversed," the study says.
Andreasson said that while the findings are preliminary, they could have implications for a wide variety of conditions.
"This will be true for most age-related inflammatory diseases," she told AFP.
"There are a lot of them, for example atherosclerosis ... metabolic syndrome, frailty, arthritis, Alzheimer's disease," he added, "very excited" about possible applications.
But research is still in its early stages, and there are a few unanswered questions. 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 unclear whether they were toxic, although no harmful side effects were seen in the mice tested.
Andreasson said his team is currently working on several questions raised by the research, including better understanding the mechanisms that cause cognitive decline and investigating the role of cell metabolism functions in aging.
Research published Wednesday in the journal Nature reveals the role of a messenger hormone in older humans and mice at much higher levels than their young counterparts.
When the hormone was inhibited in older mice, they were able to perform better as well as younger rodents in memory and navigation tests.
Researchers found that higher hormone levels affect the metabolism of immune cells called macrophages, encouraging them to store energy rather than consume it.
This effectively starves cells and sends them to a damaging inflammatory hyperdrive that contributes to age-related cognitive decline and various age-related diseases.
The hormone prostaglandin E2 (PGE2) is "the main regulator of all kinds of inflammation, both good and bad, and its effect depends on the receptor that is activated," Katrin Andreasson, senior author of the study, told AFP.
"In this study, we identified the EP2 receptor as the receptor that causes energy depletion and incompatible inflammation," added Andreasson, a professor of neurology at Stanford University.
Very exciting
Having isolated the role played by PGE2, Andreasson and his team then set out to see if there was a way to prevent its negative effects.
They administered two experimental compounds to mice that could block 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 mice genetically modified by deletion of the EP2 receptor.
As well as older mice that receive the compounds or delete the receptor from their genes, young mice when tested for navigation and spatial memory were also impaired with diseases such as aging and Alzheimer's.
"Our study suggests that maladaptive development of inflammation and cognitive decline in aging are not static or permanent, but can be reversed," the study says.
Andreasson said that while the findings are preliminary, they could have implications for a wide variety of conditions.
"This will be true for most age-related inflammatory diseases," she told AFP.
"There are a lot of them, for example atherosclerosis ... metabolic syndrome, frailty, arthritis, Alzheimer's disease," he added, "very excited" about possible applications.
But research is still in its early stages, and there are a few unanswered questions. 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 unclear whether they were toxic, although no harmful side effects were seen in the mice tested.
Andreasson said his team is currently working on several questions raised by the research, including better understanding the mechanisms that cause cognitive decline and investigating the role of cell metabolism functions in aging.
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