Turning off certain immune cells can ‘age’ the brain, scientists claim

From brain training apps to botox, many people will try anything to turn back the clock.

But a new study suggests that the key to slowing the aging process could lie with certain cells in our immune system called myeloid cells.

These cells play a critical role in fighting infection and cleaning up debris, but they often go into overdrive as we age and cause chronic inflammation.

The research indicates that turning off these cells can ‘age’ the brain and delay the onset of a variety of conditions, including heart disease, Alzheimer’s disease, cancer and vulnerability.

While the findings are at a very early stage, the researchers hope they can help drug manufacturers develop a compound to slow aging.

Research indicates that turning off myeloid cells can 'age' the brain and delay the onset of a variety of conditions, including heart disease, Alzheimer's disease, cancer and frailty (stock image)

Research indicates that turning off myeloid cells can ‘age’ the brain and delay the onset of a variety of conditions, including heart disease, Alzheimer’s disease, cancer and frailty (stock image)

WHAT ARE MYELOID CELLS?

Myeloid cells are found in the brain, circulatory system and peripheral tissues, where they play an essential role in clearing dead cells, providing nutrients to other cells, and keeping an eye out for invading pathogens.

However, as we age, our myeloid cells begin to dysfunction, causing damage to innocent tissues.

In the study, the researchers blocked the interaction of a hormone called PGE2 and a receptor on myeloid cells in the mice and human cells in culture.

Amazingly, this was enough to restore youthful metabolism and restore age-related mental decline in old mice.

In the study, Stanford Medicine researchers studied myeloid cells in aged mice, as well as myeloid cells in cultures of people over the age of 65 and under 35.

Myeloid cells are found in the brain, circulatory system, and peripheral tissues, where they play an essential role in clearing dead cells, providing nutrients to other cells, and keeping an eye out for invading pathogens.

However, as we age, our myeloid cells begin to malfunction, damaging innocent tissues.

In the study, the researchers blocked the interaction of a hormone called PGE2 and a receptor on myeloid cells in the mice and human cells in culture.

Amazingly, this was enough to restore youthful metabolism and restore age-related mental decline in old mice.

Professor Katrin Andreasson, professor of neurology and neurological sciences and senior author of the study, explained, “If you modify the immune system, you can age the brain.”

PGE2 is a hormone that belongs to a group known as prostaglandins and does many different things in the body, depending on the cells it binds to.

For example, when PGE2 binds to a receptor called EP2 on myeloid cells, it starts inflammatory activity in the cells.

Myeloid cells are found in the brain, circulatory system, and peripheral tissues, where they play an essential role in clearing dead cells, providing nutrients to other cells, and keeping an eye out for invading pathogens.  However, as we age, our myeloid cells begin to dysfunction, causing damage to innocent tissues in the process

Myeloid cells are found in the brain, circulatory system, and peripheral tissues, where they play an essential role in clearing dead cells, providing nutrients to other cells, and keeping an eye out for invading pathogens. However, as we age, our myeloid cells begin to dysfunction, causing damage to innocent tissues in the process

In the study, the researchers found that the cells of older mice and older people had much higher numbers of EP2 on their surface and also produced more PGE2.

Unfortunately, because the hormone binds to these receptors, it leads to an increase in inflammation, damaging innocent tissues.

Professor Andreasson explained: ‘This powerful path stimulates aging. And it can be switched back. ‘

Using two compounds, the researchers blocked PGE2’s ability to bind to EP2 and were able to reverse this inflammation and age-related cognitive decline.

In fact, older mice were able to perform just as well on memory and spatial navigation tests as young mice.

Of particular interest was one of the two compounds, which proved to be effective even though it does not cross the blood-brain barrier.

According to the team, this suggests that resetting myeloid cells outside of the brain can have a huge effect on what is happening in the brain.

Unfortunately, the compounds are not approved for human use and have potentially toxic side effects, the researchers said.

However, the team hopes they can provide a roadmap for drug manufacturers to develop a secure compound that can be given to humans.

HOW CAN SCIENTISTS USE TELOMERASE TO REVERSE THE AGING PROCESS?

Scientists have decoded an enzyme thought to halt the aging of plants, animals and humans as part of a recent breakthrough study.

Unraveling the structure of the complex enzyme called telomerase could lead to drugs that slow or block the aging process, along with new treatments for cancer, researchers reported in the journal Nature in April.

Delighted scientists announced the completion of a 20-year quest to map the enzyme believed to fight aging by repairing the ends of chromosomes.

“It has taken a long time,” lead researcher Kathleen Collins, a molecular biologist at the University of California at Berkeley, said in a statement.

“Our findings provide a structural framework for understanding mutations in human telomerase disease, and represent an important step towards telomerase-related clinical therapies.”

Partial protein and part RNA (genetic material that transmits instructions for building proteins) telomerase acts on microscopic sheaths, known as telomeres, that cover the ends of chromosomes in all cells.

In humans, each cell contains 23 pairs of chromosomes, including one pair of sex chromosomes – the ‘X’ and ‘Y’ – that differ between men and women.

Australian-American biologist Elizabeth Blackburn, who shared the Nobel Prize in Medicine in 2009 for discovering telomeres and their protective function in the 1970s, compared them to the tiny plastic caps that keep shoelaces from fraying.

Ultimately, however, shoelace tips and telomeres break down: Each time a cell divides, the telomeres wear out a bit more, until the cell stops dividing and dies. This, biologists agree, is likely central to the natural aging process.

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