Scientists claim that switching off certain immune cells can ‘age’ the brain

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 down the aging process in certain cells in our immune system, myeloid cells, may lie.

These cells play an important role in fighting infections and clearing up debris, but they often become too strong as we age, causing chronic inflammation.

The research indicates that shutting down these cells can ‘age’ the brain and delay the onset of several conditions, including heart disease, Alzheimer’s disease, cancer and weakness.

Although the findings are very early, the researchers hope that their drug manufacturers can help develop a compound that slows aging.

Research suggests that switching off myeloid cells can 'age' the brain and delay the onset of various conditions, including heart disease, Alzheimer's disease, cancer and fragility (stock image)

Research suggests that switching off myeloid cells can ‘age’ the brain and delay the onset of various conditions, including heart disease, Alzheimer’s disease, cancer and weakness (stock image)

WHAT ARE MYLOYDE CELLS?

Myeloid cells are found in the brain, circulatory system and peripheral tissues, where they play an important role in clearing dead cells, giving nutrients to other cells and paying attention to invasive pathogens.

However, as we age, our myeloid cells begin to malfunction, 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 the culture.

Surprisingly, it was enough to restore youthful metabolism and restore the age-related mental decline in old mice.

In the study, researchers from Stanford Medicine studied myeloid cells in old mice, as well as myeloid cells in cultures of people older than 65 and younger than 35.

Myeloid cells occur in the brain, circulatory system and peripheral tissues, where they play an important role in clearing dead cells, giving nutrients to other cells and alerting to invasive pathogens.

However, as we age, our myeloid cells begin to function, 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 the culture.

Surprisingly, it was enough to restore youthful metabolism and restore the 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 adapt the immune system, you can age the brain.”

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

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

Myeloid cells are found in the brain, circulatory system and peripheral tissues, where they play an important role in clearing dead cells, giving nutrients to other cells and paying attention to invasive pathogens.  However, as we age, our myeloid cells begin to malfunction, causing damage to innocent tissues.

Myeloid cells are found in the brain, circulatory system and peripheral tissues, where they play an important role in clearing dead cells, giving nutrients to other cells and paying attention to invasive pathogens. However, as we age, our myeloid cells begin to malfunction, causing damage to innocent tissues.

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

Unfortunately, since the hormone binds to these receptors, it leads to an increase in inflammation, causing damage to innocent tissues.

Professor Andreasson explained: ‘This powerful way drives aging. And it can be turned off. ‘

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

Older mice were even able to perform as well on young repeat tests and spatial navigation as young mice.

Of particular interest was one of the two compounds found to be effective, even if it does not penetrate the blood-brain barrier.

According to the team, this suggests that the repair of myeloid cells outside the brain can have a major impact on what goes on in the brain.

Unfortunately, according to the researchers, the compounds were not approved for human use, and may have toxic side effects.

However, the team hopes they can provide a roadmap for drugmakers to develop a safe connection to give to people.

HOW MAY SCIENTISTS USE TELOMERASES TO PREVENT THE AGING OF AGING?

Scientists have decoded an enzyme thought to stop 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 slowing or blocking the aging process, along with new treatments for cancer, researchers reported in April in the journal Nature.

Joyful scientists have announced that the 20-year quest to prevent the enzyme thought to prevent aging has been completed by repairing the points of chromosomes.

“It’s been a long time coming,” lead researcher Kathleen Collins, a molecular biologist at the University of California, Berkeley, said in a statement.

“Our findings provide a structural framework for understanding mutations in human telomerase diseases, and are an important step toward telomerase-related clinical therapy.”

Partial proteins and partial RNA (genetic material that gives instructions for building proteins) telomerase works on microscopic sheaths, known as telomeres, which cover the points of the chromosomes present in all cells.

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

Australian-American biologist Elizabeth Blackburn, who shared the 2009 Nobel Prize in Medicine for the discovery of telomeres and their protective function in the 1970s, compared them to the small plastic caps that do not weaken shoelaces.

Eventually, however, shoelaces and telomeres break off: each time a cell divides, the telomeres wear out a little more until the cell stops dividing and dies. Biologists agree that it is probably central to the natural aging process.

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