Turning off certain immune cells can ‘age’ the brain.

Turning off certain immune cells can ‘age’ the brain.

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From brain training apps to botox, many people will try everything to go back in time.

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

These cells play a vital role in fighting infections and cleaning up debris, but they are often depleted as we age, causing chronic inflammation.

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 frailty.

Although the findings are at an early stage, the researchers hope they can help drug makers develop a compound to slow aging.

Research indicates that shutting down 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 indicates that shutting down myeloid cells can ‘age’ the brain and delay the onset of various conditions, including heart disease, Alzheimer’s disease, cancer and fragility (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 cleaning up dead cells, supplying nutrients to other cells, and monitoring invading pathogens.

However, as we age, our myeloid cells begin to malfunction, causing damage to innocent tissues in the process.

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

Surprisingly, this was sufficient to restore juvenile metabolism and restore age-related mental decline in old rats.

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

Myeloid cells are found in the brain, circulatory system and peripheral tissues, where they play an essential role in cleaning up dead cells, supplying nutrients to other cells, and monitoring invading pathogens.

However, as we age, our myeloid cells begin to malfunction, causing damage to innocent tissues in the process.

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

Surprisingly, 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 adjust the immune system, it can reduce the age of the brain.’

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

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

Myeloid cells are found in the brain, circulatory system and peripheral tissues, where they play an essential role in cleaning up dead cells, supplying nutrients to other cells, and monitoring invading pathogens. However, as we age, our myeloid cells begin to show dysfunction, inflicting damage on innocent tissues in the process.

Myeloid cells are found in the brain, circulatory system and peripheral tissues, where they play an essential role in cleaning up dead cells, supplying nutrients to other cells, and monitoring invading pathogens. However, as we age, our myeloid cells begin to show dysfunction, inflicting damage on innocent tissues in the process.

In the study, the researchers found that cells from older mice and humans had a much higher number of EP2 on their surfaces and also produced more PGE2.

Unfortunately, as the hormone binds to these receptors, it leads to increased inflammation, causing damage to innocent tissues.

Professor Andreasson explained: ‘This powerful path leads to aging. And it can be reduced. ‘

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

The older mice were even able to perform as well on recall tests and space navigation as the young mice.

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

According to the team, this suggests that redefining myeloid cells outside the brain can have a big effect on what happens inside the brain.

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

However, the team hopes to be able to provide a roadmap for drug manufacturers to develop a safe compound to administer to humans.

HOW CAN SCIENTISTS USE TELOMERASE TO REVERSE THE AGING PROCESS?

Scientists have decoded an enzyme that supposedly stops aging in plants, animals and humans as part of a recent groundbreaking study.

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

Enthusiastic scientists announced the completion of a 20-year mission to map the enzyme that prevents aging by repairing the tips of chromosomes.

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

‘Our results provide a framework for understanding mutations in human telomerase disease and represent an important step towards clinical therapy related to telomerase.

Part protein and part RNA (genetic material that relays instructions for building proteins) telomerase acts in microscopic sheaths, known as telomeres, which cover the tips of the chromosomes found within all cells.

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

Australian-American biologist Elizabeth Blackburn, who shared the Nobel Prize in Medicine in 2009 for the discovery of telomeres and their protective function in the 1970s, compared them to the tiny plastic covers that prevent the wear of shoelaces.

Eventually, however, the ends of the shoelace and the telomeres break: each time a cell divides, the telomeres wear out a little more, until the cell stops dividing and dies. This, according to biologists, is probably fundamental to the natural aging process.

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