New scientific research explains why we are aging at such a rapid rate

Population Aging occurs at an accelerated rate, so it is important to understand what is happening in the body at the molecular level over time. It is known that in many processes mTOR protein complexa key agent in many body functions and especially in metabolism, reports Agencia Sinc.

New work carried out by researchers from the National Center for Cancer Research (CNIO) has observed in animal models that when the activity of this protein complex is increased, but only moderately, aging is accelerated and the animals’ lifespan can be extended. is reduced to 20%.

Given the central role of mTOR in metabolismThis study provides clues to why diseases associated with aging appear or worsen in people with high body mass indexindicator related to obesity And inflammation.

It also provides information on why calorie restriction – a type of diet associated with longer lifespan in animals – may contribute healthy aging, because certain genes that are activated by nutrient restriction interact with mTOR. The study was published in Natural aging.

Premature aging of animals

The activity of the mTOR protein complex is regulated depending on the amount of nutrients available in the cell. The authors developed a system to trick mTOR into regulating its activity in animal models.

Inside cells, chemical signals are constantly coming and going through proteins, and mTOR is a key agent in cellular participates in energy use and cell metabolism. It is also known to affect longevityalthough it is still not entirely clear how.

To manipulate mTOR activity at will, the team focused not on mTOR itself, but on a protein that would send it a signal indicating the amount of nutrients available in the cell. Researchers have genetically modified this protein to “lie” and send a signal to mTOR that there are more nutrients in the cell than there actually are.

Thus, the mTOR chemical signaling pathway is activated as if the animals were eating more, although in fact their diet does not change. When animals with this mTOR-cheating protein reach adulthood, cell function begins to deteriorate and the characteristic symptoms of aging appear: thinning skin and damage to the pancreas, liver, kidneys and other organs.

20% shorter service life

Cells of the immune system come to repair them, but they are overloaded with the amount of damage, accumulate and, instead of repairing, cause inflammation, which further increases the problems in these organs.

The result of this vicious cycle is that the lifespan of these animals, in which mTOR is working more than usual, is reduced by 20%, which on a human scale would be equivalent to about 16 years.

The study sought to break this cycle by blocking immune reaction this causes inflammation. The organ damage then improved enough to extend a person’s life by several years.

For this reason, the authors argue that targeting chronic inflammation is “a potential therapeutic intervention that controls deteriorating health.” Ana Ortega-Molinafirst author and currently a researcher at the Center for Molecular Biology of Severo Ochoa.

Results extrapolated to humans

What happens when the information the mTOR receives is affected by mimicking nutrient excess is reminiscent of the changes typical of natural aging. The research team compared their model to naturally aging colonies of mice, both their own and non-genomes. National Institute on Aging (NIA) in Bethesda (USA), an institution that participates in the work.

For example, the activity of lysosomes—the organelles through which a cell removes and processes its waste—is reduced in both naturally aged animals and genetically modified ones.

“When there is an excess of nutrients, it is logical that the cell turns off the recycling activity of lysosomes, because this recycling begins especially when there are no nutrients,” explains the lead author. Alejo EfeyanHead of the Metabolism and Cell Signaling Group at CNIO.

This decrease in lysosome activity also occurs during human aging, as confirmed by a group of researchers. Consuelo Borras and Daniel Monleonfrom the University of Valencia, comparing blood samples from young people and people over seventy years of age.

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