07 June 2019

Turning age

The fracture of the human aging curve occurred at 50 years

At this time, according to scientists, the work of genes associated with aging is changing

Polina Loseva, "The Attic"

The search for a molecular "aging program" has not yet been crowned with success. Therefore, it is still impossible to talk about the age of the onset of aging, nor about a universal way to stop it. Scientists from the UK, Finland and the USA analyzed the work of genes in the brains and muscles of people from 20 to 90 years old and found that before and after 50, the activity of genes associated with age differs significantly. Apparently, at the age of 50 there is some significant restructuring at the genetic level. At least some of the candidates for "pills for old age" can postpone it.

An unambiguous answer to the question "When does the body begin to age?" still not found. Moreover, if we perceive aging as an accumulation of damage, then we can assume that it begins right from conception, that is, it appears together with life. But this approach does not allow us to predict at what point it is worth starting to struggle with old age. For elderly people whose body already carries the burden of age-related diseases, the "old age pill", even if it is found, may not help. Therefore, it is necessary to act earlier.

A group of researchers collected data on genes that work in the nerve and muscle cells of people 20-55 and 50-91 years old, and built their own model of aging. Scientists have selected those genes whose work changes with age. Among them, we identified those that are somehow related to two key parameters of cell life – the ability to breathe (absorb oxygen and produce energy) and insulin sensitivity. It is believed that it is the violation of cellular respiration that causes breakdowns in cells and their death. And the increased activity of insulin causes the cell to increase its metabolism, as a result of which toxic metabolic products accumulate in the cell.

People aged 20-55 had about 700 such genes, about two-thirds of them worked weaker with age, and one-third, on the contrary, were more active. In the older group, aged 50-91, 76% of these genes unexpectedly "lost" their connection with age-related changes. Based on this, scientists have suggested that a "midlife crisis" in aging occurs around the age of 50, when some genetic program that was previously active suddenly stops working.

To test whether it is possible to postpone the shutdown of this program, the researchers acted on the culture of muscle cells with different drugs-candidates for "remedies for old age". All of them somehow block signaling pathways associated with insulin–like growth factor and the protein complex mTORC - the main stimulators of cellular metabolism. They found 24 molecules that had a real effect on cells and affected the work of 46% of the "aged" genes.

Thus, the results of the study give hope that at least at the genetic level, half of the midlife crisis can be postponed "for later".

Article by Timmons et al. Longevity‐related molecular pathways are subject to midlife 'switch' in humans published in the journal Aging Cell.

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