Scientists have identified 25 genetic mutations that could help explain how humans evolved to live such long lives compared to our cousins cousins.
Humans can live up to 120 years, while the species of some closest primates live half of that period.
Worldwide, it is now believed that there are as many as half a million centenarians.
Scientists say the new finding could also help them develop new drugs to treat age-related diseases, which could help us live even longer.
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Scientists have identified 25 genetic mutations that could help explain how humans evolved to live such long lives compared to our cousins cousins (stock image)
Scientists have developed a new method to identify 25 genes associated with wound healing, blood coagulation and cardiovascular disorders.
Senescence, or biological aging, refers to the general deterioration of an organism, which leads to an increased susceptibility to diseases and, ultimately, to death.
It is a complex process that involves many genes.
Flies can expect to live for four weeks, horses for thirty years, while some hedgehogs can live up to two centuries.
Researchers led by the Institute of Evolutionary Biology (EBI) identified some of the genes that may have been crucial to extend the life of our species, as well as primate with a longer life.
They studied the genomes of seventeen primate species, including humans, according to the study published in the journal Molecular Biology & Evolution.
From the point of view of aging, primates are interesting because although they are very similar, there are great differences between species in terms of longevity.
Of all the species studied, only three (humans and two macaques) lived longer than the common ancestor.
This shows that they have experienced a relatively rapid process of life evolution, said Arcadi Navarro, a research professor at the Catalan Institution for Research and Advanced Studies (ICREA) and the leader of the study.
Of all the species studied, only three (humans and two macaques) lived longer than the common ancestor (stock image)
The scientists compared these species with those of the fourteen other primate species in order to detect the mutations present in those with a longer life.
"This would be very suggestive evidence that these genes have helped extend their lives," said Dr. Navarro.
After the comparison, twenty-five mutations were identified in the genes associated with wound healing, coagulation and a large number of cardiovascular conditions.
"The results are significant, because it requires a flexible and adaptable control of the coagulation mechanisms in the species that live longer," said Gerard Muntane, lead author of the study and postdoctoral researcher at the OIE.
He said that "they confirm the theory of the pleiotropy of aging".
This proposes that "certain mutations can have different effects depending on the stage of life: they help us in the early stages but damage us in later stages, once the reproductive stage is over," he said.
The authors suggest that the results could help to develop new therapeutic targets for the treatment of diseases related to aging.
HOW COULD SCIENTISTS USE TELOMERASE TO REVERSE THE AGING PROCESS?
The scientists decoded an enzyme designed to stop aging in plants, animals and humans as part of a recent study.
Unraveling the structure of the complex enzyme, called telomerase, could lead to drugs that slow down or block the aging process, along with new treatments for cancer, researchers reported in the journal Nature in April.
Excited scientists announced the completion of a 20-year mission to map the enzyme believed to prevent aging by repairing the tips of chromosomes.
"It has taken a long time to arrive," said lead researcher Kathleen Collins, a molecular biologist at the University of California at Berkeley, in a statement.
"Our findings provide a structural framework for understanding mutations in human telomerase disease and represent an important step toward clinical therapy related to telomerase."
Part of the protein and part of the RNA (genetic material that transmits instructions to build proteins) telomerase acts on microscopic sheaths, known as telomeres, that 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 the "Y", which differ between males and females.
The 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 with the tiny plastic capsules that prevent the laces from fraying.
Eventually, however, the tips of the shoes and the telomeres break: every time a cell divides, the telomeres wear out a little more, until the cell stops dividing and dies. This, according to biologists, is probably central to the natural aging process.