New study finds that long-lived elderly people have more effective DNA repair mechanisms than normal people. This is a schematic diagram of DNA.
A new study, which for the first time sequenced the complete genes of 81 super-centenarians, found that their genomes do have an overwhelming presence. On the one hand, their bodies have more efficient DNA self-repair mechanisms, and on the other hand they have fewer malignant mutated genes that together protect them from deadly diseases during the aging process.
This study explored the genes of a total of 81 elderly people over the age of 105 and even 110, so they are called super centenarians. When it comes to genetic variations, the first thing that comes to mind is diseases related to aging, but there are also good variations. This study then mentions some genetic variations that serve to protect the body from disease. These genetic variations, or things that are different, are either inherent or occur later in life.
The 81 supercentenarians came from all over Italy, and the researchers took blood samples for complete genetic sequencing, compared their genes with those of another group of 36 adults from the same geographic area as them, with an average age of 68, and then compared them with data from another previous genetic analysis of centenarians. That previous study analyzed the genes of 333 Italian centenarians.
It turned out that there were some similarities between these supercentenarians and the centenarians whose genes were analyzed in the previous study: they had five common variations in two genes, COA1 and STK17A. The analysis shows that it is likely that the changes in these genes in turn affect the characterization of three other genes.
The first change was an increase in the activity of the STK17A gene. This gene is associated with three aspects of cellular health: coordinating the cellular response to DNA damage; promoting auto-apoptosis of damaged cells; and managing intracellular levels of reactive oxygen metabolism. Reactive oxygen is a byproduct of the aerobic metabolism of living organisms. Excessive levels of this substance are detrimental to cellular and genetic structure. These mechanisms are important for cellular health and many diseases are associated with imbalances in these three mechanisms.
The second genetic change is that the activity of the COA1 gene is reduced. This gene is important for the process of communication between the nucleus and the mitochondria. Mitochondria are like the energy factories of the cell and mitochondrial dysfunction is a key factor in aging.
Finally, the characterization of the biliverdin reductase A (BLVRA) gene was increased in these long-lived elderly. The function of this gene is to eliminate reactive oxygen species that are harmful to health.
In addition to these genetic changes, the researchers also examined the genetic variants that were detrimental to health in these elderly people.
They focused on seven common genetic variants that are detrimental to health. In the group of people over 100 years old, six of them had lower levels than the general population. The researchers believe that this is one of the factors that prevented them from developing such deadly diseases as heart disease during the aging process.
The study’s first author, Professor Massimo Delledonne of the University of Verona, Italy, said, “This is the first study to completely sequence the genes of a particularly long-lived group of older adults, providing a comprehensive understanding of their innate genetic background and acquired genetic changes, and to compare and analyze them with the genes of the general population.”
Principal investigator Claudio Franceschi, professor emeritus of immunology at the Università di Bologna, Italy, concluded, “Our analysis shows that both effective DNA self-repair mechanisms and fewer malignant mutated genes are the two aspects that protect these individuals from the diseases of aging and living to such an advanced age.”
The study was published May 4 in the journal eLife.
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