The increased activity of proteins that lengthen the telomeres is associated with the acceleration of aging, and not its slowdown, as previously thought. This conclusion was made by a group of American scientists from the University of California at Los Angeles, Boston University, Stanford University, and the Hebrew SeniorLife Nonprofit Research Institute. An article by researchers is published in the journal Nature Communications, and is briefly described in a press release on EurekAlert !.
Telomeres are the terminal regions of chromosomes that prevent DNA loss during cell division. However, each time during mitosis, telomeres are reduced, which leads to a gradual increase in genome instability. In the end, the cell stops dividing and dies. It is believed, however, that an enzyme called telomerase can extend cell life by lengthening telomerase DNA.
Another marker of aging is methylation, the process of the attachment of methyl groups to DNA. In this case, suppression or activation of certain genes may occur. For example, genes that promote neurodegeneration are activated with age, and DNA is suppressed, which prevents atherosclerosis. By the level of methylation, you can determine the biological age of a person, which does not always coincide with the chronological. People with a high proportion of methylated DNA are at high risk of premature death.
Researchers evaluated the methylation level in 9907 people and conducted a genome-wide search for associations, which study the associations between the phenotypic trait – in this case, the proportion of methylated DNA – and different gene variants on all chromosomes. SNPs — point mutations affecting a single nucleotide — were identified that were associated with high methylation levels. It turned out that one of the loci characterized by SNP data was the TERT gene, which encodes part of telomerase.
TERT point mutations associated with high methylation levels are also associated with elongated telomeres. According to scientists, this means that anti-age therapy, based on increased activity of telomerase, on the contrary, will contribute to aging. Thus, the opinion is refuted that human rejuvenation can be achieved by preventing the shortening of the terminal sections of the chromosomes.