The increased activity of telomere-lengthening proteins is associated with the acceleration of aging, and not its slowdown, as previously thought. This conclusion was reached by a group of American scientists from the University of California at Los Angeles, Boston University, Stanford University and the Institute for Aging Research at the non-profit organization Hebrew SeniorLife. The researchers' article was published in the journal Nature Communications, briefly described in a press release on the EurekAlert! Website.
Telomeres are the ends of chromosomes that prevent DNA loss during cell division. However, each time during mitosis, telomeres contract, which leads to a gradual increase in genome instability. Eventually, the cell stops dividing and dies. It is believed, however, that an enzyme called telomerase can prolong cell life by lengthening telomerase DNA.
Another marker of aging is methylation, the process of attaching methyl groups to DNA. In this case, suppression or activation of certain genes can occur. For example, with age, genes that contribute to neurodegeneration are activated and DNA is suppressed, which prevents atherosclerosis. The level of methylation can be used to determine the biological age of a person, which does not always coincide with the chronological one. People with a high proportion of methylated DNA are at high risk of premature death.
The researchers assessed methylation levels in 9,907 people and conducted a genome-wide association search that examines associations between a phenotypic trait - in this case, the proportion of DNA methylated - and different gene variants on all chromosomes. SNPs - point mutations affecting one nucleotide - have been identified that have been associated with high levels of methylation. It turned out that one of the loci for which these SNPs were characteristic was the TERT gene, which encodes a part of telomerase.
Point mutations in TERT associated with high levels of methylation are also associated with elongated telomeres. According to scientists, this means that anti-aging therapy based on increasing telomerase activity, on the contrary, will promote aging. Thus, the opinion is refuted that human rejuvenation can be achieved by preventing the shortening of the terminal sections of chromosomes.
