Paper in Nature Genetics demonstrates that mutations in TERC conferes a shorter telomere length, which is associated with age-related diseases.
Scientists report the identification of variants associated with biological aging in humans. The team analyzed more than 500,000 genetic variations across the entire human genome to identify these variants, which are located near a gene called TERC.
The study, published in Nature Genetics, was conducted by researchers from the University of Leicester and King’s College London, working with University of Groningen in The Netherlands. The paper is titled “Common variants near TERC are associated with mean telomere length.”
There are two forms of aging—chronological aging and biological aging, whereby the cells of some individuals are older (or younger) than suggested by their actual age—explains British Heart Foundation professor of cardiology at the University of Leicester Nilesh Samani who co-led the project. “There is accumulating evidence that the risk of age-associated diseases including heart disease and some types of cancers are more closely related to biological rather than chronological age.
“What we studied are structures called telomeres, which are parts of one’s chromosomes. Individuals are born with telomeres of certain length, and in many cells telomeres shorten as the cells divide and age. Telomere length is therefore considered a marker of biological aging.
“In this study what we found was that those individuals carrying a particular genetic variant had shorter telomeres, i.e., looked biologically older. Given the association of shorter telomeres with age-associated diseases, the finding raises the question whether individuals carrying the variant are at greater risk of developing such diseases.”
TERC is already known to play an important role in maintaining telomere length. “What our study suggests is that some people are genetically programmed to age at a faster rate,” remarks professor Tim Spector from King’s College London and co-leader of the study. “The effect was quite considerable in those with the variant, equivalent to between three to four years of biological aging as measured by telomere length loss.
“Alternatively genetically susceptible people may age even faster when exposed to proven bad environments for telomeres like smoking, obesity, or lack of exercise and end up several years biologically older or succumbing to more age-related diseases.”