Gene variant that causes aging discovered

London, UK, February 9 -- A new breakthrough study that proposes to end the diseases associated with aging of the skin has revealed a gene variant that causes biological aging in humans.

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Researchers from the University of Leicester and King's College London and the University of Groningen in the Netherlands jointly carried out this study that can help in better understanding cancer and aging in humans.

It may be noted that aging is categorized into chronological and biological aging. While chronological aging is the time elapsed since birth, biological aging is caused due to body cells that may make one look younger or older than their chronological age.

Dr Nilesh Samani, professor of cardiology in the Department of Cardiovascular Sciences at the University of Leicester and co-author of the study said, “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.”

“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,” he further said.

More than 500,000 genetic variations analyzed
The research team carried out a genome-wide investigation of more than 500,000 genetic variations in 12000 humans to find the gene that caused biological aging.

They found that a gene variant called TERC that is significant for maintaining telomere (end of chromosome) length caused biological aging in homo-sapiens.

According to the researchers, people having this gene variant had shorter telomeres that caused rapid aging.

Professor Tim Spector from King's College London, who also co-authored this research, informed, “The effect was quite considerable in those with the variant, equivalent to between 3-4 years of 'biological aging" as measured by telomere length loss.”

Useful study
“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,” said Dr Nilesh Samani.

“It is the first step to understanding why people age. Once we have a full understanding we should be able to manipulate it in a manner to influence how someone ages,” he added.

Smoking, inactiveness and obesity may trigger faster aging when combined with the TERC gene variant, and this finding can help in finding a cure for many diseases associated with early aging.

The present research has been published in the online journal Nature Genetics and was supported by the grants from the Wellcome Trust and the British Heart Foundation.