15 February 2010
ByAppeared in BioNews 545
Scientists have identified a genetic variant that may influence the rate at which a person will age. The finding, published in last week's edition of the journal Nature Genetics, could help identify which individuals are most susceptible to common age-related conditions, such as heart disease and Alzheimer's disease.
The research team headed by Professor Nilesh Samani, from the University of Leicester, and Professor Tim Spector, from King's College London, found that individuals with variants located near a gene known as TERC (telomerase RNA component) tended to have cells with shorter telomeres, a trait previously shown to make them age faster.
Professor Spector said: 'the effect was quite considerable in those with the variant, equivalent to between three-four years of biological ageing as measured by telomere length loss'. Those with two copies of the variant had the equivalent of six to seven years of extra biological ageing.
Telomeres are long sections of repetitive DNA which cap the ends of chromosomes to protect them from damage during cell division, rather like the plastic caps on the ends of shoelaces. Previous research has shown that ageing of human cells is delayed by the presence of an enzyme called telomerase, which acts to restore telomere length.
Professor Samani said that the study's findings could help explain the link between telomere length and biological age. 'In this study what we found was that those individuals carrying a particular genetic variant had shorter telomeres i.e. looked biologically older,' he told the Daily Telegraph.
In the search for genetic variants associated with telomere length, the researchers scanned the whole genome of more than 10,000 individuals for around 500,000 different genetic variants. They found that a number of gene variants located near the TERC gene occurred more frequently in those with shorter telomeres. This suggests that 'some people are genetically programmed to age at a faster rate', according to Professor Spector.
Professor Samani further described the finding as 'the first step to understanding why people age' and said that 'once we have a full understanding we should be able to manipulate it in a manner to influence how someone ages'.
These manipulations may take the form of screening programmes to identify people who are likely to develop age-related conditions early in life. Individuals at high risk could be offered preventative life-style advice and pre-emptive drugs to reduce their risk of developing these conditions.
Last year three US scientists won the 2009 Nobel Prize in Physiology and Medicine for their work showing that cells with damaged telomerase age faster and that ageing of human cells is delayed by the presence of telomerase.