EU-funded scientists make breakthrough in ageing research
The physical process of ageing is one of the greatest mysteries of life, and now a partially EU-funded research team has thrown light for the first time on the process by identifying genetic variants that are associated with biological ageing in human beings. The breakthrough research, published in the journal Nature Genetics, may have important implications for the understanding of age-associated diseases. The research team, from the University of Leicester and King's College London in the UK, along with the University of Groningen in the Netherlands, analysed more than 500,000 genetic variations across the entire human genome to isolate the variants which are found near a gene called TERC (telomerase RNA component). EU support came from the projects GENECURE ('Applied genomic strategies for treatment and prevention of cardiovascular death in uraemia and end stage renal disease'), which received EUR 2.25 million in funding under the 'Life sciences, genomics and biotechnology for health' Theme of the Sixth Framework Programme (FP6), and ENGAGE ('European Network for Genetic and Genomic Epidemiology'), which has been allocated EUR 12 million of funding under the Health Theme of the Seventh Framework Programme (FP7). Professor Nilesh Samani of the Department of Cardiovascular Sciences at the University of Leicester, who was joint leader of the project, said, '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 ageing. 'In this study what we found was that those individuals carrying a particular genetic variant had shorter telomeres, i.e. [they] looked biologically older. Given the association of shorter telomeres with age-associated diseases, the finding raises the question of whether individuals carrying the variant are at greater risk of developing such diseases.' Professor Tim Spector from King's College London, who co-authored the study, said, 'The variants identified lie near a gene called TERC which 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. The effect was quite considerable in those with the variant, equivalent to between three to four years of 'biological ageing' 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.'
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Netherlands, United Kingdom