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Ageing genes may affect cancer and heart risk

8 April 2013
Appeared in BioNews 699

Genes that influence the so-called 'biological age' of cells may also influence susceptibility to many age-related diseases.

In an international study, scientists identified seven genetic variants which regulate the length of DNA caps found at the ends of chromosomes, known as telomeres.

Dr Jess Buxton, from Imperial College London, who analysed over 5,500 samples for the study, said that the research had 'shown that some people have genetic variants that mean they have shorter telomeres and are at higher risk of age-related disease'.

Telomeres are lengths of repetitive DNA that are important in the correct replication of DNA when a cell divides. The cell machinery which replicates DNA is unable to copy the full chromosome and so a short bit of the telomere is lost during each division. In this way, the telomere acts as a buffer region and stops the essential genetic information contained in the chromosome from being lost. It also works to signal for the cell to stop dividing when the telomeres get too short.

The length of the telomere provides an indicator of the biological age of a cell, and the shortening of telomeres can be considered as the process of biological ageing. Accordingly, older people generally have shorter telomeres than young people.

But human telomeres are not of uniform length and at birth will depend on what people inherit from their parents. Furthermore, the rate at which telomeres shorten is different in different people. This means that two people of the same calendar age may have different biological ages.

In this study, researchers from 14 research centres around the world analysed DNA samples from over 48,000 people, and identified seven genetic variants linked to telomere length. On analysing medical records they found that, on average, people carrying the telomere-shortening variants had a higher risk of developing a number of age-related diseases including cancer, multiple sclerosis and coronary artery disease.

According to Nilesh Samani, professor of cardiology at the University of Leicester, and lead author of the study, 'this research strongly suggests that biological aging plays an important role in causing coronary artery disease'.

He added that the work 'at least partly explains why some patients develop it early and others don’t develop it at all even if they carry other risk factors'.

Dr Veryan Codd, senior research associate at the University of Leicester, who coordinated the study said that the suggestion of a causal link between telomere length and susceptibility brought into play 'the possibility that manipulating telomere length could have health benefits'. Although there is, Dr Codd noted, 'a long way to go before any clinical application'.

And the relationship between telomere length and health remains complex, Dr Codd added: 'We have to remember that some diseases are actually associated with longer telomere length'.

The study is published in Nature Genetics.

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