The quest for immortality may seem the stuff of science fiction, but evidence is emerging that our lifespans could be extended well beyond current averages.
Although some studies point to an inescapable limit of around 150 years old for humans, this still leaves us with a clear gap between our current life expectancy and our potential maximum.
A new study, published in Genome Research, has identified a group of genes that could play an essential role in bridging this divide.
The study, led by University College London (UCL) researchers in the UK, looked at genes that have previously been linked to long lifespans in small organisms like fruit flies, finding a link in humans as well.
The genes in question play an essential role in building proteins in our cells. Co-lead author Dr Nazif Alic from the Institute of Healthy Ageing at UCL says that quietening the actions of genes such as these can affect longevity.
"We have already seen from extensive previous research that inhibiting certain genes - involved in making proteins in our cells - can extend lifespan in model organisms such as yeast, worms and flies," he says.
This is the first time scientists have demonstrated the same link in humans. The results emerged from a review of genetic data from previous studies involving 11,262 people who had lived an exceptionally long life, to an age above the 90th percentile of their cohort.
They found that people with reduced activity of genes linked to two RNA polymerase enzymes were more likely to live very long lives.
They found evidence that the genes' effects were linked to their expression in specific organs, including abdominal fat, liver, and skeletal muscle, but also that the effect on longevity was much broader, transcending direct associations with specific age-related diseases.
Does this mean we can simply switch these genes off if we want to have a crack at a second century of life? Not quite.
There's a trade-off involved with the activity of these genes, with loss of function earlier in life associated with disorders known as ribosomopathies.
This is an example of a concept known as antagonistic pleiotropy, where genes that shorten our lives are selected for in evolution if they help us early in life and through our child-bearing years.
"Here, we have found that inhibiting these genes may also increase longevity in people, perhaps because they are most useful early in life before causing problems in late life," says Alic.
Clearly we need to hold on to these genes in our youth, but the findings suggest that existing drugs such as rapamycin, an immune regulator which acts to inhibit certain polymerase enzymes, could be used to promote healthy lifespan once we've cleared the hurdle of middle-age.
Professor Karoline Kuchenbaecker from the UCL Genetics Institute is enthusiastic about the results of this study, saying that bridging the gap between animal models and human applications, as this study did, is essential in the study of healthy ageing.
"Ageing research in model organisms, such as flies, and in humans are often separate efforts," she says. "Here we are trying to change this.
"In flies, we can experimentally manipulate ageing genes and investigate mechanisms. But ultimately, we want to understand how ageing works in humans. Bringing the two fields together has the potential to overcome the limitations of both fields."
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