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PETBioNewsNewsDead end for the 'longevity gene'?

BioNews

Dead end for the 'longevity gene'?

Published 3 October 2011 posted in News and appears in BioNews 627

Author

Dr Louisa Petchey

Image by Peter Artymiuk via the Wellcome Collection. Depicts the shadow of a DNA double helix, on a background that shows the fluorescent banding of the output from a DNA sequencing machine.
CC BY 4.0
Image by Peter Artymiuk via the Wellcome Collection. Depicts the shadow of a DNA double helix, on a background that shows the fluorescent banding of the sequencing output from an automated DNA sequencing machine.

A gene associated with increased lifespan in a number of organisms is now thought to have no effect on longevity after a second look revealed significant flaws in the original studies on which the assumptions were based. The findings will disappoint the manufacturers of many anti-ageing creams that claim to work by activating the gene, but are unlikely to put a stop to research...

A gene associated with increased lifespan in a number of organisms is now thought to have no effect on longevity after a second look revealed significant flaws in the original studies on which the assumptions were based. The findings will disappoint the manufacturers of many anti-ageing creams that claim to work by activating the gene, but are unlikely to put a stop to research. The gene is still known to play an important role in protecting against the damage of high-fat diets and other age-related diseases.

The existence of a 'longevity gene' was supported by evidence from a number of different studies, but 'none seem to stand up to close scrutiny', according to Dr David Gems from the Institute of Healthy Ageing at University College London, who headed up the UK-based investigation. 'Far from being a key to longevity', the gene has 'nothing to do with extending life', he said.

The gene, called SIRT1 in humans, is also found in yeast, worms and flies and produces proteins called sirtuins. Previous research showed that higher levels of sirtuins in these model organisms increased lifespan compared to their normal or 'wild type' counterparts, in some cases by 50 percent. But when Dr Gems and colleagues looked at the strain of worm used to study the effects of higher sirtuin expression, they found it had an extra genetic mutation that was causing the increase in lifespan.

It was a similar story with the fly studies. When researchers checked that the level of sirtuin was the only difference between the wild type and test strains, they were unable to detect any difference in the length of time they lived for. The study, also refuted the claim that resveratrol, found in anti-ageing creams and red wine, is able to activate sirtuins, or that they are responsible for the increase in fly lifespan induced by dietary restriction, which was found to work independently of sirtuins.

But disproving these previous findings is no bad thing according to Dr Gems: 'Revising old ideas can be as important as presenting new ones to assure scientific progress. This work should help to redirect scientific efforts toward those processes that really do control ageing'.

Professor Johan Auwerx from the Ecole Polytechnique Federale de Lausanne in Switzerland agrees that the findings put 'a final nail in the coffin' for the role of sirtuins in longevity, but believes that they still have a 'long life as a subject for further exciting research'. Writing a commentary on the study, published in the same issue of Nature, Professor Auwerx and colleagues point to the 'overwhelming body of evidence' that sirtuin activation promotes metabolic fitness that may help us overcome the effects of unhealthy diets and lifestyles. 'Don't write sirtuins off', they conclude.

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