Genetically altered mice that can live a third longer than average have thrown light on the mechanisms of ageing. Italian scientists produced the mice by removing a gene that appears to control how the body repairs chemical damage. Research in organisms such as worms, yeast and flies has shown a link between increased lifespan and a vigorous response to oxidative stress - damage by reactive chemicals in the body, especially forms of oxygen. But until the publication of this study in the journal Nature, no such link had been demonstrated in mammals. Pier Pelicci from the European Institute of Oncology in Milan and colleagues from Perugia University and New York, found that mice lacking in the protein p66shc were more resistant to oxidisation and therefore lived longer than normal mice. Although the researchers are not yet sure why this happens, they believe the normal function of the missing gene may be to repress repair of the damage. The genetic mutation could produce a repair pathway that is permanently switched on, according to the study. US scientist Leonard Guarente of the Massachusetts Institute of Technology commented in the same issue of Nature that, 'We may be at a watershed in the study of ageing. Although the conclusions must be regarded as provisional until larger groups of animals are studied, the results support the proposal that oxidative damage is involved in ageing.' He added: 'They also indicate modification of the response to oxidative damage can have a considerable effect of life span, without apparent negative side-effects.
Sources and References
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'Methuselah' mice resist ageing with gene defect
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The p66shc adaptor protein controls oxidative stress response...
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Scientists link a single gene to longer life in mice
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Researchers identify lifespan-boosting gene
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