A protein appears to be capable of extending the 'green years' by delaying the ageing process: it is a molecule guarding the pattern of active genes in young cells. Over the years, this pattern of gene activity goes haywire and we age. This is shown by a study on mice conducted by David Sinclair of Harvard Medical School in Boston, according to which by enhancing the production of the molecule, 'sirt1', mice stay young longer, and their lifespan is extended by 24 to 46 per cent. According to reports in the journal Cell, the sirt1 protein is responsible for keeping the DNA young and controlling that only the 'youth genes', those genes that normally need to be switched on in various organs and tissues to make them function well, are active.

This protein is an old acquaintance of ageing experts such as Sinclair, who became famous for his discovery in animals of the 'anti-ageing' virtues of resveratrol, an antioxidant in red wine. Experts have discovered that the function of sirt1 is twofold: it maintains the stability of the genome by controlling the correct gene set-up in the cells of each tissue; it also turns on the 'green light' for those genes that need to be switched on and red for those that need to remain switched off. Sirt1 also mediates the repair of DNA damage that accumulates over the years. Sinclair's group saw that by mutating the activity of sirt1 in mice, the pattern of gene activation changes to become similar to that found in the brains of elderly mice; in other words, the 'youth' genes are switched off and the 'old age' genes are switched on. The researchers therefore observed that by increasing the amount of sirt1 in the mice, they live longer. The hope, they concluded, is that these improvements in longevity can be reproduced by administering drugs that stimulate sirt1.

Taken from Corriere della Sera Scientific source: Evidence for a Common Mechanism of SIRT1 Regulation by Allosteric Activators Science 8 March 2013: Vol. 339 no. 6124 pp. 1216-1219