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You would be wrong. While we do have a few theories about why we, and other species we share the planet with, have evolved to grow old and die, we understand very little about the mechanism that makes living cells lose their ability to mend broken and damaged DNA. In a new study published Friday in the journal Science, a team of researchers has identified a molecule, named NAD+, which plays a key role as a regulator in protein-to-protein interactions that control DNA repair. Moreover, experiments in mice reveal that treating the animals with a precursor of NAD+, called NMN, significantly boosts their cells ability to repair age-related and radiation-caused DNA damage. Our results unveil a key mechanism in cellular degeneration and aging, but beyond that they point to a therapeutic avenue to halt and reverse age-related and radiation-induced DNA damage, the studys senior author David Sinclair, a professor at Harvard Medical Schooland the University of New South Wales School of Medicine in Sydney, said in a statement . The researchers then concluded that as the amount of NAD+ in cells declines with age, there arent enough of these molecules to prevent harmful interactions between proteins called DBC1 (which is found across a wide range of organisms, from bacteria to humans) and PARP1 (a protein that is known to control DNA repair). When this happens, damages to DNA accumulate over time, causing cell damage, mutationandeventually, death. It should be noted that the findings of the study do not bring us any closer to curing death, per se. However, they do open the door for the creation of drugs and intervention techniques that can reverse DNA damage associated with space travel and cancer treatments, and, to a certain extent, even reverse aging. This is the closest we are to a safe and effective anti-ageing drug that's perhaps only three to five years away from being on the market if the trials go well, Sinclair said . Related Articles

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