Researchers at the Albert Einstein College of Medicine, and colleagues, have found a clear link between living to 100 and the inheritance of a hyperactive version of an enzyme that rebuilds telomeres. Telomeres are relatively short sections of specialized DNA that sit at the ends of all chromosomes. Telomeres have been compared to the plastic tips at the ends of shoelaces that prevent the laces from unraveling. Each time a cell divides, its telomeres erode slightly and become progressively shorter with each cell division. Eventually, telomeres become so short that their host cells stop dividing and lapse into a condition called cell senescence. As a result, vital tissues and important organs begin to fail and the classical signs of aging ensue. In investigating the role of telomeres in aging, the researchers studied Ashkenazi Jews because they are a homogeneous population that has been well studied genetically. Three groups were enrolled: 86 very old, but generally healthy, people (average age 97); 175 of their offspring; and 93 controls (offspring of parents who had lived a normal lifespan). "As we suspected, humans of exceptional longevity are better able to maintain the length of their telomeres," said Dr. Yousin Suh, senior author of the paper. "And we found that they owe their longevity, at least in part, to advantageous variants of genes involved in telomere maintenance." More specifically, the researchers found that participants who have lived to a very old age have inherited mutant genes that cause their telomerase-making system to be extra active and able to maintain telomere length more effectively. For the most part, these people were spared age-related diseases such as cardiovascular disease and diabetes, which cause most deaths among elderly people.
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