Short Telomeres and Accelerated Aging

All of the rare accelerated aging conditions appear to be caused by one aspect of "normal" aging exaggerated and run wild to cause great biochemical damage. Researchers now think they understand what underlies another of these conditions: "Sufferers of the disease, called dyskeratosis congentia, tend to have problems in tissues in which cells multiply rapidly - skin, hair, nails, tongue, gut and bone marrow - and usually die between the ages of 16 and 50 from bone marrow failure, or the inability to replenish their blood cells. ... Each time a cell divides, the protective caps at the ends of chromosomes shorten - and when these caps are gone, so are we. Now, by using an unconventional strategy to shorten telomeres in mice, [researchers] have not only created the first faithful mouse model for studying [dyskeratosis congentia], but they have revealed the molecular defect behind the disease. ... these results suggest that in patients suffering from dyskeratosis congenita, the enzyme telomerase can't elongate telomeres as fast as the nucleases chew them away. ... Clearly, the next step is to understand how telomeres are degraded in human cells. We need to identify the nucleases at work and find out how they are regulated."



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