Scientists Extend Telomeres: How Can This Help Turn Back Aging?

Scientists say they've found a way to increase the length of telomeres -- the caps that protect chromosomes in our cells from deterioration -- that have been linked to disease and aging when they shorten.

Lengthening those telomeres could lead to treatments for a number of age-related or genetic conditions, researchers at Stanford University say.

Telomeres protect chromosomes, structures on the ends of DNA strands that hold all our genetic information, from becoming damaged during the process of cell division.

However, with each successive cell division the telomeres become shortened until they reach a point where they can no longer protect chromosomes from deteriorating.

This complicates cell studies in laboratories searching for treatments for aging-related diseases difficult, as researchers can only monitor a few cell divisions before the subject cells die.

The Stanford researchers, in an effort to increase the length of telomeres, used a modified form of RNA containing the code sequence for the active component of telomerase.

Known as TERT, the component is an enzyme created by stem cells that maintains the health of telomeres as they are passed to the next generation.

Just three applications of the modified RNA in human cells over several days increased the telomere length by up to 10 percent, the researchers report in the FASEB Journal.

"Now we have found a way to lengthen human telomeres by as much as 1,000 nucleotides, turning back the internal clock in these cells by the equivalent of many years of human life," says Helen Blau, a professor of immunology and microbiology. "This greatly increases the number of cells available for studies such as drug testing or disease modeling."

The lengthening effect is temporary, lasting around 48 hours, then the newly lengthened telomeres begin shortening again during each successive cell division in the normal way, the researchers say.

The fact that cells in which the telomeres have been lengthened don't keep dividing indefinitely is important, they point out, because if they did they would be too dangerous for any therapies in humans because of a risk of cancer.

"This suggests that a treatment using our method could be brief and infrequent" and still be effective, says study co-author John Ramunas, a postdoctoral scholar.

There are a number of possibilities for such treatments, Blau says.

"This new approach paves the way toward preventing or treating diseases of aging," she says. "There are also highly debilitating genetic diseases associated with telomere shortening that could benefit from such a potential treatment."

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