Photo by Asdrubal luna on Unsplash.

Despite our best efforts, the quest for immortality has been fruitless and the fountain of youth remains undiscovered. Instead, science has focused on slowing the clock. Now, researchers at Arizona State University have discovered a new method that promises to delay the rate of aging with a greater understanding of the mechanics behind DNA. It’s a discovery that represents a step forward in living longer, healthier lives.

To understand aging, it’s important to understand a little about DNA. The body needs cells to divide and they do so by following instructions contained in chromosomes, which are X-shaped threads of DNA. The bad news is that with each division a little bit of genetic information is lost. This results in decreased performance and an eventual ‘gumming up’ of the works. This degradation cause the signs commonly associated with aging.

Our lives would be short indeed if no defence mechanism existed to protect chromosomes during division. Fortunately, each arm of a chromosome is capped with telomeres  – repeating sequences of DNA – that take the hit during division and protect the rest of the chromosome. However, with time, telomeres also degrade and can no longer contain the damage.

Scientists have found direct correlation between telomere length and longevity, which is why research has focused on slowing down their deterioration, repairing damage and bolstering their strength. Of particular interest is an enzyme called telomerase that replenishes telomeres and could further improve their longevity if it could be modified.

Arizona State researchers took a close look at telomerase and discovered that it acted like a car driving with the handbrake on. Their discovery was an extension on the common knowledge that each enzyme encodes a repeating sequence of six nucleotides on to the tip of chromosomes. The scientists found a pause signal that operates after each sequence to ensure that cell division occurs correctly. However, once the division occurs, the pause continues to have a residual effect, reducing the efficiency of the enzyme.

“Telomerase has a built-in braking system to ensure precise synthesis of correct telomeric DNA repeats,” says Julian Chen, the lead researcher for the study. “This safe-guarding brake, however, also limits the overall activity of the telomerase enzyme. Finding a way to properly release the brakes on the telomerase enzyme has the potential to restore the lost telomere length of adult stem cells and to even reverse cellular aging itself.”

The hope is that by targeting this signal they can improve the function of telomerase and improve the lifespan of adult stem cells. The researchers do sound a note of caution since the pause signal plays a critical role in ensuring cells stay healthy. Removing it altogether could have disastrous consequences, including cancer, which has been known to co-opt telomerase to maintain its growth.

Clearly, more research needs to be done, as the team at Arizona State works on recommendations on how to avoid potential pitfalls. Though we may not be able to stop the clock, the future of successful aging is a bit brighter as new developments to slow its ticking continue to discovered.