Biology

Anti-aging research uncovers new role for telomeres

Anti-aging research uncovers n...
A new study suggests that telomeres, protective caps on the tips of chromosomes, might play a different role in aging than previously thought
A new study suggests that telomeres, protective caps on the tips of chromosomes, might play a different role in aging than previously thought
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A new study suggests that telomeres, protective caps on the tips of chromosomes, might play a different role in aging than previously thought
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A new study suggests that telomeres, protective caps on the tips of chromosomes, might play a different role in aging than previously thought

Aging affects everybody, so it’s easy to understand why so much scientific attention is focused on studying it. Scientists in Canada now claim to have found that telomeres play a different role in cellular aging than previously thought.

One of the main points of interest in anti-aging biology are what’s known as telomeres. These are sections of “junk” DNA that form caps on the ends of chromosomes, protecting important genetic information from damage when a cell divides. But a piece of the telomere is eroded away with each cell division, and when it gets too short the cell stops dividing entirely, entering a dormant state known as senescence. The build-up of these senescent cells contributes to a range of symptoms we associate with aging, such as frailty and age-related diseases.

The implication of this model is that telomeres take on a pre-emptive protection role – they signal to cells to stop dividing as soon as one telomere wears out. But there is evidence to suggest that cell division can continue with as many as five dysfunctional telomeres.

So for the new study, the researchers investigated what’s going on. They reproduced cellular aging in a population of cells in the lab, inducing all of their telomeres to become dysfunctional. Then, they closely watched what was happening inside each cell.

The team found that telomeres don’t seem to halt cell division in advance to prevent damage to the genome – instead, an accumulation of that DNA damage is what triggers senescence.

“What’s most surprising is that, before really entering senescence, the cells divide one last time,” says Francis Rodier, corresponding author of the study. “In fact, the cell division caused by telomere dysfunction is so unstable that it ends up creating genetic defects. Contrary to what was believed, senescent cells have an abnormal genome. That’s what we show in our study.”

It’s a departure from current models, but in essence the new find is just a different means to the same end. Telomere length is still associated with aging, and finding ways to repair them could still yield new anti-aging therapies, as could clearing out or rejuvenating senescent cells.

The research was published in the journal Nucleic Acids Research.

Source: Université de Montréal

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Ralf Biernacki
That one more division makes a crucial difference; it means that senescent cells, rather than being just torpid cells that no longer divide but function more-or-less normally, are in fact seriously damaged and dysfunctional mutants. This goes a long way towards explaining why treatments that exterminate senescent cells are so beneficial.