Drazgul said:

You shouldn't focus on treating age-related diseases, focus on treating aging itself. It's the worst disease.

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Senescent cells -- cells that have stopped dividing -- accumulate with age and accelerate the aging process. Since the "healthspan" (time free of disease) in mice is enhanced by killing off these cells, the scientists reasoned that finding treatments that accomplish this in humans could have tremendous potential.

The scientists were faced with the question, though, of how to identify and target senescent cells without damaging other cells.

The team suspected that senescent cells' resistance to death by stress and damage could provide a clue. Indeed, using transcript analysis, the researchers found that, like cancer cells, senescent cells have increased expression of "pro-survival networks" that help them resist apoptosis or programmed cell death. This finding provided key criteria to search for potential drug candidates.

Using these criteria, the team homed in on two available compounds -- the cancer drug dasatinib (sold under the trade name Sprycel®) and quercetin, a natural compound sold as a supplement that acts as an antihistamine and anti-inflammatory.

Further testing in cell culture showed these compounds do indeed selectively induce death of senescent cells. The two compounds had different strong points. Dasatinib eliminated senescent human fat cell progenitors, while quercetin was more effective against senescent human endothelial cells and mouse bone marrow stem cells. A combination of the two was most effective overall.

Next, the team looked at how these drugs affected health and aging in mice.

"In animal models, the compounds improved cardiovascular function and exercise endurance, reduced osteoporosis and frailty, and extended healthspan," said Niedernhofer, whose animal models of accelerated aging were used extensively in the study. "Remarkably, in some cases, these drugs did so with only a single course of treatment."

In old mice, cardiovascular function was improved within five days of a single dose of the drugs. A single dose of a combination of the drugs led to improved exercise capacity in animals weakened by radiation therapy used for cancer. The effect lasted for at least seven months following treatment with the drugs. Periodic drug administration of mice with accelerated aging extended the healthspan in the animals, delaying age-related symptoms, spine degeneration and osteoporosis.

The authors caution that more testing is needed before use in humans.

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Nocebo said:

Are the senescent cells automatically replaced by the body after they're destroyed? I assume they are. Does this also work on cells that have become senescent from dividing too many times (telomere shortening)?
Or would telomeres still need to be lengthened?

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