A new class of anti-aging drugs has been identified in a study by a team from The Scripps Research Institute and the Mayo Clinic. In mice, the drugs reduce frailty, improve heart function and extends a healthy lifespan.
The drugs, which the researchers have dubbed "senolytics," work by causing senescent cells to die. These cells secrete harmful substances that damage other cells, including stem cells, said study contributor Laura J. Niedernhofer, a Scripps Research scientist in Jupiter, Florida.
Since these substances are already approved for human use, researchers say clinical trials should be relatively easy to arrange in a short time. They are the cancer drug dasatinib, sold under the brand name Sprycel; and quercetin, a nutritional supplement with antihistamine and anti-inflammatory properties. And even stronger drugs may be discovered, now that researchers know what to look for.
"If senolytic agents can indeed be brought into clinical application, they could be transformative," the study stated. "With intermittent short treatments, it may eventually become feasible to delay, prevent, alleviate, or even reverse multiple chronic diseases and disabilities as a group, instead of one at a time."
Laura J. Niedernhofer / The Scripps Research Institute
The study was published Monday in the open-access journal Aging Cell. The co-first authors of the study are Yi Zhu and Tamara Tchkonia of the Mayo Clinic.
Old mice (24 months) given both drugs improved their heart function in five days. The ejection fraction, a measurement of how much blood is pumped, rose by about 10 percent. Mice irradiated to mimic cancer treatment experienced improved exercise capacity, as measured by treadmill performance, for seven months on a single dose. Control mice had endurance 15 percent below normal, treated mice had normal endurance.
And a special kind of mouse that ages at six times the rate of normal mice greatly extended their healthy lifespan, or "healthspan." The mouse type, which Niedernhofer developed, mimics a human disease called progeria and dies in six months, compared to up to 3 to 3 1/2 years for normal mice. Treated mice of this type had their healthspan increased by 10 percent, and more than 15 percent greater bone density.
"Probably, these secreted factors from senescent cells inhibit regeneration, so just getting rid of the bad players, these senescent cells, is sufficient to have a positive impact," Niedernhofer said.
The first treatments could reach the clinical within a year or two, said Paul D. Robbins, another Scripps Florida researcher on the study. This would be based on treating specific conditions, not as a general anti-aging drug, because federal regulators don't consider aging to be a disease.
For example, cancer patients who become frail after undergoing chemotherapy could be tested to see if these drugs restore their strength, Niedernhofer said.
The study is "exciting," representing a new strategy for life extension, said Kang Zhang, a professor of genetics and ophthalmology at UC San Diego. However, further research is needed, said Zhang, who is also codirector of the university's Biomaterials and Tissue Engineering Center.
"I want to be cautious," Zhang said. "I want to see more replication studies over a longer time, and to look for long-term effects."
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