For more than a decade, researchers have believed that aging cells damage the tissue around them, and that this damage underlies a number of age-related disorders. Now a new study in mice appears to confirm this. The study shows that selectively eliminating those aging, or “senescent,” cells, could help prevent the onset of everything from muscle loss to cataracts
Scientists at the Mayo Clinic in Rochester, Minnesota, identified senescent cells in mice that had been genetically engineered to age rapidly using a biomarker, called p16Ink4a, specific to these cells. For the length of the animals’ lives, they were injected with a drug that induced only those biomarker-containing senescent cells to commit suicide, while leaving others untouched.
The results were striking: in tissues that contained the labeled cells, including everything from fat to muscle to eyes, selective removal appeared to postpone age-related damage. Treated mice had no cataracts, and showed increased muscle mass, strength, and subcutaneous fat when compared to mice that hadn’t received the drug.
Fightaging – At any given time a whole bunch of cells in your body need to be destroyed before they cause harm – cells that are past the productive stage of their life cycle and have become senescent, cells that are damaged and malfunctioning, and so forth. The majority of these cells are indeed destroyed, either by the immune system or through self-destruction mechanisms that evolved to trigger when vital cellular processes begin to run ragged. But this protective culling fails with age, and the accumulation of cells that should have been destroyed but were not is one of the driving forces of degenerative aging.
This fact is reflected in the proposed apoptoSENS research program, one of the seven branches of the Strategies for Engineered Negligible Senescence. Where the body isn’t keeping up with cells that should be destroyed, appropriate forms of biotechnology can could be developed to perform this necessary work – and thereby remove and reverse this contribution to aging. The first array of therapies will probably look much like the targeted cell killing strategies under development in the cancer research community: using bacteria, viruses, nanoparticles, or the patient’s own immune system to selectively seek out and destroy cells based on their surface markers.