Baker exploited the fact that many senescent cells rely on a protein called p16-Ink4a. He created a genetic circuit that reacts to the presence of p16-Ink4a by manufacturing an executioner: a protein called caspase-8 that kills its host cell. Caspase-8 is like a pair of scissors – it comes in two halves that only work when they unite. Baker could link the two halves together using a specific drug. By sneaking the drug into a mouse’s food, he activated the executioners, which only killed off the cells that have lots of p16-Ink4a. Only the senescent ones get the chop.
Maggie Koerth-Baker at 7:29 am Friday, Nov 4Bonus fun: Read Ed Yong's write-up of the study. Then read this version written by a reporter at the New York Times. Then think about how much you would have misunderstood about this study if you'd only read the New York Times story.
Image: The Apple Mouse, a Creative Commons Attribution Share-Alike (2.0) image from moparx's photostream
There was some interesting research out of the Mayo Clinic announced this week. The study focused on a new method to combat aging, though not, significantly, one that could extend life. Instead of living forever, Darren Baker and colleagues would just like to help people enjoy the time they do have—by reducing the physical downsides of aging, such as lost muscle and stiff joints.
Their method centers around something called senescent cells coach bags, normal cells that have basically shut down all growth, but continue to release chemicals into the body. Some scientists have suspected this process of cellular senescence contributes to the negative physical effects of aging and Baker's team was able to provide some big support for that theory. They killed senescent cells in the bodies of fast-aging mice. Those mice went on to age more gracefully, delaying the physical breakdown of their bodies. Ed Yong explains:
It really should go without saying that there's a big jump between getting something to work in mice and getting it to work in people. So do not expect your doctor to be able to kill off your senescent cells anytime soon, if ever. There's also potential risks to this therapy and a lot we don't yet know about it. Will this work as well in mice that age at a normal rate? Will killing senescent cells allow us to delay or eliminate other signs of aging, or just muscle loss and cataracts? If you kill of senescent cells, will damaged cells continue to grow, producing cancer?
Baker tested out this system in a special strain of genetically engineered mice that age very quickly. It worked. The senescent cells disappeared, and that substantially delayed the onset of muscle loss, cataracts, and fat loss. Typically, around half of these mice show signs of muscle loss by five months of age. Without their senescent cells, only a quarter of them showed the same signs at ten months. Their muscle fibres were larger, and they ran further on treadmills. Even old mice, whose bodies had started to decline, showed improvements.
When you're thinking about a study like this, it's probably best to treat it as an interesting discovery about the way mammal biology might work, rather than something that has any immediate practical medical applications for humans. From that perspective, this is pretty cool science.
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