Scientists Get Their First Look at the Enzyme That Could Help Battle Aging

Home / Research Updates / Scientists Get Their First Look at the Enzyme That Could Help Battle Aging

Nothing in your body lasts forever. Every single cell in your body will die eventually, and eventually, you’ll run out of replacements. When that happens, various parts of your body will stop working correctly, and at some point, the whole thing will shut down. Aging happens to all of us, and there’s nothing we can do about it.

Except, maybe there is. Researchers from UC Berkeley have discovered the 3D structure of the enzyme telomerase, which could lead to new advances in aging research, as well as possible new insights into cancer.

 The reason we age—or at least, one of the reasons—is because our cells can only multiply a certain number of times. Each time our cells split, a tiny part of the ends of our chromosomes doesn’t make the cut. Over successive cell divisions, our DNA gets shorter and shorter. The only thing protecting our genes are the endcaps, called telomeres.

Telomeres don’t code for any genes, but they protect the more useful bits of our DNA from getting damaged during replication. The problem is that when our telomeres run out, our cells can’t replicate anymore. But some of our cells—typically stem cells and cancer cells—don’t have this concern, because they have an enzyme called telomerase that keeps making the telomeres longer.

Telomerase was discovered in 1997, but it’s so complicated that researchers have been unable to determine what it looked like until now. The researchers used a new imaging technique called cryo-electron microscopy (cryo-EM), which involves cryogenically freezing a sample before looking at it with an electron microscope. This technique can illuminate structures too sensitive for normal electron microscopes.

Now that we know the structure of telomerase, we can start creating drugs and therapies to target it. We might be able to artificially extend the lifespan of our cells—and by extension, ourselves—or stop the runaway replication behind cancers. It’s still a long way to go before we start seeing those things, but this is an important and crucial first step.