This isn't _really_ news. It's been known for a while that cells can be made "immortal" by repairing telomeres [0]. In fact, for stem cells and cancer cells to keep their immortal properties they use various mechanisms to repair telomeres [1]. The major issue is that the more times a cell divides, the greater the likelihood that it will develop cancer. Some theories postulate that the Hayflick division limit on cells is actually a defense against cancer.<p>The Wikipedia articles on telomeres and telomerase have plenty of further resources[2][3].<p>[0] <a href="http://learn.genetics.utah.edu/content/chromosomes/telomeres/" rel="nofollow">http://learn.genetics.utah.edu/content/chromosomes/telomeres...</a><p>[1] <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370421/" rel="nofollow">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370421/</a><p>[2] <a href="https://en.wikipedia.org/wiki/Telomere#Cancer" rel="nofollow">https://en.wikipedia.org/wiki/Telomere#Cancer</a><p>[3] <a href="https://en.wikipedia.org/wiki/Telomerase" rel="nofollow">https://en.wikipedia.org/wiki/Telomerase</a><p>edit: formatting
This is of interest because it provides a much better methodology for lengthening telomeres, with more control than genetic engineering, and therefore a faster path to establishing why telomerase therapy extends life in mice.<p>Average telomere length in tissue is a measure of health in general: since telomere length decreases with each cell division it is a proxy for some combination of cell division rates and rate of influx of fresh new cells with long telomeres provided by the stem cell population maintaining a tissue. Since average telomere length is often measured in white blood cells it goes up and down with health and generally downward with age. Stem cell activity declines with age, so this shouldn't be surprising.<p>Lengthening telomeres via telomerase may extend life in mice for any number of reasons, some of which actually have nothing to do with telomeres. Telomerase, like all biomolecules, has a lot of roles, not all of which are fully understood. Alternative and more controllable methods of lengthening telomeres should help narrow down what is going on in those studies. Is it greater stem cell activity, something to do with telomerase influencing mitochondrial function, something completely different?<p>In general if you're thinking of aging as accumulated molecular damage, telomere shortening looks like a consequence not a root cause. It may cause further issues itself, but targeting it is probably not as effective as going for the actual root causes that lead to it. The interesting question is why telomerase therapy does do comparatively well in extending life in mice.
This indeed is news! It's not the idea of telomere extension or telomerase, but a quick hit, temporary way of inducing that extension. Every other time I've seen this discussed, it involved some sort of modified virus or persistent agent.
I suspect that telomeres are just one component in a system that maintains an organism's biological stability, and that simply lengthening them without reference to the rest of the system will just get you a young, cancer-ridden body.
but, how to find mutations somewhere along the thousands of pairs of compounds along a DNA strand?<p>I guess if you could compare many strands you could find the spots that are the same in all.<p>But then to somehow repair them all?