I wrote here a while ago on the topic of “senescent cells”, which has been a hot topic for quite a while now. It’s an appealing hypothesis - that there’s a population of cells that has lost its oomph and are not only not contributing to their respective tissues, but could even be actively dragging them down. They have stopped going through the cell cycle; they have different protein expression profiles and different secretory profiles, and there’s evidence that clearing them out might improve overall health. Why, you ask, hasn’t evolution gotten around to this useful effect already? Probably because natural selection is no longer really operating very strongly on cellular events that only happen in older individuals. By a certain age you’ve either passed on your genetic heritage already or you’re increasingly less likely to do so at all, and you are thus basically invisible to natural selection.
Here’s some of the latest news in the field, the start of a clinical effort to try senolytic therapy in Alzheimer’s patients. I’m very much in favor of Alzheimer’s ideas that don’t involve direct attacks on the amyloid pathway, since I think that so far the evidence is that those aren’t very useful at all. This trial is the very first tiptoe into the clinic - five people, open-label, Phase I. You can’t start off much more tentatively than that! These patients were given a combination of dasatinib and quercetin (“D&Q”, in the lingo of the field), which are two of the better-characterized compounds in this field. The former is a well-known inhibitor of several tyrosine kinases, and the latter is, well. . .I’m not sure what quercetin does, to be honest, but it has been investigated in this field and in many others. The combination of the two has cleared senescent cells selectively in culture and in animal models.
Full article (open access):