All of the current crop of research resulting from heterochronic parabiosis studies and telomerase studies are most likely just hitting different ways of orderi

All of the current crop of research resulting from heterochronic parabiosis studies and telomerase studies are most likely just hitting different ways of ordering stem cells back to work. So you get increased tissue maintenance, and surprisingly less cancer than one might expect from putting damaged stem cells to work in damaged environments and damaged tissues. The decline in stem cell activity is just one of the things that happens in aging, and it seems likely that this reduced activity is a response to various forms of cell and tissue damage. Researchers are now starting to identify some of the cellular cross-talk and signaling that mediates this reaction. Putting stem cells back to work doesn't deal with lipofuscin in long-lived cells. It doesn't deal with glucosepane cross-links that our biochemistry cannot break down. It doesn't reduce nuclear DNA damage and the accompanying cancer risk. It may be somewhat helpful for amyloid accumulation via increased immune activity, such as the beta amyloid in Alzheimer's and transthyretin amyloid linked to heart failure, based on some studies. It doesn't appear to do much for accumulations of senescent cells or mitochondrial DNA damage in cell population. It doesn't reverse immune system dysregulation (inflammaging) all that much, though again there are some studies suggesting that cell transplants can suppress inflammation and this may be one of their modes of action. So there are whole swathes of damage linked to age-related disease that this line of work doesn't help. It should probably be thought of as a parallel line of stem cell research, with expected outcomes and development akin to that achieved through cell transplant therapies. It is good, helpful progress, but not the cure for aging on its own. Separately, examining epigenetic changes in blood and tissues appears so far to be a plausible road to a robust biomarker of aging. Such a thing is very much needed in a field in which the only way to tell right now if a possible rejuvenation treatment works is to wait and see. That costs a lot, millions and years even in mouse studies, and so the pace at which new ideas can run through the system is pretty slow. A lot of things are just never tried or validated. If instead you could run a treatment on mice, then a month later run a blood test with a reasonable expectation that the results correlated well with remaining life expectancy, then a lot more can be done with any given amount of time and money.