The popular press here covers the ambition of the scientific mainstream to modestly slow aging. Many researchers don't even want to talk about extending life, but only a small expansion of healthspan. This lack of ambition, and refusal to engage with the large body of evidence that suggests we can do far better, is why we need organizations like the SENS Research Foundation. It is possible and plausible to extend healthy life and overall lifespan indefinitely by implementing the approach of repairing the cell and tissue damage that causes aging. Yet all too much of the rhetoric and effort in the scientific community still goes towards tinkering with the operation of metabolism to slightly slow the pace at which damage accumulates - a clearly far inferior approach, that can at best produce only marginal outcomes.

With all of that, it is still a little odd to see senescent cell clearance, a part of the SENS repair strategy, showing up in articles like this, and given no greater weight than, say, treating people with metformin, which can't possibly have anywhere near as beneficial effect. Journalists typically don't distinguish between the potential value and outcome of different approaches to aging - it is all the same to them, just a flat list. That's something of a problem when the differences are enormously important and the expected outcomes are night and day. If there is to be significant progress towards healthy life extension in our lifetimes, the better strategies, those involving damage repair, must gain far greater support.

Imagine a day in the not-too-distant future. You're in your late 40s, and it's time for a special doctor's visit. The physician reviews your lifestyle, sleep habits and health history and orders some blood work to compare certain biomarkers with baseline measures taken when you were in your 20s. Then she gives you a personalized prescription for change that includes a diet that mimics the effects of fasting and a drug that helps your cells clear out malfunctioning proteins. The goal? To make you age more slowly and lengthen your "healthspan." If it sounds like science fiction, you're right - for now. But researchers in the field of geroscience, which explores the relationship between aging and diseases like cancer, heart disease and Alzheimer's, see that day coming. They are marshalling evidence that the same cellular processes that drive aging also result in those diseases, and that it's possible to slow the damage down. "The idea is that if you can treat the underlying causes of aging, you can delay all of these things as a group.That's a whole different way of thinking about medicine." The goal is not to extend lifespan, though that may indeed happen. Instead it's to extend the length of time you're healthy and active. Working with a range of organisms from yeast to worms to rodents, scientists have homed in on several interrelated processes they suspect drive aging. Proteostasis, for one, is a fancy name for the quality-control system at work in your cells. Like a factory, a cell has ways to ensure the proteins it makes are up to snuff. If they're not, the malfunctioning proteins are supposed to be broken down and used to build new proteins or as energy. Researchers are looking for interventions, whether lifestyle or drugs, that might repair this age-related quality-control decline. Another area of exploration is inflammation. Low-grade, chronic systemic inflammation in the absence of an infection is a factor in most age-related diseases; it's even known as "inflammaging." The sources of it aren't well known, but scientists are investigating possible contributors, including a state called cellular senescence. Researchers wondered what would happen if senescent cells were removed. In mice, they've shown that certain drugs called senolytics can do just that - and slow the progression of age-related changes and even partially reverse them. Other drugs, too, are being eyed for their potential. A top contender, which has increased both lifespan and healthspan in mice by targeting a protein that controls key cellular functions, is rapamycin, used in people to prevent rejection of transplanted organs. Researchers now studying whether rapamycin has a similar effect in pet dogs, which might be great models for aging research because they share an environment with humans and are genetically varied.

Link: http://health.usnews.com/wellness/articles/2016-08-09/the-future-of-aging