The short answer: It really depends on what we define as aging.
Professor Fabio Rossi, University of British Columbia, is Director, Research in the School of Biomedical Engineering and Canada Research Chair in Regenerative Medicine. He obtained his MD from his hometown university in Genoa, Italy. During undergraduate studies, he investigated the mechanisms underlying chondrocyte differentiation in the laboratory of Ranieri Cancedda. Next, he joined the PhD program at the European Molecular Biology Laboratories in Heidelberg, where he studied the influence of avian retroviral oncogenes on cellular differentiation under the supervision of Thomas Graf. His interest in this topic led him to continue his training at Stanford University, in Helen Blau’s laboratory, where he pioneered the use of β-galactosidase complementation as a reporter of protein-protein interactions in live cells. He moved to the University of British Columbia to open his laboratory in 2001.
Can our life span be extended, and if yes what is the limit? There is no doubt that human life expectancy has increased tremendously by improving hygienic conditions, nutrition and disease prevention/management. The number of centenarians in developed countries with a good social support system is still increasing, so likely we did not address all environmental factors that accelerate aging yet. However, we are at a point in which, once the external age-accelerating factors are removed, the intrinsic limits dictated by the fact that evolution can only optimize biological processes, such as inflammatory responses and tissue maintenance, during reproductive age are becoming more obvious, and we are closer to accurately identifying when the human organism just runs out of gas.
It seems unlikely that there will be a silver bullet, a single intervention that will magically refill our tank, expanding life expectancy. The biological constructs that we call our bodies run a number of parallel, interlinked processes and by “messing” with any of them to “fix” aging we are likely to trigger changes that will cause problems, like increased incidence of cancers. In a way, this conundrum is what spurred the nascent “senolytics” industry.
Senolytics are drugs that get rid of senescent cells, which are cells that are no longer able to proliferate and that secrete factors altering their environment. Think of them as old grumpy cells yelling at their younger neighbours to stay off their lawn! This approach assumes, supported by some data, that while we may not easily change the mechanisms that lead to their appearance, the senescent cells themselves are the result of some kind of mistake and should not be there; therefore, we can get rid of them after they show up. The consensus is that senescent cells are bad, they corrupt youthful cells in their vicinities and interfere with their functions.
This monolithic consensus, however, is starting to show some cracks: It has been reported that cells that look senescent by most of the accepted criteria are actually playing important roles in processes taking place in young tissues, and in particular in regeneration—the first process to fail in aging, and the restoration of which is the holy grail of aging research. So are aging cells really the bad guys, or are they good guys that were deployed to fix the wrong problem? What are we going to break in the process of eliminating them?
Our ability to “reverse” aging will likely rest on the answer to this question.
The much simpler approach seems to be preventing aging, or at least some aspect of it. We may have an inbuilt limit to how old we can become, at least in our present evolutionary state. But perhaps we don’t necessarily have to reach that limit as frail, diseased husks of what we once were. The recipe for a healthier aging is already pretty clear, and it includes caloric restriction and age-appropriate exercise. But this actually requires will power, which does not come in pill form.
So what alternatives do we have to remain healthy longer, and perhaps to slow down the cognitive decline that is the real bane of our late years?
My point of view, admittedly slightly biased by my research interests, is that the most promising way to do that over the next century lies in new approaches to engineering our systemic immune environment. Inflammatory responses in aging are starkly different from those observed in young adults, affecting key systems such as muscles and joints, the brain, and regeneration in general. Bringing them back to “normal” may be our best bet to solve aging-related problems without too many side-effects. In fact, this is likely how caloric restriction, currently the most beneficial anti-aging strategy, works—by altering inflammatory responses.
In fact, those very cells that are responsible for the most outwardly visible effects of aging such as saggy, thinning skin (they go by a variety of names such as stromal or mesenchymal cells, or fibroblasts) are also hubs that control the quality of inflammation. Acting on these cells and understanding in depth why their responses change with age may therefore address multiple age-related problems.
So then, is aging more reversible than we thought? I think the more exciting question isn’t one of reversal but prevention. If you have to reverse it, you may have already lost.
My blog is just one of many covering this topic as part of Signal’s sixth annual blog carnival. Please click here to read what other bloggers think about this.
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