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Reporting from a Comparative Biology of Aging Conference


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Posted 21 October 2015 - 02:40 PM


Josh Mitteldorf here reports on the presentations given at a recent conference on the comparative biology of aging. He has a programmed aging point of view, considering aging to be an evolved genetic program that produces damage and dysfunction. On the other hand I as a long-time observer of the field, along with the majority the research community, consider the evidence to point to aging to be the result of accumulated cell and tissue damage, and where epigenetic and other changes are observed in old individuals, these are reactions to that damage. To the degree that this division steers research and development priorities, it is the most important debate in aging research.

Comparative biology is a field that has grown with advances in genetic biotechnology, and the plummeting cost of good genetic data is producing a wealth of information on long-lived species for those researchers who want to better understand how exactly age-related degeneration progresses from first cause to final outcome at the most detailed level of genetic and cellular mechanisms. The purpose of science is to generate knowledge, so all this is good and according to plan, but it seems to me to be largely unlikely to lead to great breakthroughs in methods to build rejuvenation therapies. We already know how to do that, which specific forms of cell and tissue damage to repair, and the problem there is directing more funding and attention to that work, not a need for more data. The comparative biology community may be well placed to answer questions about which forms of damage are more important than others, aiding prioritization in repair approaches, but even there it would be faster just to spend more efforts on repair and then see what happens as a result.

The conference was opened by a theoretical lecture by Tom Kirkwood, father of one of the more popular theories of aging. He admonished us that evolution is a mathematical science that yields specific and quantitative information about what aging can and cannot be. These provide a powerful mathematical underpinning for the understanding of aging.

The next morning, Annette Baudisch told us that in reality, nature has produced every combination of aging strategy that you can imagine, and some that you probably never imagined. The kind of aging that humans know is gradual and accelerating, leading to death on a timetable that is predictable within about 10-15%. But this brand of aging is a small minority in nature. There are salmon and octopuses and annual plants that reproduce in a burst and then die suddenly. There are beetles and jellyfish that are able to "age backward", reverting to a larval state under stress, then beginning life again with a fresh start. Baudisch coined the term "negative senescence" for a phenomenon that is not the same thing as this: most trees and some turtles and lobsters just grow ever larger and more fertile over decades or even centuries.

Closing the conference was a keynote address by Steven Austad. Austad warned us that much of what we have long assumed about the biology of aging is not to be taken literally without exception; and some of it is merely persistence of myth. He showed us the classic plot of animal size versus lifespan. In mammals, life span rises slowly, with about the 1/4 power of an animal's weight, which corresponds to a slope of 0.25 in the log plot. There are outliers where animals have managed to find strategies to suppress their death rates from predators and disease. Most birds live longer than comparably-sized mammals, and the most dramatic examples are people and bats. I had known that mice are outliers on the downside. Since mice provide food for a great number of predators, and they freeze to death over the winter; their life spans are below the trend line. What I learned from Austad is that the exceptions extend to all small rodents. For rodents less than 8 kg, there is no correlation at all between size and life span. No one, to my knowledge, has explained this.

As in his past work, Austad offers so much useful good sense in his keynote, and yet he clings to a view that aging is driven by an accumulation of damage, that it can be slowed but never reversed, that there are no genetic mechanisms that have evolved solely for the purpose of assuring a fixed (shorter) life span. The three points are related but not identical. Curiously the idea that damage is the root of aging is not the influence of evolutionary theorists, but far older, rooted in ancient concepts of impermanence. I know it is theoretically possible, and hope that it will prove generally true in practice, that the body knows how to repair all the important kinds of damage that accrue in aging, and is capable of restoring itself to a youthful state, given the appropriate signaling environment.

Austad's present research is based on the observation that misfolded proteins tend to accumulate in our cells, and are related to dysfunction and disease, most prominently Alzheimer's. Long-lived varieties need to keep proteins in the right conformation, with "chaperone" molecules that are particularly effective. Austad is isolating and transplanting some of these chaperone molecules from his menagerie of 500-year-old clams. Despite differences in theoretical perspective, I have found the community of aging biologists to be especially personable and gracious. I have known Austad and Kirkwood in the deep past, and Baudisch more recently because she belongs to the next generation. Before I had any reputation or credibility in the field, all of them responded to me personally and respectfully.

Link: http://joshmitteldor...-with-rotifers/


View the full article at FightAging




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