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I pointed out a paper in passing a few weeks back, in which researchers put forward a model to explain how some species can evolve extreme longevity, or even agelessless (or negligible senescence).

How can evolution, biased to early reproductive success at all reasonable cost, produce such a species?

As it turns out, there may be some plausible scenarios - which is a good thing, given the fact that many extremely long-lived animal species exist, and that some might indeed be ageless. Problems arise for any theory that cannot explain the outliers. Chris Patil has given this work a great deal more attention over at Ouroboros, and you should take look.

The evolution of negligible senescence:

The authors describe in detail two organisms - the Bristlecone pine and Arctic quahog - that exhibit density-dependent recruitment. In both species, sessile adults live in crowded but stable conditions in which new opportunities for maturation arise rarely. In such situations, it behooves an individual organism to outlive its neighbors, so that when they die its seedlings or larvae have a place to dig in and grow up. In such contexts, the authors argue, natural selection can trigger an anti-aging arms race that results in negligible senescence as a consequence of runaway selection.

The evolution of negligible senescence, part II: Organisms that are remotely like us:

But does the evolutionary theory that explains the emergence of negligible senescence in trees and clams have anything to teach us about how long-lived species arise from short-lived stock? If so, are those lessons in any way portable to mammals? Possibly.

...

One famous example of a species with far greater longevity than similarly sized species of comparable body plan, the naked mole rat, is also territorial and eusocial. It is tempting to speculate that mole rat queens, like their peers among the harvester ants, have evolved long lifespans in order to wait out their competitors in other burrows.

...

Mole rats are no less similar to humans than lab mice are. Therefore, biogerontologists are very interested in learning the detailed mechanisms by which mole rats have delayed senescence, since it’s likely (more likely than for clams and trees, anyway) that these details might be of some practical use to us.

The most important lesson to learn from an examination of the huge range in animal - even mammal - longevity is that it is possible to design better humans with the biotechnology of tomorrow. Longer lived, less diseased, less prone to aging. That is the driving goal behind much of the mainstream work in metabolism, genetics and aging these days. It'll be a long time in the making, however - a truly massive undertaking of great scope and complexity.

While that great work is underway, we should devote more resources to the easier path to longevity: learning how to repair the humans we have now.

My attention was drawn to a Spanish article on one of the many research groups investigating the role of p53 in aging and cancer. There has been a great deal of interest in finding ways around the "cancer or aging, choose one" limitation to this set of biochemical mechanisms, thought to apply until recently. This Spanish article is somewhat in advance of the scientific publication; I'm not sure why that is the case.

The translation via Google is fair (suggestions taken on a better translation automaton):

In this line, Serrano said that the genomes of a chimpanzee and humans are virtually identical at 99.8%. However, the maximum life of a chimpanzee is 60 years and the human rarely exceeds 110. The average of a chimpanzee is 40 years and that of a human, 80. There must be something in our genes very subtle changes made to live 50 years to live 100. Then, along with the team of Mary Blasco, we are going to make some genetic manipulation to see if we can increase longevity in mice much more. That is our challenge If we get a mouse in the privileged environment of a laboratory comes to live three years to live six passes, it would be proof that longevity is flexible and would know how to enlarge it.

So it seems compelled to ask the molecular biologist in this battle if they have undertaken together against cancer and aging, it is just a matter of putting telomerase a mouse to make it immortal. The answer is no, because telomerase makes more cancer. To ensure a tumor, which has activated telomerase, and if a mouse has more telomerase than normal, for example, on transgenic mice, we know that you have more tumors. What we have done is to use the superratones Manuel, because p53 protects cancer and a 18% lengthens the life of mice, and if we add to this the gene of immortality, telomerase, which got these mice [to] live an average of 50% more, without cancer, which are words older. That is what we have discovered now.

Because this extension of life, 50% in superratones is the longest that has been described in mammals.

You get the gist, despite the breakdown of translation in the last few sentences: there are combinations of metabolic and genetic states in mammals not selected for by evolution that nonetheless lead to a clearly superior beast, from our perspective at least. Well, more or less. If you head over to the Methuselah Foundation forums, you'll find that Michael Rae wrote a long piece on this research back in mid-2007, before the life span studies were complete:

The standard reading is that the "Super p53" mice are getting less cancer, but are having their [life spans] restrained by lack of tissue replenishment due to stem cell loss, while the telomerase transgenics are on the opposite horn of the same dilemma. It seems at least possible that if one overlaid the strong cancer resistance conferred by the former, with the increase in stem cell mobilization and proliferative capacity of the latter, you'd wind up with a long-lived, slow-aging mouse.

There are a lot of caveats and details both prior and after that statement, many of which still apply even with these final life span study results. It's not all completely clear-cut, as is often the case, but I can see this impressive work garnering a great deal of attention in the popular press once it jumps the language gap for the English-speaking world.