Evidence to date suggests that we retain diverse populations of stem cells - and the resulting processes by which new cells and tissue are generated - throughout our lives. Stem cells don't go away as we age, but rather age-related changes in our biochemistry act to suppress the action of those cells. When we better understand these biochemical changes, it may be possible to restore the regenerative capacities of the aged through comparatively simple manipulation of signaling processes in the body. Here are a couple more papers to add to the weight of science behind this supposition:

Neurogenesis in the aging brain:

Neurogenesis, or the birth of new neural cells, was thought to occur only in the developing nervous system and a fixed neuronal population in the adult brain was believed to be necessary to maintain the functional stability of adult brain circuitry. However, recent studies have demonstrated that neurogenesis does indeed continue into and throughout adult life in discrete regions of the central nervous systems (CNS) of all mammals, including humans. Although neurogenesis may contribute to the ability of the adult brain to function normally and be induced in response to cerebral diseases for self-repair, this nevertheless declines with advancing age. Understanding the basic biology of neural stem cells and the molecular and cellular regulation mechanisms of neurogenesis in young and aged brain will allow us to modulate cell replacement processes in the adult brain for the maintenance of healthy brain tissues and for repair of disease states in the elderly.

Epidermal stem cells are retained in vivo throughout skin aging:

In healthy individuals, skin integrity is maintained by epidermal stem cells which self renew and generate daughter cells that undergo terminal differentiation. It is currently unknown whether epidermal stem cells influence or are affected by skin aging. We therefore compared young and aged skin stem cell abundance, organisation, and proliferation. We discovered that despite age associated differences in epidermal proliferation, dermal thickness, follicle patterning, and immune cell abundance epidermal stem cells were maintained at normal levels throughout life. These findings, coupled with observed dermal gene expression changes, suggest that epidermal stem cells themselves are intrinsically aging resistant and that local environmental or systemic factors modulate skin aging.

Cancer is the big potential problem associated with any "put the stem cells back to work" strategy. It is probable that evolutionary pressures have led to biochemistries in which generative processes diminish with age, thereby reducing the risk of cancer due to damaged stem cells. It's a balanced trade-off between losing capacity and the harm caused by runaway, damaged cells. But we have to fix cancer anyway, if we'd like to live much longer, healthier lives - and the near-term for cancer medicine is very rosy, even if complete prevention and absolute cures are still decades in the future.

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.

The full content of the December 2007 issue of Rejuvenation Research is presently freely available. These promotions don't last too long, so take a look while it's available - there's a lot of good reading in there. For example, Aubrey de Grey's piece on the balkanization of gerontology (PDF):

In my view, the divide between biogerontologists and other gerontologists concerning the desirability of combating aging is a symptom of the pitifully limited amount of communication between these subfields. Though they study facets of the same phenomenon, these researchers' actual contact is very nearly nil. It is thus no surprise that such fundamental differences of opinion persist. Whether anyone is really to blame for this "balkanization" of the field is debatable: it exists in a more limited way even within biogerontology, and the reasons are probably the same, revolving around the much higher priority (in career terms) of maintaining prestige among those who know and understand one’s work best than of disseminating it to others.

There has long been a recognition that this balkanization is regrettable, and token measures have been taken to diminish it: for example, the Gerontological Society of America (GSA) brings together all the gerontological specialties under one roof every November. But token is all these measures are: as anyone who has attended the GSA’s annual meeting will tell you, the event is indistinguishable from a coincidence of three or four conferences going on in the same building at the same time.

Alternately, William Bains' pointed commentary on views of death and aging (PDF):

no one will ever be in a position to ask, "Should I live forever?" We will be asked another, harder question. It is my contention that we should debate that question, and yes debate it in terms of its possible, long-term, science fictional implications if you like, but do not pretend the debate is ‘about’ whether people should seek physical immortality. It is about something more complicated, less black-andwhite, and much more immediate.

...

The question is not, "Do you want to live forever?" The question is, "Do you want to die tomorrow?" Replacing "should we live forever" with "do you want to die tomorrow?" strips away the sheer nonsense that is spouted about what 'might be,' and brings us back to specifics. Many people state firmly that they do not want to live forever. Many say they would not want to live beyond 100. Usually they are less than 60 years old when they say it (few 95-year-olds hold this view; very few 99-year-olds). But these people appear genuinely to feel that they do not want to live to be 100. So they do not want to live another 50 years. Do they want to die tomorrow? No. If I ask again tomorrow, will they want to die the day after? No.

Also an interview with Paul F. Glenn of the Glenn Foundation for Medical Research (PDF):

In our view, aging research is drastically underfunded. Promising opportunities must be pursued, such as the emergence of stem cell research, which offers the possibility of new therapies for treating or renewing diseased tissues or organs.

The growth of an aging population will bring treasury-breaking healthcare costs unless health can be maintained and age-related diseases delayed or cured. Human suffering that accompanies age-related disease is not just a financial burden.

It's a pity that all this more broadly interesting content ends up behind the paid firewall. I can imagine that all parties involved in publishing Rejuvenation Research would be better served by a journal in which the content above - very interesting and accessible to the layperson - is open while the research publications remain as paid access only. If you want more people to see what you have to say, open access is the way to go, and those in the research community who pay for the journal will pay for it regardless of the non-research content.

The full content of the December 2007 issue of Rejuvenation Research is presently freely available. These promotions don’t last too long, so take a look while it’s available - there’s a lot of good reading in there. For example, Aubrey de Grey’s piece on the balkanization of gerontology (PDF):

In my view, the divide between biogerontologists and other gerontologists concerning the desirability of combating aging is a symptom of the pitifully limited amount of communication between these subfields. Though they study facets of the same phenomenon, these researchers’ actual contact is very nearly nil. It is thus no surprise that such fundamental differences of opinion persist. Whether anyone is really to blame for this “balkanization” of the
field is debatable: it exists in a more limited way even within biogerontology, and the reasons are probably the same, revolving around the much higher priority (in career terms) of maintaining prestige among those who know and understand one’s work best than of disseminating it to others.

There has long been a recognition that this balkanization is regrettable, and token measures have been taken to diminish it: for example, the Gerontological Society of America (GSA) brings together all the gerontological specialties under one roof every November. But token is all these measures are: as anyone who has attended the GSA’s annual meeting will tell you, the event is indistinguishable from a coincidence of three or four conferences going on in the same building at the same time.

Alternately, William Bains’ pointed commentary on views of death and aging (PDF):

no one will ever be in a position to ask, “Should I live forever?” We will be asked another, harder question. It is my contention that we should debate that question, and yes debate it in terms of its possible, long-term, science fictional implications if you like, but do not pretend the debate is ‘about’ whether people should seek physical immortality. It is about something more complicated, less black-andwhite, and much more immediate.

…

The question is not, “Do you want to live forever?” The question is, “Do you want to die tomorrow?” Replacing “should we live forever” with “do you want to die tomorrow?” strips away the sheer nonsense that is spouted about what ‘might be,’ and brings us back to specifics. Many people state firmly that they do not want to live forever. Many say they would not want to live beyond 100. Usually they are less than 60 years old when they say it (few 95-year-olds hold this view; very few 99-year-olds). But these people appear genuinely to feel that they do not want to live to be 100. So they do not want to live another 50 years. Do they want to die tomorrow? No. If I ask again tomorrow, will they want to die the day after? No.

Also an interview with Paul F. Glenn of the Glenn Foundation for Medical Research (PDF):

In our view, aging research is drastically underfunded. Promising opportunities must be pursued, such as the emergence of stem cell research, which offers the possibility of new therapies for treating or renewing diseased tissues or organs.

The growth of an aging population will bring treasury-breaking healthcare costs unless health can be maintained and age-related diseases delayed or cured. Human suffering that accompanies age-related disease is not just a financial burden.

It’s a pity that all this more broadly interesting content ends up behind the paid firewall. I can imagine that all parties involved in publishing Rejuvenation Research would be better served by a journal in which the content above - very interesting and accessible to the layperson - is open while the research publications remain as paid access only. If you want more people to see what you have to say, open access is the way to go, and those in the research community who pay for the journal will pay for it regardless of the non-research content.