The world works in strange ways; as soon as I mention twice the paucity of AGE-breaker and AGE-inhibitor work, more research groups start to come to my attention. Before diving into the example below, you might want to first refresh your memory on the buildup of advanced glycation endproducts (AGEs) and their contribution to aging.

• Beneficial effects of C36, a novel breaker of advanced glycation endproducts cross-links, on the cardiovascular system of diabetic rats

Unfortunately, past evidence suggests that excitement over work in rodents should be muted at best - the history of ALT-711 or alagebrium demonstrates that different types of AGEs are important in shorter-lived mammals versus humans. So far, promising work in mice and rats has translated poorly into human therapies - in most cases, through trying to address the wrong AGEs.

You'll noticed that this group, as for a number of others, is focused on diabetes. This is very much the way of the world in medical research. Regulation - both directly by decree and indirectly through raising costs of development - forces researchers down the road of focusing upon specific common diseases. You can't raise significant funds through the normal channels for work aimed at addressing an aspect of aging itself so long as major regulatory bodies will not approve the end result of your work for use. So, for example, most AGE research aims at diabetes because diabetic metabolism generates - and suffers due to - AGEs at an accelerated rate, but more pertinently because funds can be raised.

So it is that a range of the most promising potential research into addressing aging, not just AGE-breakers, is happening by stealth, in groups whose officially declared purposes span the known diseases of aging. Progress towards the more interesting goal of repairing age-related damage in our bodies proceeds at a fraction of the pace it might, because there is little freedom in medical research and development these days. It's a tragedy; unless this state of affairs is overturned, it will ensure age-related suffering and death comes for us much sooner than would otherwise be possible.

Posted by Reason at 7:00 PM
Permanent Link | View Comments (0) | Post Comment | TrackBack (0)

Everything is connected to everything else: our biochemistry is a web of tightly interacting processes, systems and feedback loops. You can't consider any one process in isolation of the whole if you'd like to learn more about how we work. This level of interaction is one reason why it is likely easier to learn to repair damage to our metabolism - the damage that causes aging - than to significantly change our metabolic systems to generate damage more slowly, and thus age more slowly.

With that in mind, I thought I'd point out a selection of papers that illustrate some of the more obvious linkages between stem cells, cancer, DNA damage, telomeres and aging - all a big ball of intricately knotted string. As cells - especially stem cells - become damaged, multiple sentinal processes try to destroy or place them into a quiescent state in order to avoid the runaway replication and mutation of cancer. But removing cells from active service reduces the effectiveness of the body, and is one cause of aging. This is an evolutionary balance of multiple competing and co-operating processes, degeneration with age on the one hand and avoidance of cancer on the other.

DNA repair in stem cell maintenance and conversion to cancer stem cells:

Genomic stability is essential for cell and organism longevity. Without genomic stability, replication errors and external stress as well as direct forms of DNA damage can induce mutations, which decrease cell survival, cause altered gene expression, and can lead to cellular transformation. All represent the antithesis of maintenance of normal stem cell function. We argue here that genomic stability is essential for stem cell maintenance and longevity. This concept is supported by human diseases associated with premature aging and animal models of DNA damage repair abnormalities all of which lead to abnormalities of stem cell survival.

...

Thus one origin of the cancer stem cell phenotype is the inability to maintain genomic stability among the stem cell population leading to mutational alterations and transformation. Capturing stem cells at this transition point represents an exciting field of discovery possibly leading to early detection and therapeutic interventions.

Two faces of p53: aging and tumor suppression:

The p53 tumor suppressor protein, often termed guardian of the genome, integrates diverse physiological signals in mammalian cells. In response to stress signals, perhaps the best studied of which is the response to DNA damage, p53 becomes functionally active and triggers either a transient cell cycle arrest, cell death (apoptosis) or permanent cell cycle arrest (cellular senescence). Both apoptosis and cellular senescence are potent tumor suppressor mechanisms that irreversibly prevent damaged cells from undergoing neoplastic transformation.

However, both processes can also deplete renewable tissues of proliferation-competent progenitor or stem cells. Such depletion, in turn, can compromise the structure and function of tissues, which is a hallmark of aging. Moreover, whereas apoptotic cells are by definition eliminated from tissues, senescent cells can persist, acquire altered functions, and thus alter tissue microenvironments in ways that can promote both cancer and aging phenotypes. Recent evidence suggests that increased p53 activity can, at least under some circumstances, promote organismal aging.

Telomeres, senescence, and hematopoietic stem cells:

The replicative lifespan of normal somatic cells is restricted by the erosion of telomeres, which are protective caps at the ends of linear chromosomes. The loss of telomeres induces antiproliferative signals that eventually lead to cellular senescence. The enzyme complex telomerase can maintain telomeres, but its expression is confined to highly proliferative cells such as stem cells and tumor cells.

The immense regenerative capacity of the hematopoietic system is provided by a distinct type of adult stem cell: hematopoietic stem cells (HSCs). Although blood cells have to be produced continuously throughout life, the HSC pool seems not to be spared by aging processes. Indeed, limited expression of telomerase is not sufficient to prevent telomere shortening in these cells, which is thought ultimately to limit their proliferative capacity.

Posted by Reason at 6:43 PM
Permanent Link | View Comments (0) | Post Comment | TrackBack (0)

It wasn't so long that we were talking about the uncertain longevity of lobsters, but for today it's the turn of the humble clam:

A British scientific team discovered the 405-year-old clam, named after the Chinese dynasty and not the former Liberal Democrat leader, at the bottom of the ocean, and hope its longevity will reveal the secrets of ageing.

...

The record-breaking shellfish, 31 years older than the previous oldest animal, another clam, was caught last year when scientists from the Bangor University School of Ocean Sciences were dredging the seabed north of Iceland.

...

Richard Faragher, a gerontologist at Brighton University working with the Bangor team, said: "Most of what we know about the ocean quahog is what it tastes like. We need to find out how it retains muscle strength, remains cancer-free and keeps its nervous system intact over such a long period of time."

As for the lobster (and the bowhead whale, for that matter) this is a good illustration of the limits of present knowledge, for all that the biotechnology revolution is well underway. There's an awful lot of trees in this forest.

Another potentially useful consequence of scientific examination of species of extreme longevity is an increase in public understanding of the range of life spans in the animal world. As scientists demonstrate specific biochemical reasons for differences in longevity between species, that work helps to generate support for medical engineering research aimed at increasing the healthy life span of our own species.

Posted by Reason at 7:22 PM
Permanent Link | View Comments (0) | Post Comment | TrackBack (0)

Advanced glycation end-products, AGEs, are a wide variety of inconvenient biochemical waste products produced by the operation of your metabolism (and, to a much lesser degree, eaten as a part of your diet). AGEs gum up important biomolecular machinery and disable essential macromolecules by glueing them together. Some AGEs can be broken down by your cells, but accumulate faster than they can be removed. Others cannot be broken down at all, and the slow accumulation renders vital functions in your cells ever more hampered and faulty.

So far, there's nothing radical that can be done about this process - no working, sort-the-problem-out AGE-breaker therapies for humans. The best advice is to try and avoid metabolic disease - exercise, keep fit, eat a calorie restriction diet and don't pack on the fat, in other words - because that condition and the diabetes that follows ramps up the rate of AGE accumulation.

Here's a closer look at some of the details.

Cross-link breakers as a new therapeutic approach to cardiovascular disease:

Fibrillar proteins, such as collagens type I and III, and elastin are components of the extracellular matrix. They form an intricate widespread network that provides a basis for maintaining the physical structure of the heart and vessels and also play an important role in determining cardiovascular function.

Physiologically, collagen and elastin fibres are enzymatically cross-linked to form [the] matrix. In addition to these enzymatically formed cross-links, collagen fibres may be linked non-enzymatically, most notably by formation of AGEs (advanced glycation end-products). AGEs are formed by a reaction between reducing sugars and body proteins; they are formed increasingly in diabetes mellitus and hypertension and they accumulate with aging.

There are several mechanisms whereby AGEs may affect cardiovascular structure and function. These include increased myocardial and vascular stiffness and (upon reaction with their receptors) inflammatory reactions, release of growth factors and cytokines, and increased oxidative stress. Therefore breaking AGEs appears as a promising tool in the therapy of cardiovascular injury related to diabetes, hypertension and aging.

Nothing radical to be done at present: that's a pretty grim picture, considering the widespread suffering caused by AGE buildup. Work is presently underway on AGE-breaker and AGE inhibitor drugs, but it's a small, slow-moving field in comparison to regenerative medicine or other well-funded initiatives.

Posted by Reason at 7:21 PM
Permanent Link | View Comments (1) | Post Comment | TrackBack (0)

The defeat of cancer is an important part of any comprehensive approach to repair the damage of aging. Ultimately, we'd all like perfect cancer prevention, but it may be that comprehensive and effective cancer cures will be enough to sustain the first few additional decades of the longevity revolution. That would put us at around 2040, entering "sky's the limit" territory with biomedicine and molecular nanotechnology. Cancer will go the way of smallpox shortly after that.

With regard to cancer cures, two of the most interesting lines of research at present involve engineered viruses and dendrimer-based therapies, both of which I've noted in past months:

• Cancer Cells are Different, So Target the Differences
• Stomping on Cancer With Viruses

Forced to pick the most promising technology base, I would have chosen dendrimers - they offer comparative efficiency in the process of producing new therapies because many components can be attached to a single dendrimer. Complex theraputic concepts - such as seeker molecules or two-stage toxins triggered by biochemicals specific to cancer cells - can be developed in isolation by specialists and the end results combined or built upon by other groups.

A virus doesn't have to be a one-trick pony, however. Engineered viruses that can do more than one job are examined in a recent Wired article:

Researchers at Stanford University and Jennerex Biotherapeutics have tweaked the cancer-killing vaccinia virus JX-963 so that it also stimulates the body to generate cancer-fighting white blood cells. The company intends to take the virus into clinical trials based on a promising animal study.

...

Scientists claim to have made recent progress targeting cancer cells with modded cold, herpes and smallpox viruses. These viruses infect and kill cancer cells while leaving healthy cells alone.
...

With the new JX-963 therapy, the virus doesn't have to do the work alone -- it elicits the body's own defenses to mop up cancer cells. The chemical that the virus secretes, granulocyte-macrophage colony-stimulating factor, or GM-CSF, is a protein that stimulates the production of white blood cells.

Interesting stuff. In theory, a virus could be altered to produce a range of useful proteins once it has access to the cellular environment - that might be good enough to give dendrimer therapies a run for their money if widely used engineered virus platforms emerge in the near future.

The existence of multiple competing technologies is one of the most promising signs of progress in any field. Competition turns the wheel, and it's good to see it here - that cancer with your name on it isn't getting any further away in time.

Posted by Reason at 6:19 PM
Permanent Link | View Comments (1) | Post Comment | TrackBack (0)

If you have a long memory, you'll recall I discussed work claiming a link between solar radiation and human longevity at the end of last year:

The assumed general mechanism in biology is good, whatever you might think of the rest of the theory; it's essentially covered by the reliability theory of aging - biochemical damage, caused by radiation or otherwise, lowers remaining life expectancy by reducing or destroying the functionality of component parts in the machine that is you.

...

Some interesting studies are quoted in the article on solar radiation, but it looks very much like a case of having a hammer and seeing nails in everything. It is logical to suppose that demonstrated variations in human longevity and disease by location of birth date in solar and seasonal cycles have something to do with the sun at root - but that certainly doesn't mean that the sun is the direct cause of the biochemical damage that leads to such variations. It might be solar radiation, or it might be one or more differences in other systems caused by variations in solar radiation - diet, weather, hormonal changes, behaviors ... just to rattle off a few. There are certainly many more.

I noticed a new paper from the same researchers today, and I thought I'd point your attention in that direction.

The light of life: Evidence that the sun modulates human lifespan:

This paper reinforces the findings of others regarding the seasonality of various diseases and that there are factors occurring early in utero that increase susceptibility to diseases later in life. The authors use the vital statistics of 320,247 Maine citizens over a 29-year period to show that those born in 3-year peaks of 11-year solar cycles live an average of 1.5 years (CL 1.3-1.7) less than those born in non-peak years. Males are more sensitive than females to this phenomenon, which is statistically demonstrable well into adult life, showing the effect of probable UVR on the early human embryo despite superimposed adult lifetime hazards.

...

This study also supports the reliability theory of aging which suggests that events affecting the genome early after conception are important in the expression of adult diseases.

Nice to see them giving the nod to reliability theory in this latest work, but it doesn't look like the authors are any closer to demonstrating likelihood of any one mechanism over another.

Posted by Reason at 7:19 PM
Permanent Link | View Comments (1) | Post Comment | TrackBack (0)

Scientists are not in the business of assigning names that make life easy for the rest of us, as illustrated by the PI3K-PTEN-Akt-TOR pathway. But you should read about it anyway, for the same reasons you read about research into calorie restriction and other aspects of metabolism and aging. It's good to know how we work, and gain an appreciation of how close scientists are to safely manipulating the core mechanisms on which a mammal is built:

Cancer, diabetes, and aging are related by their use of the PI3K-PTEN-Akt-TOR signaling pathway. This pathway controls how cells grow when nutrients are available and plays a role in how caloric restriction is able to extend lifespan. If parts of the pathway malfunction due to somatic or genetic mutations, cancer or diabetes can result. Thus, the pathway presents an exciting new frontier in medicine as researchers discover how to treat diseases by stopping the propagation of harmful signals and promoting the transmission of beneficial ones.

...

When nutrients are plentiful, growth factors spur the pathway to direct the cell toward growth and proliferation. If the pathway becomes overactive, however, cancerous growth results. Persistent activation by excess nutrients can lead to insulin resistance and diabetes. The pathway also appears to be involved in cellular senescence and aging in flies and worms and quite possibly in humans as well. Designing therapies to treat cancer, diabetes, and the aging process will be a challenge given the ubiquitous nature of this signaling pathway.

A challenge if you're of the school that believes the only way to tackle aging is to slow it down somewhat by redesigning metabolism, a hugely complex task that produces results of very limited benefit to those who are already old.

There is an alternate way forward, however: learn to repair the metabolism we have, and that we have invested so much time in understanding. Reversing or fixing the known biochemical changes that are the root of aging is arguably no harder - and arguably very much easier - than changing our metabolism. Yet progress along this path would greatly benefit those already old by producing therapies capable of rejuvenation rather than just a slowing of aging.

Work that leads to a greater understanding of our biochemistry will never be a waste - but it is very possible for the research community to head down a path that will never produce rejuvenation therapies in time to help those of us reading this now. Our job is to do our best to avoid that outcome.

Posted by Reason at 8:16 PM
Permanent Link | View Comments (2) | Post Comment | TrackBack (0)

Evidence of specific age-related declines in our biochemistry that are put off, avoided, reduced or otherwise slowed by the practice of calorie restriction - known as "dietary restriction" in some scientific circles - should no longer be a surprise. Here's another piece of welcome research for those who like to cut out the empty calories:

Effects of dietary restriction on hematopoietic stem cell aging are genetically regulated:

Diminished stem cell functions with age may be a major cause of anemias and other defects. Unfortunately, treatments that increase stem cell function can also increase the incidence of cancers. Lifelong dietary restriction (DR) is known to decrease spontaneous cancers and lengthen lifespan. This study examines the effect of DR on the ability of bone marrow cells to repopulate irradiated recipients and produce erythrocytes and lymphocytes.

...

Hematopoietic stem cell (HSC) numbers are highly variable in aged BALB mice, however, the observed loss of marrow function is due to a major loss in repopulating ability per HSC. DR greatly ameliorates this loss of function with age. In contrast, function per HSC in B6 mice is neither affected by age nor by DR.

Thus, DR increases or maintains increased marrow repopulating ability with age in the 3 different genotypes tested, but effects on function per HSC depend on genotype. The fact that DR increases or maintains stem cell function with age, while decreasing cancer, has far-reaching health implications.

Good news all round.

You'll recall that age-related decline in the capacity of stem cells to repair and generate new tissue likely has as much to do with the aging of their cellular support environment as any inherent change in the cell population. Are the stem cells becoming damaged, are they ramping down as a part of an evolutionary program to avoid cancer, or is the cellular environment controlling it all? A great deal of work is presently focused on answering these questions, and then doing something about it.

Posted by Reason at 5:57 PM
Permanent Link | View Comments (0) | Post Comment | TrackBack (0)

Some of you might have seen a recent documentary on longevity science on Canadian TV, and noticed some of the less enthused resulting press. So did Kevin Perrott, organizer of the Edmonton Aging Symposium and Methuselah Foundation volunteer, and sent in this letter to the Globe and Mail:

As a participant in the documentary "Living Forever: The Longevity Revolution" on David Suzuki's "The Nature of Things" on the CBC network, it was with great interest that I read a review on the program by your Arts columnist, Kate Taylor.

To be sure, given the content of the program and where the concept of 'aging' sits in the heart of western civilization, I am unsurprised at the negative impression she received from the program, but I find it personally gratifying that nothing of what she wrote was of much substance and really simply indicated her own bias. Still, our culture and society hold progress in high esteem and in the name of such forward motion I feel compelled to describe a different perspective than that written in the thoughts of Ms Taylor.

To start, Ms Taylor seems at a loss as to why anyone would want to live past 100. I'm not sure about Ms Taylor, but 100 years isn't enough for me to accomplish everything I want to do or see. For certain, just the little pleasures in life would be enough for me to wake up and be 100 years-old-and-a-day. There is always another book to read, embrace with a loved one, sunset to see, piano to play, planet to explore and belly laugh to share amongst innumerable other moments and precious activities that make life worth living. I'm surprised that as an accomplished writer this simple answer is opaque to Ms Taylor.

Ms Taylor muses how society would cope with the massive demographic shift of having many more people living a century or more. Firstly, as these therapies would effectively cure many age-related diseases, turning them from expensive chronic conditions to acute and preventative syndromes, the 80% of our health care dollar spent dealing with the degenerative diseases of old age would be dramatically reduced, freeing billions of dollars of capital. I would refer Ms Taylor to some serious, high-profile gerontologists in the U.S. who have proposed a "Longevity Dividend" (S. Jay Olshansky et al.) who are urging congress to allocate funds to slow aging showing that even a tiny decrease in the rate of aging would result in tremendous economic shifts to the good. Secondly, there are of course many sociological consequences of having healthy supercentenarians in our midst. Many more grandparents would live to be great-grandparents which would obviously bolster the sense of family continuity. Many more healthy consumers would bolster the economy. Many more healthy individuals, who have lived through the hormone-ridden decisions of youth to arrive at the 'been there done that' period of senior citizenship, would find themselves able to offer their experience to mentor upcoming generations from the perspective of hale and hearty bodies rather than the invisibility of cowering in the shadows of the institutions they currently inhabit.

How indeed would society cope with a generation of individuals who have lived a century or more? Perhaps our world may achieve a more 'mature' perspective and many perennial problems which have escaped solution may be approached from a different direction with the attitudes of altruism and cooperation we find more prevalent at advanced ages. For a small taste of what one might expect in spades from healthy supercentenarians, have a look at CivicVentures.Org. Ms Taylor and perhaps you might envision a different world than one where the elderly simply take up space.

Given that Ms Taylor is not a scientist, nor does her bio list any training in science, it is perhaps understandable that her treatment of the facts and feasibility behind the technologies discussed in the program is superficial at best. The disinterest and lack of understanding of the subject matter is exemplified when she asks the question "Where will all these kidneys come from?" with reference to the segment of the program dealing with cryobiology. She doesn't even bother to mention his name when she refers to Dr. Greg Fahy where he describes the technology for freezing organs for use in later life as they are required. Her question as to where the 'kidneys' would come from indicates that she never heard/understood a word of most of his interview. Dr. Fahy clearly says that such organs would be tissue-engineered from a patient's own cells, something which has already seen success in Anthony Atala's work at the University of Pittsburgh Medical Center where he grew the first organ, a bladder, outside the body and transplanted it to help a child lead a more normal life. There are plenty more well publicized examples of promising tissue-engineering technology. It is likely that many have not heard of the rapid progress in the use of printing technology to actually 'print' solid organs, but a look at the work of Gabor Forgacs of the University of Missouri in 'bioprinting' with 'bioink' might be an interesting read. (New Scientist, April 13, 2006)

Ms Taylor does bring up one very important point; that of the potential disparity in the availability of these therapies. However, is such potential disparity in availability really an argument against development? Is the fact that we can't share with the Third World a reason to forgo the development of valuable medical technologies for people suffering today? It would seem that the problems are not related in the least. I don't think distribution problems have much to do with ethical questions of developing technologies that will eventually benefit billions of people. If we followed the logic that therapies should not be available to any unless they are available to all, therapies would never be developed. Restricting the development and availability of therapies will result in exactly the effect that Ms Taylor fears, the wealthy will access such technologies in countries that do not have such issues through medical tourism while the situation for the poor remains unchanged at home or is worse. Developing the therapies at home and making them accessible as quickly as possible to as many as possible is what we should be shooting for, not restricting access and forgoing development.

I was somewhat taken aback by Ms Taylor referring to the program as an example of "immature journalism" when actually her own story exemplifies a remarkable lack of interest in wanting to delve any deeper into the background than is needed to satisfy her own closed-minded preconceptions of what the value of the elderly is. She ultimately willfully blinds herself to the fact that old people suffering from age-related disease in need of therapies are PEOPLE, loving and beloved, parents and grandparents, individuals who have contributed to her well-being and the world. Off-hand remarks such as "What is it all those extra centenarians are going to do, other than consume more fossil fuels?" indicate that she has obviously not thought things through, or about how abysmally unethical it is to talk about PEOPLE as if they have nothing to offer when they reach old age. Such a viewpoint is sadly endemic in our society, and changing such a viewpoint is one welcome consequence that would result from having many healthy oldsters around a century or more.

Finally, Ms Taylor berates Dr. Suzuki for featuring a program where more people suffer less and live longer than previous generations, intimating that the focus of environmentalism would be ill-served by having yet more healthy elderly people on the planet. She completely ignores the fact that the elderly are the ones whose perspective is most valuable in the preservation of the environment as they have seen the changes wrought by years of empire building by the relatively young. If people knew they would live to be centuries old, perhaps they may think twice about making decisions which foist onto future generations the environmental fallout from their greed and poor stewardship. Dr. Suzuki is right on the money in suspecting that older individuals would care substantively more than those who we know from past experience care little.

Sadly, the attitude expressed by Ms Taylor is all too prevalent in a society that glorifies youth and denigrates the elderly. As is the case however, the young soon enough grow old and will experience the motivation necessary to work for changes that will create a world where getting older is truly something that enriches, rather than diminishes, the individual and society. If we all work together, we will avoid the worst pitfalls and bring about such a day all the sooner.

Kevin Perrott PhD Student
Department of Biochemistry
University of Alberta

I should have mentioned that Perrott isn't content with organizing impressive conferences on the repair of aging and improving the lot of the Methuselah Foundation, but has also gone back to the grindstone of earning a doctorate. He is changing careers to become a molecular biologist for aging research, and thereby help to get the job done in person. Now there is dedication to the cause, ladies and gentlemen - he's an example for all of us.

Posted by Reason at 5:10 PM
Permanent Link | View Comments (1) | Post Comment | TrackBack (0)

Yesterday I stumbled onto a press release on the topic of funding from the Ellison Medical Foundation and the American Federation for Aging Research. I am very struck by the tone of the piece:

The Ellison Medical Foundation has awarded AFAR more than $2.8 million to support 45 postdoctoral fellows (both MDs and PhDs at any level of postdoctoral training) over the next three years in the fundamental mechanisms of aging. With this new commitment, the Ellison Medical Foundation/AFAR partnership has increased five-fold the number of researchers it will support.

...

There are so many promising scientists yet we are only able to fund eight percent of the applicants who seek grants. There's a potential to lose a tremendous brain trust of future leaders in aging research. The Ellison Medical Foundation has taken a lead role in helping the next generation of researchers establish careers and an aging society will benefit

...

In the face of this opportunity we currently see declining federal support for scientists. Those just beginning their careers are especially vulnerable as support dries up. Our hope is that this decline is temporary, yet even a temporary reduction in support for scientists just beginning their careers, or those deciding whether to stay in science or build a career elsewhere, could result in the loss of most of a whole generation of scientists.

...

"While AFAR-supported grant programs have traditionally focused on early-career scientists, it is also important to sustain that investment in our scientists at all stages of their careers," said Stephanie Lederman. This generous grant can make all the difference in allowing years of painstaking research to continue."

"Mid-career scientists, with newly acquired tenure, are at a unique career stage. Freed from worry about getting tenure and job stability, they have more intellectual freedom than they have ever had before. We hope to empower them to try riskier research with great potential pay-off, for themselves and for an aging society."

This might as well be language lifted from a mythical government release on the Full Employment Act for Gerontologists. It's all so grey and tired - rescue the scientists, pay the scientists, help the scientists. Note the utter absence of any sort of discussion of goals or results. What are these scientists actually doing? What is the value of it? Where are they going? When will they get there? What does it mean to me?

This sort of thing is exactly why there is little public support for or understanding of mainstream aging research. I've long said that basic research is no different from any other human endeavor. It isn't magic, immune to planning - you can set goals, plans and schedules. You can invest in research in exactly the same way as commercial companies invest in research day in and day out. Those who claim that you can't set goals, timelines, explain matters to the public, create excitement and make real fireworks fly in an area of fundamental research are generally much more interested in the steady flow of dollars or their own particular hobby than in actually getting something meaningful accomplished.

The drift of mainstream American science into government dependency has drained it of vigor and accountability to produce real progress. There's a reason why most of the interesting, productive scientists largely work outside that system, in the market or philanthropic ventures.

Another thought: the languishing of aging science - in comparison to, say, regenerative medicine, tissue engineering or cancer research - makes $2.8 million a big deal. $10 million from the Glenn Foundation to establish the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging was a big splash in the pond.

With those numbers for comparison, note that the Methuselah Foundation has $4.8 million pledged to Strategies for Engineered Negligible Senescence (SENS) research. I will venture to say that the Foundation has succeeded in building up to that level of funding by being everything that the Full Employment Act for Gerontologists is not. There is a plan, there are goals, there are timelines, there is accountability for failing to deliver - and a real effort to explain what all this work and funding really means to folk like you and I.

Posted by Reason at 7:27 PM
Permanent Link | View Comments (2) | Post Comment | TrackBack (0)

Charles Platt, who presently works with Suspended Animation, Inc., has a long history with the cryonics community. Over at CryoNet, you'll find a three part report on the recent Alcor conference:

• Part One
• Part Two
• Part Three

There might be a touch too much insight into the sausage-making process for some folk. Small communities of passionate people tend to produce the sort of history, disagreements and debates worthy of a writeup - and that might not appear too noble at first glance, or from certain angles. There's no such thing as too much transparency or constructive criticism, however - for any service, never mind one upon which you are relying for a chance at life. It seems to me that Alcor is more transparent than many organizations seeded by a small, motivated community.

The cryonics industry, small and still very dependent on passion and volunteerism, suffers from all of the problems you normally find in those circumstances. Resources are tight, bad apples can have a disproportionate effect, and so forth. That the industry has sustained itself and even managed some growth and professionalization over a number of decades speaks well of those folk who stepped up and got the job done when a crisis loomed. But that's no way to run for the long term; one day, through accident or decline, there will be no-one there capable of saving the day.

This is why the cryonics industry needs publicity, economic offshoots, spin-off technologies, demonstrated progress in research related to the core ideal of cryopreservation and restoration, and other means of becoming larger and more viable. The goal must be more eggs in more baskets, such that there will always be resources on tap to handle the unexpected.

Posted by Reason at 10:31 AM
Permanent Link | View Comments (0) | Post Comment | TrackBack (0)

You'll find a rather interesting paper (abstract and full PDF are available) at the Annals of the New York Academy of Sciences on the topic of manipulating autophagy to repair some classes of age-related damage to cells and cellular components.

Aging denotes a post-maturational deterioration of cells and organisms with the passage of time, an increased vulnerability to challenges and prevalence of age-associated diseases, and a decreased ability to survive. Causes may be found in an enhanced production of reactive oxygen species (ROS) and oxidative damage and not completed housekeeping.

Caloric restriction is the most robust anti-aging intervention known so far. Similar beneficial effects on median and maximum life-span were obtained by feeding animals a 40% reduced diet or by every-other-day ad libitum feeding. In both instances, animals are