Longevity Meme News and Commentary

David Deutsch Speaks With Aubrey de Grey

Fri, 09 May 2008 19:59:11 CST

Via Thoughtware.TV, a video interview on the science of the Strategies for Engineered Negligible Senescence (SENS), a path to repairing the biochemical damage of aging and greatly extending the healthy human life span: "Renowned Quantum Physicist, and father of the Quantum Computer, David Deutsch [speaks] with Aubrey de Grey about the scientific details, and feasability of life extension technology SENS ... Filmed in the Natural History Museum, Oxford, with kind permission of the trustees." Beneath the dinosaur skeletons, in fact. SENS is far more than just research and medical technology, just as the challenge in engineering longevity is far more than a matter of science. SENS is also very much about educating the public of the potential of today's science, raising support for directed funding in longevity science, and forging a new research community enthused to intervene in the aging process as soon as possible rather than just passively documenting it.

View the Article Under Discussion: http://www.thoughtware.tv/videos/show/1989
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The Future of Regeneration

Fri, 09 May 2008 16:31:34 CST

If only the future of longevity science was as widely supported, understood and acclaimed as the future of regenerative medicine and tissue engineering. The Times Online notes that "within decades stem-cell technology will make it possible to grow replacements for virtually any part of the human body ... the emerging field of regenerative medicine would enable a patient's own cells to be used to build hearts, livers and kidneys, complete with their own blood supply, to replace diseased organs. The advance could make many transplants unnecessary and allow the regeneration of brain tissue and limb parts. ... We know the human genes that can do this do exist, because human foetuses can do it. If a finger is lost before three months' gestation in the womb, it will grow back. The genes are there; we just need to know how to reactivate them. When we started on this work in the 1960s, we knew all these things would become possible . . . it will not be far off. The biggest stumbling block has been money, but now there is huge investment in the field and things are moving rapidly."

View the Article Under Discussion: http://www.timesonline.co.uk/tol/news/uk/science/article3867838.ece
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Improving Targeted Nanoparticles

Thu, 08 May 2008 17:54:39 CST

A great deal of tomorrow's better, more effective medicine will rest on targeting nanosystems that can deliver therapies to specific cell populations in the body. Much of this development is taking place in the cancer research community, but you can be sure there are a thousand and one other uses: "Using nanoworms, doctors should eventually be able to target and reveal the location of developing tumors that are too small to detect by conventional methods. Carrying payloads targeted to specific features on tumors, these microscopic vehicles could also one day provide the means to more effectively deliver toxic anti-cancer drugs to these tumors in high concentrations without negatively impacting other parts of the body. ... Most nanoparticles are recognized by the body's protective mechanisms, which capture and remove them from the bloodstream within a few minutes. The reason these worms work so well is due to a combination of their shape and to a polymer coating on their surfaces that allows the nanoworms to evade these natural elimination processes. As a result, our nanoworms can circulate in the body of a mouse for many hours. ... We are now using nanoworms to construct the next generation of smart tumor-targeting nanodevices."

View the Article Under Discussion: http://www.sciencedaily.com/releases/2008/05/080506200531.htm
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CIRM Funds For the Buck Institute

Thu, 08 May 2008 17:20:25 CST

The Buck Institute for Age Research is one of the recipients of research funds awarded by the California Institute for Regenerative Medicine (CIRM): CIRM "has awarded $20.5 million to the Buck Institute for Age Research to build a 'CIRM Center of Excellence' on its Novato campus. ... The Buck Institute's proposed research program for the Center of Excellence is guided by the promise that human embryonic stem cells may provide a model system to study and understand the process of human aging and age-related disease. ... The specific aims are to use human embryonic stem cells or their differentiated progeny to study how cells self-renew and to examine processes involved in the biology of aging including DNA repair, genome integrity and programmed cell death. The long-term goal of the program is to unravel the mysteries of aging and age-related human diseases by understanding the fundamental biological process of aging in appropriate human cell models." Which is an excellent summary of the slow boat, look-but-don't-intervene approach, and shows why those researchers invested in this approach - rather than the much more direct repair of damage approach and the goal of curing aging as soon as possible - believe, incorrectly, that any successful intervention in aging is a long way away.

View the Article Under Discussion: http://www.buckinstitute.org/site/index.php?option=com_content&task=view&id=462
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A Discussion on Animal Longevity

Wed, 07 May 2008 12:47:12 CST

Researchers talk about the basis for animal longevity at the Post-Gazette: "What is it about tortoise biology that makes them so long-lived? The same thing can be asked of some even more intriguing creatures in the Methuselah Club, including the rough-eye rockfish (up to 205 years), the bowhead whale (211 years) and the ocean quahog clam (225 years). ... In the bowhead whales, researchers have been able to chart the slow change in the orientation of amino acids in their eyelids, he said, while the rockfish and quahog lay down age-related rings, the rockfish in an ear bone and the quahog on its shell. ... Dr. de Magalhaes said he did a survey two years ago of hundreds of species of mammals, and 'what we showed is there is really no correlation between metabolic rate and life span in mammals.' ... 'I'm a little bit skeptical about the idea that telomeres contribute that much to aging,' said Dr. de Magalhaes, given the fact that mice, which live about four years, have longer telomeres than humans. ... scientists have been able to create mice with short telomeres and with long telomeres, and 'the mice with long telomeres don't have a significant difference in life span.' Unfortunately, the article doesn't delve into mitochondrial biochemistry, which looks like it might be much of the root of differences in life span, in mammals at least.

View the Article Under Discussion: http://www.post-gazette.com/pg/08128/879500-51.stm
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$7 Million For Longevity Research

Wed, 07 May 2008 12:20:36 CST

The Methuselah Foundation has reached $7 million pledged to Strategies for Engineered Negligible Senescence research, aimed at the repair and reversal of molecular and cellular damage that causes aging. "Congratulations are due to all the Methuselah Foundation volunteers and generous donors who have made our ongoing SENS research programs a reality. Thank you all! You can find out more about the SENS research funded and organized by the Methuselah Foundation at our website, and in the most recent progress report ... The Foundation currently sponsors research in two of the seven strands of the SENS program: preventing the harm caused by mitochondrial mutations (MitoSENS) and degrading damaging, long-lived cellular debris (LysoSENS). ... A selection of [further] projects within the SENS plan are ready to be launched as Foundation-sponsored research programs. [As] for MitoSENS and LysoSENS, these projects will start small (likely with only a single researcher), with the aim of delivering high leverage in terms of the credibility of the approach."

View the Article Under Discussion: http://blog.methuselahfoundation.org/2008/05/7_million_pledged_to_sens_long.html
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Rebooting the Immune System Repairs MS

Tue, 06 May 2008 16:26:31 CST

This is interesting news from the Australian, considering past work on rebooting the human immune system to repair otherwise irreversible damage: "Dr Freedman, who specialises in treating [multiple sclerosis (MS)], wanted to study how the disease unfolds. He set up an experiment in which doctors destroyed the bone marrow and thus the immune systems of MS patients. Then stem cells known as hematopoeitic stem cells, blood-forming cells taken from the bone marrow, were transplanted back into the patients. ... We weren't looking for improvement. The actual study was to reboot the immune system. ... Once MS is diagnosed [you've] already missed the boat. We figured we would reboot the immune system and watch the disease evolve [but] have yet to get the disease to restart ... Not a single patient, and it's almost seven years, has ever had a relapse ... We are trying to find out what is happening and what could possibly be the source of repair." This is still a comparatively unsafe procedure, but with enough incentive, resources will be allocated to make it safer and better. This is good, because benefits to health and longevity are likely to result from a safe way of rebooting an age-damaged immune system.

View the Article Under Discussion: http://www.theaustralian.news.com.au/story/0,25197,23658555-12377,00.html
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Regenerating the Trachea

Tue, 06 May 2008 15:53:47 CST

Regenerative medicine moves forward, organ by organ: "The trachea and other respiratory tubes, like most tubes in the body, have an intricate, three-layer architecture. The inner layer, or epithelium, interacts with whatever is flowing through the tube; in the case of the trachea, air. The middle layer is composed of muscle that constricts or relaxes the tube, and the outer layer consists of connective tissue that supports microvessels and small nerves. ... researchers found that it is not necessary to recapture the ordered layering to heal injuries. Instead, they concentrated on restoring cellular health. When cells are intact and have regained their biological function, they need only reside near the injured tissue to enhance overall repair. [Scientists] achieved this repair state by delivering a mixture of new healthy cells derived from the epithelial lining and the nourishing blood vessels. The combination of epithelial and endothelial cells take over the biochemical role lost with cell damage. The healthy cells release growth factors and other molecules necessary for healing tissue, and can modulate their delivery in response to physiological feedback control signals."

View the Article Under Discussion: http://web.mit.edu/newsoffice/2008/trachea-0505.html
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Interviewing the CSO of CIRM

Mon, 05 May 2008 11:20:27 CST

Over at Nature, an interview with the new chief science officer of the California Insitute for Regenerative Medicine: "I really think that we're getting awfully close to working with patients now. We will never institutionally neglect basic science, but the shift to translational work is definitely now a priority ... The unknown is that we have no control over the cells once they're transplanted or transfused. I feel very strongly that the animal models of disease do not reflect the heterogeneity of the environments into which we will be putting the cells in diseased humans. Pharmacologically induced Parkinson's disease is not the same as the natural human disease, for example. ... The immunogenicity issue of the transferred cells is far from solved. People are also concerned about tumorigenesis, and there's been a lot of in vitro progress in addressing that. ... I think people underestimate how expensive this research is. Yes, it's a lot of money, but it's certainly not unlimited. We have to figure out a way to be involved in clinical trials, and how best to use our resources in clinical trials. ... We've got to make concrete decisions, at least as far as phase I trials, in the next couple of months."

View the Article Under Discussion: http://www.nature.com/stemcells/2008/0804/080410/full/stemcells.2008.59.html
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What If Cryonics Wasn't Cold?

Mon, 05 May 2008 11:02:06 CST

The purpose of cryonics is to preserve the body and brain with as little small-scale damage as possible for revival via plausible future technologies, most likely medical nanomachinery. To save lives, in other words. Depressed Metabolism has previously argued that it's something of an accident of history that the cryonics industry uses cold-based preservation rather than a form of warm chemical preservation, and here elaborates on future molecular nanotechnologies that may achieve warm biostasis: "To see how one approach would work, imagine that the blood stream carries simple molecular devices to tissues, where they enter the cells. There they block the molecular machinery of metabolism - in the brain and elsewhere - and tie structures together with stabilizing cross-links. Other molecular devices then move in, displacing water and packing themselves solidly around the molecules of the cell. These steps stop metabolism and preserve cell structures."

View the Article Under Discussion: http://www.depressedmetabolism.com/2008/05/01/warm-biostasis-through-nanotechnology/
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Calorie Restriction and Dietary AGEs

Fri, 02 May 2008 20:51:29 CST

It looks plausible that some portion of the health and longevity benefits of calorie restriction stem from a reduction in the intake of dietary advanced glycation end products (AGEs). AGEs are created in the body as a metabolic side-effect, but also found in your food: "Increased oxidative stress (OS) underlies many chronic diseases prevalent in aging. Data in humans confirm the hypothesis that [AGEs] and other oxidants derived from the diet may be major contributors to increased OS in normal adults as well as those with diabetes mellitus or kidney failure. Mice fed a diet with a lowered (approximately 50%) content of AGEs or a typical calorie-restricted (CR) diet, accumulated a smaller amount of AGEs [and] did not have increased oxidant stress or cardiac or kidney fibrosis with aging. However, the findings in mice fed a CR diet with an increased content of AGEs resembled those in mice fed a nonrestricted diet that had the usual higher content of AGEs. Thus, there was an inverse correlation between the dietary AGE content, [oxidative stress], organ damage, and life span."

View the Article Under Discussion: http://pmid.us/18448795
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More Stem Cells Than Thought, Perhaps

Fri, 02 May 2008 10:46:08 CST

Ouroboros on just how many stem cells we have: "It is widely accepted that stem cells are involved in tissue regeneration. It is also widely accepted that (in most organs) stem cells are vanishingly rare. So: if there doesn't happen to be a stem cell adjacent to a site of damage, how can stem cells be involved in the process of tissue repair? There might be more stem cells than we think, because we've been missing them for some reason. This possibility is strongly supported by the recent findings of Zuba-Surma et al., who have discovered a population of tiny pluripotent cells (termed, appropriately, very small embryonic-like, or VSELs) scattered throughout the body. ... Note that both VSEL number and potency diminish with age, consistent with the decrease in proliferative and regenerative capacity that we see in older animals. ... Required skepticism: VSELs are both brand new and (so far as I can tell) idiosyncratic to a single group's work. Before we get too worked up about this, I'd like to see the work reproduced by other labs and in other systems. Hopefully that sort of confirmation is already underway." The easier stem cells become to source, the faster research and development will proceed.

View the Article Under Discussion: http://ouroboros.wordpress.com/2008/05/01/widdle-biddy-stem-cells/
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Targeted Chelation Versus Lipofuscin Buildup?

Thu, 01 May 2008 17:44:31 CST

In a similar fashion to the way in which antioxidants change from dubious to demonstrably beneficial for lifespan when targeted to mitochondria, it is proposed that chelation targeted to the cell's lysosomes can slow the accumulation of lipofuscin in your cells. You might recall that lipofuscin buildup with age contributes to age-related degeneration by eventually destroying the ability of cells to function. "Since the sensitivity of lysosomes to oxidative stress can be manipulated by altering the intralysosomal level of redox-active iron, it follows that lipofuscin formation might also be influenced. It is suggested that pulse doses of iron chelators that easily penetrate membranes could be used to diminish lipofuscinogenesis." But don't run out to buy chelation products - ingesting that stuff won't send it anywhere near your lysosomes, just as swallowing antioxidant products won't affect your mitochondria. More engineering is needed, and in this case a technology demonstration to confirm the proposal.

View the Article Under Discussion: http://dx.doi.org/10.1089/rej.2007.0621
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Stress and the Damage of Aging

Thu, 01 May 2008 17:01:37 CST

Stress speeds some modes of age-related decline, probably via the mechanisms of chronic inflammation: "Responses to stress anticipate adaptation to an unacceptable disparity between real or imagined personal experience and expectation, including adaptive stress, anxiety, and depression. However, if stress persists, it may lead to chronic diseases, ranging from inflammation and cancer to degenerative diseases. For some time, only remarkable stress was acknowledged to induce immune and vascular alterations, such as infection or hypertension. Now it is known that moderate stress independent of conventional risk factors can induce a potent alteration of health conditions and consequently shorten life quality and lifespan. ... Stressful life conditions turn out to induce a diffuse (systemic) pro-inflammatory status. Subclinical chronic inflammation is an important pathogenic factor in the development of metabolic syndrome, a cluster of common pathologies, including cardiovascular disease." As for other lifestyles that induce chronic inflammation, you can wait (and suffer) while researchers build drugs that block the mechanisms at fault, or you work to change your circumstances to cause less damage over the long run.

View the Article Under Discussion: http://dx.doi.org/10.1089/rej.2008.0667
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Plan For a Longer Life

Wed, 30 Apr 2008 22:04:57 CST

Life expectancy is increasing, and the rate of increase is accelerating. People live longer than they expect to live. If you lay the foundations of your future - savings, investment, work - with an eye to your grandparent's lifespan and strategies, then you're not planning well. "As greater longevity is increasingly becoming a fact of life, people are leaving themselves vulnerable to financial hardship at a time when they are most in need ... Nearly half the population of the UK said they were only expecting to live to the same age as their parents' generation ... Interestingly, whilst people do not realise the possibility of themselves living longer than their parents, they do recognise that their children will live longer lives than they will. However, 18-24 year olds grossly underestimate this, with only 25% of them thinking that their children will live longer, whilst 44% 55 year olds thought this. ... People acknowledge increased longevity for younger generations but do not realise that this is a very real issue for them today." Plan for an interesting future - and recognize that you have more than enough time to save and invest all you will need, even in the best scenarios of radical life extension.

View the Article Under Discussion: http://www.easier.com/view/Finance/Pensions/News/article-176667.html
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