Longevity Meme Newsletter, January 07 2008

January 07 2008

The Longevity Meme Newsletter is a weekly e-mail containing news, opinions and happenings for people interested in healthy life extension: making use of diet, lifestyle choices, technology and proven medical advances to live healthy, longer lives.



- Another Swing Round the Sun
- Video FAQs on SENS and Other Longevity Science
- Creating Wealth or Persuading Wealth
- Discussion
- Latest Healthy Life Extension Headlines


Here we are again, those of us who made it, a year older and a year more experienced; another swing round the sun completed. We are somewhat more damaged by the workings of our metabolisms and biochemical happenstance, that much closer to catastrophic failure of one of the many intricate biological systems we depend upon. I hope we've managed to use that time well - it passes us at great cost, when considering what it will take to create more of it:



Five new sets of educational videos are up at the Methuselah Foundation website. Each is a short explanation of a single important concept in longevity science or the Strategies for Engineered Negligible Senescence (SENS), presented by Foundation chair and biomedical gerontologist Aubrey de Grey. Take a look:


If you find them useful, send the links to your friends or embed them on your own websites or forum posts. They are hosted by VideoJug, so can be embedded pretty much anywhere.


We are fortunate to live in an era in which there is a chance to greatly extend our healthy, active lives through pushing forward the frontiers of medical science. But doing so will require significant resources - and where are those resources going to come from?


"Where do resources for research originate? From the wealth of those who step up to make a difference. Those of us who strive to improve the lot of longevity research are faced with a fairly simple economic choice whenever we would like to pour more wealth into the pot, to help more hands make progress arrive more rapidly. Do we work to create that needed wealth, or do we work to persuade those with wealth to invest in research that will benefit their future health and longevity? How long will each path take? What is the likelihood of success in either case? I can assure you that even if you don't think that you think about these things, you do. We are all creatures of rational economic action, at every level of choice from persuading a friend versus chipping in a dollar yourself up to making investments to grow capital versus raising funds from investors and philanthropists."


The highlights and headlines from the past week follow below.

Remember - if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!




To view commentary on the latest news headlines complete with links and references, please visit the daily news section of the Longevity Meme: http://www.longevitymeme.org/news/

Tissue Engineering Replacement Skin (January 04 2008)
ScienceDaily looks at the work of a German group in the tissue engineering field: "We pluck a few hairs off the back of the patient's head and extract adult stem cells from their roots, which we then proliferate in a cell culture for about two weeks. Then we reduce the nutrient solution until it no longer covers the upper sides of the cells, exposing them to the surrounding air. The increased pressure exerted by the oxygen on the surfaces of the cells causes them to differentiate into skin cells ... In this way, the researchers can grow numerous small pieces of skin, produced individually for each patient, which add up to a surface area of 10 to 100 square centimeters when pieced together. ... The researchers expect to grow skin grafts for 10 to 20 patients a month in 2008. ... At present, chronic wounds are treated by grafting on the patients' own skin, which is normally taken from the thigh. This leaves scars on both the thigh and the treated wound ... we can achieve the same chances of recovery without hurting the patient. Moreover, the artificial skin grows onto the wound without scarring."

On the Methuselah Mouse Prize (January 04 2008)
Thoughts on the Methuselah Mouse Prize for longevity research from the Economist: "To encourage people to take his ideas seriously, Aubrey de Grey, the originator of the strategies for engineered negligible senescence, has organised a competition. He is offering a prize for the development of what he calls a Methuselah mouse. There are actually two prizes to be had. One is for longevity, the other for rejuvenation. The prize for longevity can be won by a new strain of mouse - one bred or genetically engineered to live a long time. That for rejuvenation requires treatment to begin when the mice are already in middle age. ... The winner establishes a record that others have to break. At the moment the records for longevity and rejuvenation are five years and almost four in an animal that normally lives for three. How translatable the lesson of a Methuselah mouse will be to people is a matter of debate. ... The reason mice age rapidly is that they have lots of predators and would get killed quickly anyway. Humans have few predators and tend not to get killed - at least not as easily as mice. It is therefore worthwhile for people to evolve better repair mechanisms than mice, and thus to age more slowly." Nonetheless, radical life extension in lesser mammals is an important step along the way - not just as a proving ground for the science, but as a way of educating the public as to the degree to which aging can potentially be reversed in humans.

How Can Evolution Produce Ageless Animals? (January 03 2008)
Many extremely long-lived animal species exist, and some may even be ageless. How can evolution, biased to early reproductive success at all reasonable cost, produce such a species? Some modelling in this paper: "Senescent aging is an irreversible deterioration in physiological condition with age, which many organisms express even when removed from harmful environmental influences. The inevitability of senescence for repeatedly reproducing organisms has well-developed theoretical foundations. Since reproduction carries physiological costs, natural selection in a hazardous environment favors reaping early benefits, and delaying the cost in physiological decline until later in life when there is a greater chance of being dead from exogenous factors. But some organisms show negligible senescence, and a few, such as Hydra and the Bristlecone Pine, appear to have indefinite lifespans. We ask how such species could have evolved from ancestors with senescent life histories. In large populations, juveniles attempting recruitment into the adult population can be 'crowded out' by already established adults. We show how this phenomenon can trigger a process of runaway selection on ever-reducing senescence, which can even result in the evolution of intrinsic immortality." There are good arguments for learning more about the biology of longevity in species near and far from humans.

The Economist on Repairing Aging (January 03 2008)
The Economist looks at the Strategies for Engineered Negligible Senescence (SENS) and other longevity research: "To think about the question, it is important to understand why organisms - people included - age in the first place. People are like machines: they wear out. That much is obvious. However a machine can always be repaired. A good mechanic with a stock of spare parts can keep it going indefinitely. Eventually, no part of the original may remain, but it still carries on, like Lincoln's famous axe that had had three new handles and two new blades. ... All organisms are going to die of something eventually. That something may be an accident, a fight, a disease or an encounter with a hungry predator. There is thus a premium on reproducing early rather than conserving resources for a future that may never come. The reason why repairs are not perfect is that they are costly and resources invested in them might be used for reproduction instead. Often, therefore, the body's mechanics prefer lash-ups to complete rebuilds - or simply do not bother with the job at all. And if that is so, the place to start looking for longer life is in the repair shop."

A Glance at Novel Cartilage Engineering (January 02 2008)
Globes Online gives good insight into one of the more active areas at the commercial end of tissue engineering research. Scaffold technology is maturing in a number of directions, including this one: Regentis' "replacement cartilage does not include live cells. In fact, it has expunged the tissue itself from the underlying concept behind its alternative tissue. Instead, it has formed a form of interim synthetic bridge which when applied to the injured limb, allows natural tissue to grow and regenerate. The company regulates the rate of the synthetic product's disintegration, in tandem with the growth of natural tissue. ... When body tissue has been damaged, a blood clot is usually formed which also acts a bridge for the building of new tissue and sends a signal that promotes tissue building. The problem occurs when the damage is too extensive and the blood clot can't create the bridge. Once that happens it disintegrates fairly quickly ... the implant can last for up to a year without breaking down. It is very much like the process of coating drugs with synthetic materials to enable a slow release."

More On Alpha-Synuclein and Parkinson's Disease (January 02 2008)
Parkinson's disease researchers have been expanding their understanding of - and interfering in - processes that involve alpha-synuclein. EurekAlert! here looks at some of the important mechanisms of autophagy in this context: "Alpha-synuclein molecules modified by dopamine bound tightly to the lysosomal membrane, but they got stuck there and weren't effectively transported into the lysosome ... As a result, the alpha-synuclein molecules altered by dopamine were poorly degraded, and the presence of these molecules on the lysosomal membranes interfered with autophagic digestion of other compounds as well. ... We propose that inhibition of autophagy caused by dopamine's alteration of alpha-synuclein could explain the selective death of dopamine-producing nerve cells in Parkinson's disease ... interference with autophagy has also been implicated in other neurodegenerative diseases including Alzheimer's." One thread of the Strategies for Engineered Negligible Senescence (SENS) is devoted to repairing or preventing the failure of the lysosome under load - it is a broad problem that contributes to many age-related conditions.

$100,000 More For SENS Research Donations In 2008 (January 01 2008)
From the Methuselah Foundation, news of more support for research aimed squarely at repairing the biological damage of aging: "I'm happy to report that December 2007 year-end donations to fund the Methuselah Foundation's Strategies for Engineered Negligible Senescence (SENS) research program succeeded in matching two consecutive $25,000 matching grants from Michael Cooper and Doug Arends. ... Looking to the year ahead, and plans for expansion into new branches of SENS research, Foundation supporter Ryan Scott has set up a $100,000 matching fund for all research donations made in 2008. The same rules apply as for this past December: donations are first matched 100% by Ryan's fund, and then that total is matched again at 50% by Peter Thiel's $3 million matching fund. That means that all your SENS research donations will be tripled - a $100 donation becomes $300 for new research into longevity medicine. Jump on in! These are the early years in a steep growth curve - and it's up to all of us to help make that statement true. Donations to help bring about a future of greater health and longevity can be made at the Methuselah Foundation website, where you can also learn more about how funds are spent and the results achieved to date."

More On DNA Damage, Stem Cell Aging (January 01 2008)
To what degree does accumulated DNA damage contribute to the aging of stem cells? (Versus, say, changes in their niche or other potential causes). From this freely available review paper: "Adult stem cells are extremely important in the long-term maintenance of tissues throughout life. They regenerate and renew tissues in response to damage and replace senescent terminally differentiated cells that no longer function. Oxidative stress, toxic byproducts, reduced mitochondrial function and external exposures all damage DNA through base modification or mis-incorporation and result in DNA damage. As in most cells, this damage may limit the survival of the stem cell population affecting tissue regeneration and even longevity. ... a number of human genetic abnormalities associated with aging, and those replicated in the mouse, suggest that loss of DNA repair may contribute to the aging process. This review will provide support for the argument that maintenance of the adult stem cell genome through robust DNA repair is fundamental in the prevention of aging and disease; furthermore, that failure of genomic maintenance is a leading cause of cancer, as well as senescence."

p66(Shc) and Mechanisms of Mouse Longevity (December 31 2007)
As noted back in the Fight Aging! archives, scientists have been picking away at the knot that is p66(Shc) for a while now, tying the activity of this protein to many of the other mechanisms of metabolism considered important to longevity and resistance to common age-related damage and disease. Here's more on the topic: "The notion that mice carrying a targeted mutation of the p66(Shc) gene display prolonged lifespan, reduced production of intracellular oxidants, and increased resistance to oxidative stress-induced apoptosis prompted a series of studies aimed at defining the biochemical function of p66(Shc) and its possible implication in cardiovascular diseases. Indeed, p66(Shc-/-) mice are protected against vascular, cardiac, and renal impairment attributable to hypercholesterolemia, aging, diabetes, and ischemia/reperfusion. ... On the whole, the evidence so far reported and here discussed supports the concept that pharmacological modulation of p66(Shc) expression and activity may be a novel and effective target for the treatment of atherosclerotic vascular disease as well as myocardial adaptation to hypertrophic, inflammatory and neuro-hormonal stimuli in the overloaded heart."

More Gene Therapy For Parkinson's Disease (December 31 2007)
ScienCentral on trials of one particular gene therapy aimed at ameliorating the symptoms of Parkinson's disease: "The gene therapy study was to look at an area of the brain called the subthalamic nucleus. The area is overactive when you have Parkinson's disease. ... treatment relaxed brain activity in the motor network, making a patient with severe over-activity look like a person with moderate or mild Parkinson's disease. And because patients only received the therapy on one side of their brains, the researchers used the untreated side as a control. ... The network activity in the treated side went down while the other network in fact got worse over the period of time. It was as if the disease had progressed on one side of the brain, but not the other. But just as important was to determine whether the gene therapy affected the thinking network - and results show it did not. ... [researchers] plan to start their next [phase II] clinical trial in early 2008." While this is more patch than regeneration of causative damage in Parkinson's, we should welcome advances in safely manipulating the brain. However the future of healthy life extension progresses, we are going to have to become very proficient at repairing brain biochemistry in situ.



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