Longevity Meme Newsletter, June 30 2008

June 30 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.



- Wired Article on Aging 2008
- On Stem Cell Aging
- Discussion
- Latest Healthy Life Extension Headlines


Wired printed a timely article this past week, just in advance of Aging 2008 at UCLA:


"Gandhi once said, describing his critics, 'First they ignore you, then they laugh at you, then they fight you, then you win.' After declaring, essentially out of nowhere, that he had a program to end the disease of aging, renegade biogerontologist Aubrey de Grey knows how the first three steps of Gandhi's progression feel. Now he's focused on the fourth. 'I've been at Gandhi stage three for maybe a couple of years,' de Grey said. 'If you're trying to make waves, certainly in science, there's a lot of people who are going to have insufficient vision to bother to understand what you're trying to say.'

"This weekend, his organization, The Methuselah Foundation, is sponsoring its first U.S. conference on the emerging interdisciplinary field that de Grey has helped kick start. (Its first day, Friday, will be free and open to the public.) The conference, Aging: The Disease - The Cure - The Implications, held at UCLA, is an indication of how far de Grey has come in mainstreaming his ideas."

The signs continue to be promising for the Methuselah Foundation to be the boulder that leads the avalanche, gathering legitimacy and researchers at an accelerating rate to the task of repairing aging. Those folk who helped to get this initiative off the ground back in 2004 should be feeling pretty pleased right about now. If you haven't visited the Methuselah Foundation website in a while, you should head on over and take a look:



A couple of good review papers, presently freely available online, illustrate well the present thinking on stem cells and aging:


"The weight of evidence is shifting to the view that we are packed full of functional stem cells even as we age. These stem cell populations are shut down by changes in biochemical signals and systems, possibly due to accumulated damage that causes aging and malfunction, possibly as an evolved defense against the increasing likelihood of cancer in old tissue. As cancer medicine becomes increasingly sophisticated, safe and effective, learning the signals to set our stem cells back to work begins to look like a plausible near term strategy for enhancing longevity."

Graying hair is one of the many signs that your stem cells have decided to slow down operations, as the pigment in your hair is produced by melanocyte cells (and the stem cells that create melanocyte cells) that stop coming to work one day:


"Setting any given group of aging stem cells back to work by introducing appropriate biochemical signals - or cloning many more stem cells to reintroduce into the body - are very plausible projects for the decade ahead. Either could greatly improve the immediate situation, and the second strategy has already been demonstrated in heart therapies. I can envisage cloning and reintroduction of massive numbers of melanocytes as a clinical method to reverse hair graying in the late 2010s."


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/

Steady Advances in Programming Cells (June 27 2008)
Cells would do as we desired, changing form and purpose, if we just understood the vocabulary and timing of biochemical signals. ScienceDaily relays another step forward to that end goal: researchers have "genetically programmed embryonic stem (ES) cells to become nerve cells when transplanted into the brain ... mice afflicted by stroke showed tangible therapeutic improvement following transplantation of these cells. None of the mice formed tumors, which had been a major setback in prior attempts at stem cell transplantation. ... MEF2C is a transcription factor that turns on specific genes which then drive stem cells to become nerve cells. ... To move forward with stem cell-based therapies, we need to have a reliable source of nerve cells that can be easily grown, differentiate in the way that we want them to and remain viable after transplantation. MEF2C helps this process first by turning on the genes that, when expressed, make stem cells into nerve cells. It then turns on other genes that keep those new nerve cells from dying. As a result, we were able to produce neuronal progenitor cells that differentiate into a virtually pure population of neurons and survive inside the brain."

Another Perspective on the Problem (June 27 2008)
Anders Sandberg provides a transhumanist perspective on the problem that plagues aging research, as well as other fields of medicine - a phobia of vision and directed goals: "Senior scientists and technologists are often asked about their visions and views about the future [but the] economics of research favours talking about means rather than ends, and the allowable ends will be short-term generally agreed on goods. Grants applications dutifully mentions cures for Alzheimers and increased economic competitiveness ... the biotechnology debate has become impoverished: professional competition has shifted the debate away from a 'thick' substantively rational debate about the ends of genetic engineering to a 'thin' formally rational debate about the means to achieve a few predetermined ends like safety, efficiency and health. That has left a lot of people (both for and against) disaffected and unable to participate in the mainstream thin debate since they really want to discuss thick issues. This is why I think the 'shut up, you are scaring the grant bodies' approach the wrong one. They should be scared. Otherwise we will have a science and technology where acceptable research is determined by unaccountable minorities setting 'proper' goals, rather than by a society where numerous wildly different views need to coexist. The big, dramatic and far-fetched transhumanist visions have a place here as values and ends to aim."

Aging 2008, Friday June 27th (June 26 2008)
The Aging 2008 event at UCLA is tomorrow evening, leading into the Understanding Aging conference: "Applying the new technologies of regenerative and genetic medicine, the engineering approach to aging promises to dramatically extend healthy human life within the next few decades. How do you and your loved ones stand to benefit from the coming biomedical revolution? Are you prepared? Is society prepared? At Aging 2008 you will engage with top scientists and advocates as they present their findings and advice, and learn what you can do to help accelerate progress towards a cure for the disease and suffering of aging. Doors open at 4:00 pm on June 27th, 2008, at UCLA's Royce Hall. All attendees must register in advance; entry is free and includes a complimentary drinks reception before the presentations begin. For an additional $30, attendees also have the opportunity to attend a special dinner with the speakers."

The Aging Intervention Foundation (June 26 2008)
The Aging Intervention Foundation is another new nonprofit initiative in the same sphere of advocates and scientists as the Gerontology Research Group and Supercentenarian Research Foundation: "The Aging Intervention Foundation (AIF) was created to develop new therapies to control and reverse the underlying causes of aging, as well as treat and prevent the diseases of aging. The goal is to eventually control the processes of aging, reverse their effects, and stay younger longer - and ultimately create indefinite youthful, happy and productive lifespan using innovative scientific methods that are under development today in biotech companies and research labs around the world. ... We'll accomplish these goals by creating strategic partnerships with world class organizations. The AIF will provide the vision, clearly defined project plan and goals, specific technical expertise and money. All teams will be racing together toward the common goal of greatly extending and improving our lifespan, and the quality of our lives." We should encourage these seeds to grow from their humble beginnings, as some do very well indeed, and the more that do, the faster we progress towards working longevity medicine.

More Naive B Cells For Centenarian's Children (June 25 2008)
The Telegraph reports on a new finding in the biochemistry of human longevity: "White blood cells fend off infection - in effect delaying death - so [researchers] investigated longevity by taking samples of white blood cells from 45 men and women aged between 75 and 90 who all had parents born in Sicily between 1900 and 1908. Twenty-five of the donors had one parent who had reached 100 and one who had died of old age before reaching average life expectancy for Italians - which is 67 for men and 72 for women. The remaining 20 donors served as controls having lost both parents before they reached average life expectancy ... Our main finding was the increase in naive B-cells in individuals who had centenarian parents ... Unlike mature B-cells - which are primed to attack foes the body has seen before - naive B-cells are ready and waiting to attack microbes not previously encountered." You'll recall that depletion of naive T-cells is a strong component of immune system aging. As naive cells diminish, the ability to mount a response to new challenges also diminishes.

Your Aging Epigenome (June 25 2008)
From ScienceDaily: researchers have confirmed that "epigenetic marks on DNA - chemical marks other than the DNA sequence - do indeed change over a person's lifetime, and that the degree of change is similar among family members. The team suggests that overall genome health is heritable and that epigenetic changes occurring over one's lifetime may explain why disease susceptibility increases with age." Alternately, and more likely in my opinion, epigenetic changes are cellular responses to an increasing level of biochemical damage and damage-induced changes in the operation of bodily systems. We should expect to see epigenetic changes when anything relating to the body is changed, all the way from diet and exercise to immune system aging or accumulation of amyloid between cells, and everything in between. Still, research is at its earliest stages, and any hint of correlations in epigenetic changes across larger populations is intriguing.

Update on the PAPP-A Longevity Mutation (June 24 2008)
You'll recall that mice with the PAPP-A gene deleted live 30% longer in good health than their fellows. Following up, researchers are eliminating possibilities in the search for the mechanism of action: "We determined whether 18-month-old PAPP-A knock-out (KO) mice compared to their wild-type [WT] littermates have reduced energy expenditure and/or altered glucose-insulin sensitivity. Food intake, and total energy expenditure and resting energy expenditure as measured by calorimetry, were not different between PAPP-A KO and WT mice ... However, there was an increase in spontaneous physical activity in PAPP-A KO mice. Both WT and PAPP-A KO mice exhibited mild insulin resistance with age, as assessed by fasting glucose/insulin ratios. Oral glucose tolerance and insulin sensitivity were not significantly different between the two groups of mice ... Thus, neither reduced 'rate of living' nor altered glucose-insulin homeostasis can be considered key determinants of the enhanced longevity of PAPP-A KO mice." We'll be hearing more on this topic in the years ahead, I'm sure - more healthy life with no downside through a simple genetic manipulation is an attractive idea.

tRNA and Your Mitochondria (June 24 2008)
Age-damaged mitochondria are age-damaged because they have lost genes necessary to produce proteins they need to function. This damage causes a good degree of age-related degeneration. There are a number of approaches here: fix the mitochondrial DNA, or provide the proteins some other way. New reseach suggests a novel way to accomplish the latter goal: "Scientists have determined that human cells are able to shift important gene products into their own mitochondria ... The gene products, known as tRNAs, assemble amino acids for the production of proteins within mitochondria. If the mitochondrial tRNA genes are defective or missing, and proteins are not manufactured, the mitochondria are unable to generate adequate energy. ... This was totally unexpected, to find an innate, built-in mechanism that we humans have ... If you have a mutation in a tRNA that you suspect is involved in disease, you theoretically should be able to bring a healthy tRNA from the cytoplasm into the mitochondria and correct the malfunction."

More On Risk and Information-Theoretic Death (June 23 2008)
There's dead and then there's dead and definitely not coming back. Cold water drowning victims can be restored to life if treated quickly. Cryosuspended people can plausibly be restored to active health by medicine of the future. Life renewed isn't a possibility for the buried or cremated, however: the pattern of the brain, the definition of who they are, is lost. That last is information-theoretic death, wherein all the information that is you is gone. In a future in which aging is cured, reducing the risk of this form of death becomes the primary concern. From Depressed Metabolism: "Perhaps the most logical proposal to achieve a negligible chance of information-theoretic death is to duplicate a person. If enough duplicates are made, the chance that all of them will die can be made very small. But this raises the issue of whether such duplicates are the same individual. Some people would argue that this strategy does not produce atomistic non-serial immortality. It is also not clear how the question of whether a copy of an individual is the same individual can ever be resolved by empirical observation or logical deduction. Perhaps the most realistic proposal to reduce the probability of information-theoretic death would be to separate the neurological basis of the person from its body in such a fashion that the risk of complete destruction of the person would become negligible."

Stem Cells Versus Retinal Damage (June 23 2008)
Forbes notes that Pfizer "is funding the creation of a biotech company in San Diego called EyeCyte, which will develop stem-cell treatments for eye diseases. The company is based on work by Scripps Research Institute ophthalmologist Martin Friedlander, who has pinpointed bone- and blood-marrow stems cells that, in animal experiments, have a remarkable ability to target and repair damaged blood vessels in the eye. Abnormal blood vessels are a key problem in both diabetic eye disease and macular degeneration. In the future, patients with early signs of blood-vessel damage in the eye might go to the doctor in the morning and leave a blood sample. Adult stem cells would be isolated in the lab over the next few hours, and then the patient would come back in the afternoon and get an injection of his own purified stem cells into the eye. That single injection could stave off further blood-vessel damage for years, preserving eyesight that would otherwise be lost."



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