Fight Aging!

LONGEVITY MEME NEWSLETTER
December 17 2007

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.

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CONTENTS

- Following Up On The Cato Unbound Discussion
- Progress Reports From the Methuselah Foundation
- Discussion
- Latest Healthy Life Extension Headlines

FOLLOWING UP ON THE CATO UNBOUND DISCUSSION

A collection of links and excerpts from the recent Cato Unbound debate on radical life extension can be found in this Fight Aging! post:

https://www.fightaging.org/archives/001371.php

You'll find intelligent commentary on the Cato Unbound essays and reaction pieces out in the blogosphere too; I'm always pleased to see growing discussion of the path to healthy life extension. Ongoing conversation, the broader the better, is a necessary foundation to raising support and building a better platform for research and fundraising.

https://www.fightaging.org/archives/001372.php

"If a technology existed to eliminate the physical effects of aging, it would be a boon to mankind, and it would be atrocious to forbid it. People should be allowed to experience aging if they wish, of course, but if science could make it optional, then the option should be available. And yes, I would take it. I would definitely want to live a thousand years or more. I would want all of my loved ones with me, and my only regret would be that some of them are already gone and cannot be. You and I are among the first of our species for whom physical immortality is even an outside possibility, but if the choice ever came up, I assure you that I would go for it."

PROGRESS REPORTS FROM THE METHUSELAH FOUNDATION

The Methuselah Foundation kicks off a newsletter series with an update on progress in Strategies for Engineered Negligible Senescence (SENS) research and development of the Mprize competition for rejuvenation science:

http://blog.methuselahfoundation.org/2007/12/methuselah_foundation_newslett_1.html

The scientific summaries defy easy excerpting - I encourage you to read the full progress report for MitoSENS and LysoSENS research programs. Looking forward to 2008, new research programs for other strands of SENS are in the pipeline, enabled by the steady increase in Foundation funding:

"Most people are aware of the amyloid deposits associated with Alzheimer's Disease: they are the main constituent of senile plaques, the aggregates that accumulate in the spaces between neurons as the disease progresses. Encouraging progress is being made in stimulating the body's immune system to eliminate these deposits. However, amyloid composed of different proteins also accumulates in other tissues during aging. Progress in removing these other amyloids has been much less intensive thus far, even though they are, if anything, more clearly linked to the progression of age-related illness than senile plaques are to Alzheimer's. I have been in preliminary discussion with one of the leaders in this area, with a view to initiating work as soon as possible.

"WILT, the anti-cancer therapy incorporated into SENS, entails (among other things) the elimination of genes for the enzyme telomerase, which allows cancer cells to divide indefinitely without losing material from the ends of their chromosomes. Unfortunately, about 10% of cancers solve this problem in a different way, not using telomerase, via a process known as ALT, for alternative lengthening of telomeres. Even more unfortunately, ALT is still only very poorly understood. Recently, however, some intriguing observations in two different organs have given good reason to suspect a hitherto unsuspected gene. A relatively simple sequence of initial experiments could test this, and I am already in discussions with a leading ALT researcher concerning the possibility of launching this project."

Beyond the progress in Foundation-funded SENS research, researchers continue to sign up to compete for the Mprize for rejuvenation research:

"To broaden the field of competing research, a focused program was initiated this year to actively recruit new competitors, expanding the 'mouse race' for breakthroughs in preventive and regenerative anti-aging biotechnology. Spearheading this campaign is Elliot Bergman, Ph.D., of biotech consulting firm ChemLifeSciences, as the Foundation's Competitor Development Coordinator.

"Elliot's efforts to date have brought in four new competitors for the Prize, for a total of eleven scientific teams independently racing to extend the lives of their furry subjects as of this writing. The four most recent additions are Professor Andrzej Bartke of Southern Illinois University; Professor Craig Cooney of the University of Arkansas for Medical Sciences; Alan Cash, founder of Terra Biological LLC; and Elise Sacane, co-founder of Neural Learning Systems. Each of these teams is testing a different anti-aging strategy, creating exactly the kind of wide-open, multi-strategy competition needed to weed out ineffective approaches and bring successful therapies into the spotlight.

"Several other potential competitors have been identified and are being qualified for participation. We hope to have a total of 130-15 competitors by the first quarter of 2008."

DISCUSSION

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!

Reason

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LATEST HEALTHY LIFE EXTENSION HEADLINES

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/

Reporting Progress at the Methuselah Foundation (December 14 2007)
http://blog.methuselahfoundation.org/2007/12/methuselah_foundation_newslett_1.html
The Methuselah Foundation fills us in on progress to date: "We are currently sponsoring research in two of the seven strands of the SENS program; the preventing the harm caused by mitochondrial mutations (MitoSENS) and degrading damaging long-lived cellular debris (LysoSENS) ... our teams have already seen interesting results and are moving forward rapidly. ... When these projects began in the summer of 2005, there was no strong evidence to suggest that any enzymes or organisms degrading intracellular junk existed in nature [but] reseach volunteers had successfully cultured [7-ketocholesterol (7KC)] degraders before the end of 2005. ... 2006 saw further characterization of the 7KC degraders and corroboration of the results. In summer 2007, six undergraduate research assistants and one additional PhD candidate [helped] with synthesizing additional target compounds, such as A2E and CML (a major [advanced glycation end-product]). ... [today, researchers] are preparing to move them into a cell model of age-related macular degeneration for initial safety and efficacy testing. Various other projects [are] at earlier stages. Novel targets include artificial lipofuscin and the infamous glucosepane AGE-crosslink."

Neurodegeneration and Altered Autophagy (December 14 2007)
http://www.sciencedaily.com/releases/2007/12/071214144956.htm
More evidence for autophagy as a good thing - above and beyond its apparently pivotal role in calorie restriction benefits - from ScienceDaily: "Suppressing a cellular cleanup mechanism known as autophagy can accelerate the accumulation of protein aggregates that leads to neural degeneration. [Scientists] report for the first time that the opposite is true as well: Boosting autophagy in the nervous system of fruit flies prevented the age-dependent accumulation of cellular damage in neurons and promoted longevity. ... We discovered that levels of several key pathway members are reduced in Drosophila neural tissue as a normal part of aging. Which suggests there is an age-dependent suppression of autophagy that may be a contributing factor for human neurodegenerative disorders like Alzheimer's disease. ... Keeping cells free of damaged molecules is critical for neurons because unlike many cells, they do not divide or replace themselves once created at birth. ... They rely on autophagy together with other clearance and detoxification pathways to keep themselves healthy and functioning for decades."

An Interview With Michael Rose (December 13 2007)
http://www.genengnews.com/blog/item.aspx?id=236
Gene Engineering News is broadening its scope with podcasts on late, such as this interview with researcher Michael Rose: "science is now gaining a better understanding of the human aging process, with the ultimate goal of exerting some control over it. During this week's podcast, Dr. Michael Rose, developer of the long-lived Methuselah fruit fly line and one of the pioneers in aging research, offers his insights on the science of aging. He addresses such questions as 'why we age' and 'are aging and age-related disease synonymous?' Does the concept of humans one day living to be 150-years-old or more lie in the realm of science or science fiction? A specialist in evolutionary biology, Dr. Rose talks about how can advances in evolutionary biology can help us postpone aging. He discusses why severe caloric restriction will not substantially increase the lifespans of humans although it often does so in animal models. Dr. Rose also presents his case that there is a serious, hardcore, mathematical, scientific theory that underlies aging, but that a paucity of mathematically-inclined biologists is inhibiting discussion and further advances in the scientific study of aging based [on] this theory."

Ouroboros On p53 Decline and Late-Life Cancer (December 13 2007)
http://ouroboros.wordpress.com/2007/12/13/p53-decline-in-old-age-a-cause-of-late-life-cancer/
From Chris Patil Ouroboros: "If p53 were to somehow go AWOL in a cell, it would bode poorly for cancer prevention. Lacking this critical checkpoint control, genetically damaged cells could go on cycling, perhaps developing additional genomic changes that further encourage unrestricted growth, and eventually becoming frankly neoplastic. A recent study from Arnie Levine's lab shows that the p53 response to one form of genotoxic stress (ionizing radiation) becomes less efficient [in] old mice. If this finding is general to other humans, it could partially explain why the risk of tumors increases exponentially with age. ... I wonder whether a contributing factor might be adaptation of the signaling pathways involved. Signaling pathways almost always involve some negative feedback; among other things, this serves to prevent inappropriate activation of a pathway in response to a low baseline level of stimulus, to preserve the dynamic range of the system and reset the threshold so that it can be triggered only by really noteworthy events." Patil goes on to suggest an off the cuff theory as to how declines in p53 - and increased propensity to cancer - might operate, some tests of the hypothesis, and how the system might be reset if true.

Xenotransplanting New Mitochondria (December 12 2007)
http://pmid.us/18069915
I think you'll agree this is an intriguing addition to the stable of potential methods to replace damaged mitochondria, and thus remove their contribution to aging and age-related disease: "Mitochondrial DNA [or mtDNA] mutations are the direct cause of several physiological disorders and are also associated with the aging process. The modest progress made over the past two decades towards manipulating the mitochondrial genome and understanding its function within living mammalian cells means that cures for mitochondrial DNA mutations are still elusive. Here, we report that transformed mammalian cells internalize exogenous isolated mitochondria upon simple co-incubation. We first demonstrate the physical presence of internalized mitochondria within recipient cells using fluorescence microscopy. Second, we show that xenogenic transfer of murine mitochondria into human cells lacking functional mitochondria can functionally restore respiration in cells lacking mtDNA." I'm sure you can speculate on how one would build therapies upon this basis, should it be made safe and reliable.

Kevin Dewalt's End Aging YouTube Challenge (December 12 2007)
http://kevindewalt.com/blog/2007/12/09/end-aging/
From Kevin Dewalt: "My End Aging Challenge is simple: Create and post a reply to this video on YouTube explaining why you support Dr. Aubrey de Grey's and the Methuselah Foundation's mission to end aging. I will donate $10 to the Methuselah Foundation for every video response. If you have the means, I also suggest that you offer in your video response to match me with a donation of your own for every video. After you shoot your video, follow this link to post your video reply." Good show. If you want something done, no matter how daunting or large the task, the best way to go about it is to get out there and help make it happen. Put your shoulder to the wheel and lead by example. It matters not the size and weight of that wheel, as many hands make light work. It matters greatly that you show that the job exists, and that someone is willing to work at getting it done. Where is one willing worker exists, there will soon be more.

Tissue Engineering From Now To 2021 (December 11 2007)
http://www.liebertonline.com/doi/pdfplus/10.1089/ten.2007.0335
This PDF analysis looks at challenges and advances for the next 15 years of tissue engineering, as seen by scientists in the field: "highly strategic issues often may not lie at the forefront of our day-to-day conception of the most important foci in the field, making such analyses more important to undertake. For example, the strategically most important category, angiogenic control [or engineering blood vessels], was supported by only four contributed ideas. However, its dominance over nine other concepts and its low level of present progress propelled it to the top of the list of strategic concepts. Clearly, mastering the control of angiogenesis will be at the heart of any attempts to grow larger tissue engineered constructs than have thus far been achievable. This will apply whether such growth occurs in vitro or within the body as a response to cell and/or scaffold implantation. Stem cell science is the second most strategic concept. [It] may well be that the understanding and control of stem cell development will enable us to short circuit some of the tissue engineering methods used heretofore - perhaps allowing the concurrent growth of vascular systems with parenchymal tissues."

Methuselah Foundation Pledge Total Tops $10 Million (December 11 2007)
http://blog.methuselahfoundation.org/2007/12/methuselah_foundation_pledge_t.html
From the Methuselah Foundation: "With the flood of generous year-end donations during this time of triple matching challenges, we're pleased to announce that the grand total of pledges and donations to the Methuselah Foundation has passed $10 million! This counts the Mprize for longevity science, SENS research - which itself recently passed the $5 million mark - and expense donations. This wonderful goal has been accomplished in just four years due to the hard work and generosity of many hundreds of people, volunteers, donors and supporters. We thank you all, and look forward to keeping up the accelerating pace over the next four years." The Methuselah Foundation is one of the great success stories of the transhumanist community. People moved beyond just talking about the future and stepped up to help shape that future. The $10 million dollar mark is a great milestone, and an impossibly distant milestone when we were looking at Dave Gobel's idea for the Three Hundred back in 2004 - but here we are, and onward we go. Thank you all.

Alcor Critical Care Medical Panel Transcript (December 10 2007)
http://www.acceleratingfuture.com/people-blog/?p=327
The People Database blog continues a sterling job of recording the dialogue of the healthy life extension community: "There are many ways we can define cryonics. Sometimes it is presented as a scientific experiment done on humans. The direction that we are headed in now is to present it as a long-term form of critical care medicine. ... The point is, doctors tend to be a rather stilted lot. They don't necessarily embrace things that work just because they work. They have to go through a kind of culturalization. As far as cryonics goes, leaving the realm of science fiction and entering the realm of critical care medicine, the entry point will be fairly rigorous and will involve randomized double-blind studies to show potential. Of course, you have to remember that the whole point of science is imagination. This is imaginative. Anything that is imaginative is welcome. If it can be shown to have some scientific rationality, if it can be shown to make sense, eventually it will slowly blend into a very stilted bunch of people who don't accept things readily."

SENS Research Donations Tripled Until Year End (December 10 2007)
http://blog.methuselahfoundation.org/2007/12/300_matching_to_sens_research.html
Good news from the Methuselah Foundation: "You might recall in 2006 that Peter Thiel made a $3 million Matching Challenge to SENS Research, where he matches 50% of donations to research until the end of 2009. Well, our performance and Thiel's example have prompted a supporter and Three Hundred Member, Michael Cooper, to join in. He is offering a $25,000 Matching Challenge of his own until the end of this month. ... Your donations to speed research into repairing the damage of aging and extending the healthy human lifespan will be matched 2-to-1 until the end of 2007, expanding your donation threefold. ... The two presently open Donation Challenges match donations to SENS Research cumulatively. That is, newer matching pledges are evaluated first and the amount matched is added to the incoming donation before the amount for the next matching pledge is calculated, magnifying the value of the donation substantially. At present, a $100 donation (enough for a free autographed copy of 'Ending Aging') is leveraged to $300!" If you've been thinking about stepping up to help make a real difference to the field of aging research, now is the time. If not now, when?

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