The effort will make use of existing saliva samples taken from California patients, whose average age is 65. Their DNA will be analyzed for 700,000 genetic variations called single-nucleotide polymorphisms, or SNPs, using array analysis technology from Affymetrix. Through the National Institutes of Health (NIH), the resulting information will be available to other researchers, along with a trove of patient data including patients’ Kaiser Permanente electronic health records, information about the air and water quality in their neighborhoods, and surveys about their lifestyles.
The target age group shows that the focus is on “secondary aging”:
Given the high average age of the group, the platform will also be a boon to studying diseases of aging. “One might want to ask,” Schaefer says, “what are the genetic influences on changes in blood pressure as people age, and how are those changes in blood pressure related to diseases of aging, like stroke and Alzheimer’s and other cardiovascular diseases?”
UCSF will perform separate procedures on the samples to determine the length of telomeres–sections of DNA at the ends of chromosomes that protect against damage. The length of telomeres is associated with cell division and aging. One of the coinvestigators on the project is Elizabeth Blackburn, a biologist at UCSF who shared the 2009 Nobel Prize in Medicine for her work on telomeres.
I had problems with my handwriting since elementary schools, or at least my teachers had continuous problems with it. Even during my university years I was asked sometimes to read out loud my essays, papers to them otherwise risking bad grades. Maybe it’s because I am a hidden right-handed using my left hand for writing or maybe I am just too impatient over the slow pace of handwriting (needless to say computers mostly solved this problem).
On this George Dysonphoto here you can see the SciFoo schedule in progress and I think you can easily pick the one with the ugliest handwriting on Aging and Life Extension:
Last year I was probably the only SciFoo Camper with an explicit life extension commitment. I suggested & held a session which was related a bit to partial immortalization but was rather about the systems biology perspective in general, illustrated with some examples. So throughout the terrific SciFoo Camp 2007 life extension as a conversation topic remained rather implicit (ok, close to zero) and there was not much room to discuss it in the lack of other fellow life extensionists.
In my opinion the whole point of unconferences is to form the good aggregate of people with a common interest & similar/complementer message to join forces in order to draw enough (intellectual) attention for their topic. In this context, an unconference is about topics at the first place, not just about people. Idea networking is as important as social networking.
And if something fits 100% with the idea of SciFoo it is life extension/aging just as handling terrantic scientific datasets, open science or climate change as all these topics are utterly complicated and quite urgent screaming for the attention of the smartest people.
So I emailed Timo Hannay, SciFoo organizer:
“One thing I’ve noticed is that it would be very good to organize a session on scientific life extension technologies and consequences, because the SciFoo people are ideal to see and discuss all angles of this really important topic.”
Finally Chris over at Ouroboros came up with the idea and the quick implementation of Hourglass, a blog carnival devoted to the biology of aging/biogerontology. For some reason I am not an explicit supporter of blog carnivals – many of my posts were chosen by carnival editors but I never hosted one -, but Hourglass will be the big exception in which I participate, submit posts and host it later. The reason: first it presents aging/biogerontology related posts, which fits my profile and second it was instigated by Chris Patil, whose work is a guarantee for keeping all this in the good direction. So if you want to read on the evolution of longevity and aging, calorie restricition, stem cells/tissue engineering/regenerative medicine, or on the association of long life and intelligence at once, Hourglass is for you.
Even tech people in Silicon Valley need to join their powerful forces and sources when it is about aging related neurodegenerative diseases and help research and the clinic.
I would like to provide you with a copy of the press release to be distributed via press release distribution sites on Wednesday. We will also put it on our site within a few hours after this email so you can confirm its authenticity. Please help us distribute this press release.
The Biogerontology Research Foundation, which has been started with the help of worlds’ most prominent scientists and businessmen received the charitable status from the Charity Commission for England and Wales.
The fact, which is not mentioned in the press release is that the chief scientific officer of the foundation is Dr. Michael Rose of UCI, who is famous for extending life of fruit flies threefold.Read the rest of this entry »
Will it one day be possible to take a pill to stay young? How will an average life expectancy of beyond a hundred years affect society and the planet? Join leading longevity researchers Robert Butler, David Sinclair and Richard Weindruch to investigate the facts and implications surrounding scientific developments — emerging technologies, novel therapies, and innovative medical practices — that forecast a radical extension of a healthy human life. Featuring a special performance by acclaimed singer, Marilyn Maye.
“The best way to predict the future is to invent it.” – said Alan Kay, computer legend in 1971.
Recently I had a comment dialogue with Chris on whether state-supported research or industrial business enterprises can (or should) lead to big progress in robust and healthy life extension technologies. Besides the government and corporation coin the research breakthrough could come from an aging focused foundation like the non-profit Methuselah Foundation behind the SENS approach, which supports research projects (like MitoSENS and LysoSENS) and scientists (like Mark and John) through cooperation with university labs. And finally, there is going to be another option to contribute:
Huffington Post, Fortune’s Stanley Bing: The Next Big Thing? Please pay extra attention to the language here (especially transmogrification).
Human genome schmutz: Nobody wants to get old or worse, appear old. And forget about dying. That’s the ultimate bummer. Genetic research has been held back recently by a series of disasters too terrible to mention in this venue, or even look up right now, since we’re very busy. But the three-headed midget sheep problem will be solved by 2014 and recombinant DNA, stem-cell and mitochondrial transmogrification technology will begin making inroads into the problem of aging, extending human life to its ultimate limit and even beyond, particularly for really rich people who are on everybody’s nerves already. Another enormous opportunity for confabulators here.
Well, why exactly am I working with human mitochondria and stem cells at the bench? Maybe it’s time again to recall.
The preliminary program already has over two dozen confirmed
speakers, all of them world leaders in their field. As for previous
conferences I have [co-]organised, the emphasis of this meeting is on
“applied biogerontology” — the design and implementation of
biomedical interventions that may, jointly, constitute a
comprehensive panel of rejuvenation therapies, sufficient to restore
middle-aged or older laboratory animals (and, in due course, humans)
to a youthful degree of physiological robustness. The list of
scientific sessions and confirmed speakers is as follows:
DNA damage, telomeres, cancer
Adam Arkin, Lawrence Berkeley National Laboratory; Jan Vijg, Buck
Institute for Age Research; Jerry Shay, U. Texas Southwestern;
Claudia Gravekamp, Pacific Medical Center Research Institute; Zheng
Cui, Wake Forest University School of Medicine; Rita Effros, UCLA
The cell niche
Irina Conboy, U. California Berkeley; Judith Campisi, Lawrence
Berkeley National Laboratory and Buck Institute; Leanne Jones, Salk
Institute; Ken Muneoka, Tulane University; Kevin Healy, Stanford
University Read the rest of this entry »
The successful reprogramming (dedifferentiation) of differentiated human somatic cells into a pluripotent, embryonic stem cell-like state called induced pluripotent stem cells (iPS) using just 4 (and recently 3) introduced transcription factors is the biggest news of current stem cell biology. In the paper published in Cell by the Yamanaka group (Takahashi et al.) the iPS clones derived from the facial dermis of a 36-year-old Caucasian female were highlighted. Out of 50 000 retrovirally transduced fibroblasts 10 hES cell-like colonies were observed. But what I found really thought provoking (and poorly discussed in the blogosphere) is that with the same approach iPS cells were generated from the synovial tissue of a 69-year-old Caucasian male. Interestingly out of 50 000 modified cells 17 hES cell-like colonies were found. This finding could easily be relevant from a stem cell aging point of view.
During ageing there is an overall decline in tissue regenerative potential, but it is not clear whether it is due to the intrinsic exhaustion of the adult tissue stem cells or the diminished functionality of the stem cell niche or a change in the systemic milieu. Answers could be different – tissue by tissue.
But if a terminally differentiated connective tissue cell, like the synoviocyte above could be completely reprogrammed from a 69 year old, otherwise health individual into a pluripotent state….well it could it be interpreted as an argument against the cell-intrinsic genetic aging program in adult and aged connective tissues with some cautions.
Caution 1: What if the source of the iPS cells were not really terminally differentiated, but undifferentiated stem or progenitor cells coexisting in fibroblast culture. This problem has been discussed in the paper and forms the Achilles’ heel of it.
Caution 2: The reprogrammed iPS cells from an aged person are behaving the same way as the iPS cells from a younger person with no additional cellular aging characteristics.
As the critical tail of almost every peer-reviewed paper used to say: Further study is needed.
Finally the Google PageRank algorithm, the core analysis tool of the current web is back to where its idea is originated from, scientific citation analysis. The recently launched SCImago Journal & Country Rank database uses an algorithm very similar to PageRank. It has a new metric: the SCImago Journal Rank (SJR). According to Nature:
A new Internet database lets users generate on-the-fly citation statistics of published research papers for free. The tool also calculates papers’ impact factors using a new algorithm similar to PageRank, the algorithm Google uses to rank web pages. The open-access database is collaborating with Elsevier, the giant Amsterdam-based science publisher, and its underlying data come from Scopus, a subscription abstracts database created by Elsevier.
The SJR also analyses the citation links between journals in a series of iterative cycles, in the same way as the Google PageRank algorithm. This means not all citations are considered equal; those coming from journals with higher SJRs are given more weight. The main difference between SJR and Google’s PageRank is that SJR uses a citation window of three years.
From now on every stat geek can compare journals to journals, countries to countries based on different metrics like citable documents, cites, self-cites or the new h-index and get a ticket to recursive heaven. Of course I started with the comparison of Nature and Science to find something very different. I couldn’t. I predict that self-cites will show a lot on how things are going on at different scientific journals and the stats will be used as serious arguments in many blog posts. But here let me share some graphs on the quick comparison of USA, UK and China in the category of Aging.
Here is another sign that the editors at Science Magazine are taking more and more attention to the web and the scientific blogosphere: Ouroboros (that is: Chris, Okie and Lev) was picked up in the Random Samples column of the current Science issue: “But research on aging is booming, and the field’s good health is on display at the blog Ouroboros, which is named for a symbol of endlessness. Three postdocs from leading aging research labs offer their takes on the latest results from conferences and the literature. The site is aimed at researchers, but it can also help beginners get up to speed.”
It seems that the editors are sharing my opinion that Ouroboros is one of the best science blogs out here and it is also worth mentioning that Chris Patil’s incentive of Ouroboros was Science Magazine’s SAGE KE.
Another remarkable thing is Chris’s approach of developing a group blog instead of building an individual brand and focusing exclusively on biogerontological peer review literature and conferences.
Recently I wrote a meeting report on the SENS3 conference for a very prestigious science journal, but finally it did not go through the filters. I knew that the chance for publication is small as the journal rarely publish such meeting reports and as it was in many respects an unconventional science conference. The standards were really high and the genre itself is strictly restricted: no more than 900 words and only 1-2 conference topic could be covered focusing on new data. On the whole it was a really good science writing experience for me. I finally realized how challenging it is to introduce the concept of robust scientific life extension for the mainstream science audience although it is not impossible at all.
But if a man has an interactive blog with a quality readership even an officially unpublished text could be useful, so please read my draft in its final form and think about it. Links of the video versions of the referred presentations and references are included, a perpetual advantage of the web comparing to offline publication. I’d like to say thanks for the folks who helped me with the draft: Aubrey de Grey, Michael Rae, Mark Hamalainen from within the SENS camp, Matthew Oki O’ Connor and Chris Patil, fellow scientists-bloggers and first of all, Anna.
Subject scrapline: Biotechnology
Title: Translating ageing
Summary: A recent unconventional strategic conference on translational science in ageing related damages helps to put some puzzle pieces together.
Changes in the adult tissue stem cells or in the mitochondria are two main processes under constant investigation amongst researchers curious about the ins and outs of the ageing process. At the SENS3 conference in Cambridge scientists and laymen shared their results and ideas, respectively.＊
Despite its mixed population with a scientist majority, the conference resembled a mainstream life science conference due to its topic sessions focusing on the different types of lifelong, ageing accumulated damages. SENS decodes as Strategies for Engineered Negligible Senescence, which aims to suggest a panel of interventions on how to robustly extend the mean and maximum human life span and claims to identify the adequately exhaustive list of main age-related pathologies ranging from cell depletion to mitochondrial mutations. SENS is by definition a flexible enough umbrella term to include other coming life extension technologies and concepts under its brand. Also, it is an engineering project compiled by main organizer Aubrey de Grey, a computer scientist turned theoretical biologist with a grand mission and hypotheses yet to be experimentally tested. The presentations were mainly reviewing the progress in the related branches, with enough new data to keep the experts interested.
My gmailbox says and I see no reason not to share it: The Open Aging Journal is an Open Access online journal,which publishes research articles, reviews and letters in all areas of aging science.
The journal aims to provide the most complete and reliable source of information on current developments in the field. The emphasis will be on publishing quality articles rapidly and making them freely available to researchers worldwide. All articles are deposited in at least one major international open digital repository (such as PubMed Central). All articles are indexed by Google and Google Scholar which offers additional massive world wide web exposure.
In order to slow the progress of aging and prevent age-related disease (which is not the same as figuring out a robust engineering plan for unlimited healthy life extension) biological measures (biomarkers) of aging or disease mechanisms are needed that anticipate clinical disease and are sensitive to functional organism aging.
The American Federation for Aging Research is the organizer of a one-day conference on October 2 in Manhattan focusing on current and future status of biomarkers as identifiers of rates of biological aging, predictors of longevity and predictors of susceptibility to disease.
A major cause of cell death caused by genotoxic stress is thought to be due to the depletion of NAD+ from the nucleus and the cytoplasm. Here we show that NAD+ levels in mitochondria remain at physiological levels following genotoxic stress and can maintain cell viability even when nuclear and cytoplasmic pools of NAD+ are depleted. Rodents fasted for 48 hr show increased levels of the NAD+ biosynthetic enzyme Nampt and a concomitant increase in mitochondrial NAD+. Increased Nampt provides protection against cell death and requires an intact mitochondrial NAD+ salvage pathway as well as the mitochondrial NAD+-dependent deacetylases SIRT3 and SIRT4. We discuss the relevance of these findings to understanding how nutrition modulates physiology and to the evolution of apoptosis.
Researchers report in the journal Cell that the phenom is likely linked to two enzymes—SIRT3 and SIRT4—in mitochondria (the cell’s powerhouse that, among other tasks, converts nutrients to energy). They found that a cascade of reactions triggered by lower caloric intake raises the levels of these enzymes, leading to an increase in the strength and efficiency of the cellular batteries. By invigorating the mitochondria, SIRT3 and SIRT4 extend the life of cells, by preventing flagging mitochondria from developing tiny holes (or pores) in their membranes that allow proteins that trigger apoptosis, or cell death, to seep out into the rest of the cell.
“We didn’t expect that the most important part of this pathway was in the mitochondria,” says David Sinclair, an assistant professor of pathology at Harvard Medical School and a study co-author. “We think that we’ve possibly found regulators of aging.”
Sinclair says his bravado and drive come from his grandmother Vera, who fled to Australia in the wake of the failed 1956 revolution in her native Hungary. Her son, David’s father, changed the family name from Szigeti. “My grandmother is the black-sheep rebel of the family,” he says. “She gave birth to my dad at age 15 in 1939 – imagine the scandal then – and has lived with natives in New Guinea and eaten human flesh,among other things. She once got in trouble with the police for being the first person to wear a bikini on a Sydney beach. She’s a 60s bohemian who helped raise me and taught me how to think differently and question dogma.”
For me, it was on SENS3, the presentation of Anun Hallen, who blamed only extracellular crosslinks (e.g. advanced glycation end products) for ageing. It was not the best presentation I’ve ever seen, I can tell ya. (I heard once, that there was a high school science contest in the 80′s with an overhead projector only as a presentation tool, and there was one nerd participant with only a floppy disk to present his data, so he put the disk on the overhead projector to visualize)
A supercentenarian is anyone with the chronological age of 110 years or older. Stephen Coles, M.D., Ph.D., co-founder of the Los Angeles Gerontology Research Group kindly sent me his slides of the presentation he held last week on SENS3 entitled the Secrets of the oldest old and he gave a permission to publish these slides here in the form of a slideshow. The readers can now gain now some scholarly insights on what it is to be a supercentenarian. I cut out the autopsy slides (1 week after death) showing the pretty healthy organs (brain, liver, spinal cord, heart…) of the recently died 106 yo centenarian but all slides can be viewed at the GRG homepage (click Resources). Long live the 75 validated supercentenarians and all the unvalidated ones!
Embedded on the slideshow below 9 slides of Michael Rose‘s presentation called Slowing and then stopping aging on the SENS3 conference on the 9th of September. (Photos made by me with the iPhone.) Rose’s argument was: Aubrey de Grey’s original SENS proposal is based on the non-evolutionary assumption that aging is a process of accumulating damage, while according to the evolutionary SENS version of Rose aging should be interpreted as a loss of adaption. The script is: breed mice with delayed reproduction over multiple generations (let evolution by natural selection give us the answer of how to build a long-lived animal), and then reverse engineer this answer to develop anti-aging therapies for genetically unaltered humans. The experimental basis of this proposal: Rose’s own ancient experiments with fruit flies (sorry, no reference yet, that’s what I’ve heard) showed that there is a plateau in mortality rates after many generations of breeded Drosophilas with delayed reproduction time which leads to the cessation of the aging process.
Does this method sound as one that gives us a complete engineering toolkit to achieve robust healthy life extension for early generations of humans under the reverse engineered treatment?
says Steve Coles in his short presentation, Secrets of the oldest old. They found healthy sperms in the testis of a recently died 106 year old Californian.
The immortal strand hypothesis captures stem cell scientists’ imagination these days. According to Thomas Rando The immortal strand hypothesis posits that the propensity of stem cell compartments to give rise to cancer in later life can be minimized if stem cells, during the process of self-renewal, retain those DNA strands with the fewest mutations acquired during DNA replication. Key concepts of biology are connected by the hypothesis: stem cells, cancer, aging, symmetric and asymetric cell division, DNA replication and replication-induced mutations.
At the SENS3 conference Mike Conboy from Berkeley, who is a former postdoc of Thomas Rando at Stanford gives us some muscle regeneration related data concerning the hypothesis:
Department of Bioengineering, University of California Berkeley, Berkeley, California, USA
Before cells divide, they duplicate macromolecules and organelles. When they divide, sometimes they sort the older versus newer “parts” to the daughter cells. Over 35 years ago Cairns proposed the “Immortal DNA Strand hypothesis”, where the stem daughter cell might retain the older or more “original” strands of DNA and thus limit accumulating errors of replication, while continuing to proliferate for the life of an organism. Originally based on observations in animal and plant cells, this hypothesis has remained largely unknown or unaccepted because of few additional reports, relatively few cells displaying template strand segregation and alternate interpretations of the data. We used sequential pulses of different thymidine analogs to label DNA strands of different ages in the cells in regenerating muscle, in vivo. We observed extraordinarily high frequencies of cells segregating older versus younger DNA to the daughter cells. Furthermore, this DNA inheritance asymmetry correlated with asymmetric cell divisions yielding daughters with divergent fates. Daughter cells inheriting the older templates exhibited a stem-like immature phenotype, whereas daughters inheriting the newer templates showed a more differentiated phenotype. These data provide compelling evidence of the Immortal DNA phenomenon in muscle regeneration and suggest that it may be more common in stem cell self-renewal than previously assumed. We propose that the Immortal DNA hypothesis be revisited as pertains to aging, cancer and development, and suggest implications for the SENS.
J. Schloendorn, M. Hamalainen, S.K. Kemmish, L. Jiang, J. Rebo, B. Turner, B.E. Rittmann
Center for Environmental Biotechnology, Biodesign Institute at Arizona State University, 1001 South McAllister Ave., Tempe, AZ 85287-5701, USA
Medical bioremediation is the proposal to utilize the catabolic diversity of environmental microbes to treat all conditions associated to catabolic insufficiency in aging humans. Here we report on our progress towards medical bioremediation. We have isolated several bacteria degrading 7-ketocholesterol and other oxysterols implicated in atherosclerosis. We also present a method to determine the early steps in the biochemical pathway of 7-ketocholesterol degradation, which may be used to screen different species for therapeutically interesting reactions. We have also recently begun work on other targets, such as lipofuscin components and advanced glycation end-products. We hope that enzymes derived from our work can be used to put the role of catabolic insufficiency in aging to a final test, and if such a relationship exists, provide a therapeutic opportunity. Unconventional interdisciplinary collaborations will be required to make this possible.
Key words: medical bioremediation, catabolic insufficiency, aging, atherosclerosis, 7-ketocholesterol
John Schloendorn is one out of the new wave of researchers and life scientists who can perfectly fit their scientific drive and skills with his serious life extension commitment. In fact, I dare to say that John would not be involved in life sciences if he did not have the chance to explore a healthy life extension technology.
The Buck Institute in Novato, California is a rich private research center focusing on aging with the mission of “extending the healthy years of life”. They have a real interdisciplinary staff, exactly the one that is needed for studying aging, which is a notoriously multifactorial, multicausal, atypical and complex biological phenomenon.
One of the faculty member of Buck Institute is Gordon J. Lithgow Associate Professor, and on Tuesday due to Monya Baker‘s alarm I was happy to participate on Lithgow’s clearly terrific presentation without slides but full with thoughts, facts and good comments from a grateful audience. The event was part of the Ask a Scientist Series, which is a monthly lecture series, held at a San Francisco cafe. This time the place was the Axis Cafe and here are some words out of the official intro: Understanding and dealing with disease associated with aging is arguably the greatest challenge for biomedicine in the 21st Century. In fact growing old is the single largest risk factor for human disease in developed countries. Unfortunately, we don’t know much about the biological basis of aging — but a series of remarkable discoveries in simple animal models indicates that our understanding of the subject is beginning to change. For example, it is now commonplace to extend the lifespan of lab worms and flies by genetic or chemical interventions. Come learn about the latest in the new field of geroscience and talk about opportunities for living better, more productive lives.
On the iPhone photo made by me: Mr. Lithgow is demonstrating the role of chaperone proteins in protein folding/unfolding with 2 paper glasses.
There is a formulation of the argument on why aging should be considered as an unnatural process by Atul Gawande in the current The Way We Age Now report in The New Yorker: “..scientists do not believe that our life spans are actually programmed into us. After all, for most of our hundred-thousand-year existence—all but the past couple of hundred years—the average life span of human beings has been thirty years or less. (Research suggests that subjects of the Roman Empire had an average life expectancy of twenty-eight years.) Today, the average life span in developed countries is almost eighty years. If human life spans depend on our genetics, then medicine has got the upper hand. We are, in a way, freaks living well beyond our appointed time. So when we study aging what we are trying to understand is not so much a natural process as an unnatural one.”
According to the organizers the Edmonton Aging Symposium“was a WORLD FIRST! in being streamed live onto the internet.” Now you can download where possible, the video, powerpoint and audio MP3 recordings of the streaming split up by speaker in alphabetical order. I think this is really webhistorical and good news for all open access friends of the life (extension) sciences. One critical point: Why Windows Media Video format? The following slide is from Judith Campisi‘s presentation (excellent aging blogger Chris Patil of Ouroboros is working with Campisi as a postdoc) called The double-edged sword of cellular senescence: Link
There was a Symposium Live Streaming where for the very nominal fee of $5 CAD per connection to cover bandwidth costs people could watch the majority of presentations in a Windows Media Format. If anybody participated in this trial please share with us the information on it.
Debate between Gregory Stock and Daniel Callahan, which was moderated by Aubrey de Grey
Aubrey de Grey: Damage Accumulation and Age-Related Degeneration
The organizing principle of the sessions seems to be individual SENS points with an emphasis on the “Too few cells” problem, i.e. stem cells and tissue regeneration:
1) Too Few Cells
2) Too Many Cells
3) Chromosomal DNA Mutations
4) Mitochondrial DNA Mutations
5) Junk Inside Cells
6) Junk Outside Cells
7) Protein X-Links
As my 2 main research topics are stem cells and mitochondria, I would like to highlight 2 presentations:
Irina Conboy of UC, Berkeley: Conservation of Aging Within Stem Cell Niches
Bernard Lemire: Mitochondria – Central Players in Longevity
The Coalition to Extend Life launched today an online petition to U.S. Congress and President in order to make the technological possibility of Indefinite Life Extension a national priority and public policy goal of the United States. They ask the power people to create the 4 main conditions that will make it possible.
1. a National Institute for Life Extension be created with sufficient revenues to fund research in this area.
2. the Food and Drug Administration classify aging as a disease.
3. a National Commission be organized to study the social and economic impacts of this new reality.
4. a “Manhattan Project” to cure the terminal disease of aging.
What’s new here? Indefinite life extensioncould be addressed as an independent political issue with a bunch of supporters. If you are pro, sign the petition, if you are not, never mind but do not oppose – says the background assumption. Well, I am definitely pro, so at first I felt tempted to sign the petition, because I liked point 2 and 4 from a technological point of view. But I don’t think that at this point the address is right and it should be a mail to the U.S. Congress and President with this subject. If I were the sender of a letter with a similar content like that I would write the names of tech savvy power people, Silicon Valley big guns and venture capitalists in the address field and try to motivate them in an economical fashion. On the other hand I agree with Reason in that the right for indefinite life extension falls into the category of positive rights so it is not the best move to put it into the government’s hands. Even if this positive right can be derived from our strongest, universal, concrete human and negative right, the right for life.
To sum up: If you feel yourself tempted to sign, I encourage you to do that, although I am reluctant in this respect. The idea of this online petition can become a very useful PR tool for our very niche Issue, if a critical mass of people is reached.
My favourite signature and comment from the list: Amos Avon Cooper: “I’m almost 86 years old. I’m thankful to hear your message.”
Check out Grailsearch.org, which was started at the end of January and is hosted by software engineer Jim Craig with a deep interest in aging and bioinformatics. Grailsearch is a “community web portal intended for use by biogerontologists, students of biogerontology, software engineers, biochemists or anyone else interested in working towards the search for systems solutions to the diseases of aging.” Jim was interviewed at Pimm in November, 2006, and said that: “I have adopted life extension as a hobby. I now study microbiology, proteomics and molecular design about 20 hours per week and plan to guide the next 20-40 years of my career through bioinformatics and eventually into de novo drug design with an emphasis on aging solutions.”
The initial set of blog posts on the site seems really exciting for the multi-disciplined systems biologists of the future. As my point of view on indefinite life extension technology is systemic regenerative medicine, I am strongly committed to all the computational based large scale model approaches and quantitative aspects of the human body on which I had an interesting correspondence with Jim last year.
With Grailsearch the geeky IT side of aging research and life extension has at last got a quality representative on the web!
I think you would be in a serious trouble if I ask you to explain the concrete death of an old, but otherwise healthy man in terms of the suspected biological processes of human ageing, like slowly accumulating mitochondrial and chromosomal mutations, oxidative stress, overall cell loss, intra- or extracelular junk molecules or whatever. In almost every definition of aging there is the actuarial, probabilistic and mechanism-blind term: “increased vulnerability to death”or “increased probability of dying” or something like that. But isn’t it useless and empty when we would like to explain the hows of ageing and dying? Now it is Thomas Rando‘s turn for the second time in Pimm, author of a marvellous paper on stem cells and ageing. In the slightly philosophical, but definitely scientific Box 2, called “Dying of old age”, he explains (emphasis by me): “There is no compelling explanation for the cause of death in old but otherwise healthy humans, mice, worms or flies, or any other organism for that matter. The colloquial expression ‘dying of old age’ belies our knowledge of the biological basis of this event. Surely, the cessation of respiratory and circulatory functions results quickly in irreversible damage to vital organs; however, to insist that ageing of the heart or lungs is the cause of death only sidesteps the question. Examination of tissues of an old member of a species at the time of death will reveal stereotypical biological changes and perhaps even pathological changes that were only mildly symptomatic or even asymptomatic. Why, then, did this individual die? We can measure average and maximal lifespan in species, we can evaluate the effects of genetic, nutritional or pharmacological interventions that alter those indices, and we can correlate them with changes in tissue ageing. Yet no hypothesis has emerged that yields a useful definition of dying of old age in terms of cell and tissue biology.Read the rest of this entry »
As many other heavyweight bloggers Derya Unutmaz has an A life and a B life. His A life is focusing on the molecular machinery of T cell activation, differentiation, survival and its explotation by HIV as he is an Associate Professor at Department of Microbiology at New York School of Medicine. Briefly, he is an immunologist researcher. In his B life he edits Biosingularity, which – according to the subtitle – is a weblog on advances in biological systems. It gives an uptodate and detailed review of the current biological research from a very broad range on a quality level rare in the blogosphere. As in the case of lucky science bloggers, Unutmaz’s A life motivates his B life and vice versa. I am now pleased to report that he was kind enough to answer some life extension questions as he is really supportive of that topic (emphasis added by me). Fortunately the degrees of freedom in the blog genre is higher than in mainstream journalism, so although I realized that my old questions (they were sent in last October) are not enough, the answers were so deep, that I publish them now, and set some other questions later. I am really happy to share my point of view with Professor Unutmaz concerning the role of systemic regenerative medicine in indefinite or big-scale life extension. I’d like offer his words for every life extensionist: “The most important thing to remember though is to filter the hype from truth and solid science while both raising the awareness about the possibility of human life extension and also brain storming about the ideas on how to do this best.”
1. What is the story of your life extension commitment? The story of my commitment to life extension began as I became passionate about biology and science while I was still a kid. I realized then, (about 25-30 years ago) the technology was going to keep advancing and started to think why we could not come to a point when we have the knowledge to treat all diseases, and then why not stop aging? During medical school as I learned more about the physiology and pathology I realized the complexity of biological systems. It seemed intractable but at the same time biology followed rules, it wasn’t something magical that we can not conquer. I decided my life long commitment was going to be try to figure out how biological systems worked and how we can eventually master them to a point where we can reprogram our biology.
One of the promo material of last December Cambridge Embryonic Stem Cell Symposium was the Nature Insight: Stem Cells which was a supplement in Nature Vol. 441, No. 7097 pp1059-1102 from June , 2006. In it I found the best, brilliantly argumented and conceptualized, data-rich paper of Thomas Rando from Stanford University on Stem cells, ageing and the quest for immortality. I plan to introduce the thoughts of the paper in great details in future posts of Pimm. For today I just copy here Fig. 1: Tissue heterogeneity and stem-cell functionality for homeostasis and repair and the legend because this is the essential starting point of systemic regenerative medicine. Take an hour to think about it.
You can also discuss the paper here, or comment all the reviews of Nature Insight: Stem Cells on a special Nature blog-like surface.
Now I start to answer my blogterview questions concerning life extension. Here is the first:
1. What is the story of your life extension commitment? since the age of 15. I started my first offline diary at that age with a sentence something like this: I have eventually find the aim and meaning of my life which is the extension of human life, understanding the aging process and eliminating aging-related problems. The key for that is in mitochondrial DNA mutations, which must be reversed, here is an idea how..followed by some childish argumentoid how to repair them. And I have a sharp memory about the formulation of the argument that led me to this “aim” conclusion: I, A.Cs. would like to become a good scientist, but I need 50 years for biology, 50 years for physics, 50 years for mathematics and so on…and the only way to achieve this is not concurrently but consecutively, so I need more time, a lot much more than my evolutionarily fixed biology allows me to expect. (Of course today, if I had the chance to live as long as I can, I would prefer to become a little more than a pure scientist, say 50 years for web technology, 15 years for journalism, 15 years for travelling, 20 years for playing go …any way I can fully develop my own capacities, abilities let it be mental, physical, or moral. The list is mildly determined by Zeitgeist.) Next thought was to extend the range of this possibility to family members, friends…and people all over the world, because everybody has the right to live as long as they can. Oh yeah, this business is about eliminating ageing, get enough time to explore individuality and has nothing to do with eliminating death once and for all. I don’t want to become a wholly immortal person, and my motivation was not exactly the childhood fear of death and dying.
In the early 90s, when I was a school boy, the most exciting buzzword in life sciences was molecular biology, not stem cell resesarch nor whole genomes or omics or system biology. My definite professional motivation traces its roots back to a Scientific American article with the name (for me it was in Hungarian) Sense and nonsense DNA. The basics of molecular biology (replication-transcription-translation) were crystal clear and well established and conceivable at the first sight for a teen, and the aesthetic simplicity behind it was amazingly attractive. So I decided to become not a medical doctor but a molecular biologist. Read the rest of this entry »
Al Gore’s Inconvenient Truth, a movie-long effective presentation on climate change and crisis has made him the chief environmental evangelist of U.S. Incorporation. (I liked that he is doing his Keynotes himself, my Apps.) Now I have a better offer for Al Gore: be the first networking-presentation man of healthy life extension and an official aging crisis oracle. The facts are given, and the truth is unfortunately more inconvenient, specially from the mouth of a Baby Boomer. More inconvenient because unlike weather it is something that concerns our very physical make-up. But the technologies are within range.
Here is a not very well known Al Gore documentary made by Spike Jonze himself. Part 1:
John Schloendorn has a master’s degree in biochemistry at the University of Tuebingen, Germany. Currently he is a graduate student at Arizona State University’s Biodesign Institute, USA. John is heavily involved in the LysoSENS project of the Methuselah Foundation, which aims to remove some intracellular waste products for example via microbe-derived hydrolases targeted to the lysosome. Yes, this is the aubreyesque way of thinking on and experimenting with life extension.
1. What is the story of your life extension commitment? Since I first learnt that everyone was going to fall apart brutally, it was my goal to help with fixing aging somehow. To do that I needed to learn as much about aging as possible, and also needed to learn what everyone in the field was doing, so it seemed straightforward enough to study biochemistry. By the time my graduation came closer, Aubrey was running around, telling everyone he had a plan to fix aging. The plan seemed to make sense (true to its name), or at least it seemed like by far the best plan I could find. So I contacted him a lot over the web, eventually met him and volunteered to do some basic proof-of-concept’ing of some of his ideas. LysoSENS seemed like the fastest way to do that, it had already taken some baby steps thanks to Mark Hamalainen whom you interviewed recently, and there was enough Foundation money to keep it going. One can hardly hit upon a more fortunate situation.
2. Is it a commitment for moderate or maximum life extension?LysoSENS by itself is meant to address only parts of the age-related damage we accumulate. Magically achieving all LysoSENS goals would not extend life greatly, because other exponentially rising causes of death should rapidly take over, most importantly cancer. Thus, LysoSENS by itself would presumably count as moderate life extension.Read the rest of this entry »
The successful reprogramming (dedifferentiation) of differentiated human somatic cells into a pluripotent, embryonic stem cell-like state called induced pluripotent stem cells (iPS) using just 4 (and recently 3) introduced transcription factors is the biggest news of current stem cell biology. In the paper 
Recently I wrote a meeting report on the 
My gmailbox says and I see no reason not to share it: 
The immortal strand hypothesis captures stem cell scientists’ imagination these days. 
The 
As many other heavyweight bloggers 
John Schloendorn has a master’s degree in biochemistry at the University of Tuebingen, Germany. Currently he is a graduate student at Arizona State University’s 
