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
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.”
Linda Powers is the managing director and co-founder of Toucan Capital Corp, a $120 million venture capital fund (SBIC) focused on seed and early-stage life science and advanced technology investments (the fund markets itself as the The Leading US Investor in Stem Cells and Regenerative Medicine). Out of here insights and facts presented on the SENS3 conference (I caught some of her slides with my iPhone, see below) I’d like to highlight the following ones:
- the anti-aging market today is approx. 42 billion dollars,
- the number of issued and published U.S. stem cell patents has been decreased for the first time since 2000 compared to the earlier year,
- viable business models in regenerative medicine are still missing,
- first-to-trial and -market is not always advantageous in regmed.
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?
3. What is your favourite argument supporting human life extension?
James Clement: Not only will the suffering of disease and aging be alleviated, but human society will be transformed by continuous learning, and a deeper appreciation for the value of life (human and animal) and the environment in which we live.
6. What can blogs and other websites do for LE?
JC: The vast majority of the public still thinks that extreme life extension is science fiction. Blogs and websites can help educate them as to how close we really are to ending the suffering of disease and aging. Every day, 100,000 individuals die from aging related disease. If we are to put an end to this travesty as soon as possible, we need to motivate the public to make this a priority of our society.
Unfortunately replicative senescence in dividing somatic cell populations through telomere shortening and organismal level aging is not as strictly related as the September Wired (not online yet) issue’s Artifacts From the Future section suggests:
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.
As you might know Technorati, the premiere blog search engine was redesigned about a week ago, and now it is intended to be a more universal search engine which is mirrored in the current subtitle on the page: “Zillions of photos, videos, blogs and more.”
Here is what you can find after typing the term “life extension” into the search field:
The question is whether it is enough or not enough for the users desperately seeking relevant information (see blog post 1) and desperately avoiding irrelevant information (see blog post 2)?
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.”
In recent culture, technological life extension is considered to be a form of hacking, as 2Dolphins says a “hacker is someone who enjoys the intellectual challenge of creatively overcoming or circumventing limitations — someone who makes things work beyond perceived limits through unconventional means or skills.” In hacking there is also a DIY element too.
There are now 2 broader hacking terms applied for physical life extension technologies: body hacking and life hacking. For first, see my previous post about Bodies in the Making book which handles a diverse range of practices that aren’t usually linked: tattooing, cosmetic surgery, body-building, life extension technologies, self-cutting as exemplars of the body hacking concept. Body hack in that context is something extreme, something very experimental. How extreme form it will take, that depends on the chosen technology. In the old school permalink-free blog Notes from Classy’s Kitchen it is said for instance in the November 26, 2005 post: “What Aubrey de Grey was proposing was the ultimate bodyhack, engineered immortality (or 1000 year life span at least).” Body hack also includes a form a DIY, for instance Nikolaj Nyholmof O’Reilly Radar blogged on the “protocol for “isolat[ing] stem cells from your baby’s placenta in a rent lab or at home” for the upcoming EuroOSCON Make Fest, which also plays well with one emerging theme at this year’s FOO Camp, body hacking — engineers and copper wire paired with doctors, psychologists and neurologists.”
On the other hand there is the emerging life hack movement popul
James Clement, attorney and serial entrepreneur is the new Executive Director of the World Transhumanist Association (”
The 
In recent culture, technological life extension is considered to be a form of hacking, as