The SENS Research Foundation staff have launched their newly updated website:

If this is your first time visiting our site, welcome. If you've been here before, you're no doubt noticing plenty that is new: an updated site design, a variety of new content, a new logo, and a new organizational name.

It all centers around a new tagline: reimagine aging.

For a public charity, a tagline can be an enormously powerful thing. Our vision and mission statements remain the primary guides to our planning, but the tag is everywhere, on every business card and letter and web page. More than any other document or phrase, it naturally becomes the daily reminder of who we are and what we are about.

Of course we are still "advancing rejuvenation biotechnologies" just as vigorously as when we carried that tagline over the last couple years. We still aim to introduce a new premise for the pharma and biotech industries. And now, our successes in our research, our collaborations, our conferences, and our educational programs have made us increasingly aware of the need to refocus our messaging to people being exposed to us for the first time.

So we've consulted with a number of talented and insightful PR folks, and they all offered the same basic advice: "You do a great job of telling people what you do. Now tell them why they should care." That's really the root of the aforementioned changes: we want to do a better job of communicating that, together, we can change the way we think about how to treat age-related disease. We can change the basic research premises that have so far prevented any age-related disease from being eradicated. We can improve medicine in some of the most critical but neglected areas and increase human healthspan.

It's quite a bit of change, but it all starts when enough of us reimagine aging.

Link: http://sens.org/outreach/outreach-blog/welcome-our-new-site

Aging is a global phenomenon, occurring throughout the body, which is why correlations between the pace of different manifestations of degenerative aging are likely to happen and not necessarily linked by anything other than the fundamental causes of aging:

[Researchers] studied 1,984 older adults (average age about 77 years) enrolled in a prospective observational study that began in 1997-1998. A total of 1,162 individuals with baseline hearing loss had annual rates of decline in test scores that measured global and executive function that were 41 percent and 32 percent greater, respectively, than those among individuals with normal hearing. Compared to those individuals with normal hearing, individuals with hearing loss at baseline had a 24 percent increased risk for incident cognitive impairment, according to the study results.

"Our results demonstrate that hearing loss is independently associated with accelerated cognitive decline and incident cognitive impairment in community-dwelling older adults," the authors comment. "The magnitude of these associations is clinically significant, with individuals having hearing loss demonstrating a 30 percent to 40 percent accelerated rate of cognitive decline and a 24 percent increased risk for incident cognitive impairment during a six-year period compared with individuals having normal hearing."

The authors suggest that, on average, individuals with hearing loss would require 7.7 years to decline by five points on the 3MS (the Modified Mini-Mental State Examination, a commonly accepted level of change indicative of cognitive impairment) compared with 10.9 years in individuals with normal hearing.

Link: http://www.eurekalert.org/pub_releases/2013-01/jaaj-hlm011713.php

Skin is an excellent candidate for the forefront of tissue engineering: producing tissue in thin sheets reduces the scope of many of the hurdles involved, such as blood vessel formation to support cells in the tissue interior, or the need for innovation in the growth environment and equipment used to host and encourage growing tissue. Nonetheless, it's still a work in progress. Skin is still a complicated item, for all that it might be simple in comparison to a lung or a kidney - getting the skin layers right, with the correct cell types doing the correct things in the correct places, is one challenge only recently solved, for example. That's not even to talk about the difficulties of adding hair to the mix.

One of the things we might expect to see in the years ahead is an evolution of specialized tissue printing machinery, each focused on one particular type of organ or tissue. Different shapes and forms of tissue have very different requirements for growth, so why not specialize the equipment? Here is a popular science article looking at the early development of a skin fabricator:

A 3-D machine that prints skin? How burn care could be revolutionized

Leng's modest prototype looks like a small open box of clear hard rubber, the layered floor of which contains a delta of microfabricated pathways. These lead from seven reservoir stations to a single output stream. Just like the colour cartridges in my printer, Leng's reservoirs of live cells are computer controlled to dispense precise amounts exactly where needed.

She switches on a variable pressure device that drives the material into a base stream of alginate - a medically approved derivative of algae. The cells that would be placed in the reservoirs to fabricate human tissue would ideally be drawn from the patient, but could also be compatible donor or stem cells. "The stream flows into a liquid-filled reservoir that contains calcium chloride," Leng says, as a milky-white ribbon appears in a tank at the output end. "The calcium ions bind to the alginate chain and cause it to become a gel."

The ribbon of skin-like tissue winds around a small turning spindle or drum, the speed of which can determine the tissue's thickness and even its texture. More pull from the drum makes the material tougher, like muscle tissue.

The drum could also be used to make a tissue cylinder - a vein. "Think of something like duct tape," says Guenther, who also directs the underground lab that bears his name. "You make the tissue adhesive on one side, it sticks to itself, and you create a physical tube." The alginate, which degrades over time, provides only a temporary matrix for the cells, Guenther says. The cells attach to each other, and replace the disintegrating matrix with their own.

Guenther says the prototype printer cost a few hundred dollars to make. Apart from the micro-fabricated elements in the base, the whole thing looks like it could be assembled in a handyman's basement. One early version of the receiving chamber was a fish tank purchased in Chinatown. Guenther tells me, with amused pride, that it cost $20 - then shows me a pouch as big as his hand that contains a $4,000 sheet of dermal regeneration template - the stuff used in more laborious forms of tissue engineering.

The living cells in the tissue printer were taken from neonatal rats. The first clinical trials will be undertaken with mice, then pigs. Another hurdle to be cleared is the matter of cell supply. Ideally, says Guenther, cells for a human recipient should be made from the patient's own tissue. How that or donated material could be harvested quickly enough to feed a high-capacity tissue printer still has to be worked out. Jeschke says he hopes that a trial with five to 10 human patients could be possible within two to three years.

You might also look at an article from early last year on an automated artificial skin factory in Germany that produces small skin sections for research or grafting - an early model for what will come later when tissue engineering is more advanced.

The nuts and bolts of reliably measuring life span in small, numerous laboratory animals like flies and worms are glossed over in most of the materials presented here. It's more complicated and prone to error than anyone would like it to be, and as for all such undertakings a whole field of knowledge and practice has been established over the years. Here's an interesting video presentation from the Journal of Visualized Experiments:

Individual aging is manifest at the population level as an increase in age-dependent mortality, which is often measured in the laboratory by observing lifespan in large cohorts of age-matched individuals. Experiments that seek to quantify the extent to which genetic or environmental manipulations impact lifespan in simple model organisms have been remarkably successful for understanding the aspects of aging that are conserved across taxa and for inspiring new strategies for extending lifespan and preventing age-associated disease in mammals.

The vinegar fly, Drosophila melanogaster, is an attractive model organism for studying the mechanisms of aging due to its relatively short lifespan, convenient husbandry, and facile genetics. However, demographic measures of aging, including age-specific survival and mortality, are extraordinarily susceptible to even minor variations in experimental design and environment, and the maintenance of strict laboratory practices for the duration of aging experiments is required. These considerations, together with the need to practice careful control of genetic background, are essential for generating robust measurements. Indeed, there are many notable controversies surrounding inference from longevity experiments in yeast, worms, flies and mice that have been traced to environmental or genetic artifacts. In this protocol, we describe a set of procedures that have been optimized over many years of measuring longevity in Drosophila using laboratory vials.

Link: http://dx.doi.org/10.3791/50068

Rheumatoid arthritis is a malfunction of the immune system, but like many autoimmune diseases, comparatively little progress has been made towards understanding its causes. Here researchers are using epigenetic surveys to attempt to find genes of interest:

One probable factor involves chemical "tags" that attach to DNA sequences, part of a so-called epigenetic system that helps regulate when and how DNA sequences are "read," how they're used to create proteins and how they affect the onset or progress of disease.

To complicate matters, [the] attachment of the tags to particular DNA sequences can itself be regulated by genes. "The details of what causes a particular sequence to be tagged are unclear, but it seems that some tagging events depend on certain DNA sequences. In other words, those tagging events are under genetic control." Other tagging events, however, seem to depend on cellular processes and environmental changes, some of which could be the result, rather than the cause, of disease.

To tease apart these two types of tagging events, the researchers catalogued DNA sequences and their tagging patterns in the white blood cells of more than 300 people with and without one form of RA. The team then began filtering out the tags that did not appear to affect RA risk. For example, if tags were seen on the same DNA sequence in those with and without RA, it was assumed that the tags at those sites were irrelevant to the cause or development of the disease.

Ultimately, the team identified 10 DNA sites that were tagged differently in RA patients and whose tagging seemed to affect risk for RA. Nine of the 10 sites were within a region of the genome known to play an important role in autoimmune diseases, while the 10th was on a gene that had never before been associated with the disease. "Since RA is a disease in which the body's immune system turns on itself, current treatments often involve suppressing the entire immune system, which can have serious side effects. The results of this study may allow clinicians to instead directly target the culpable genes and/or their tags."

Link: http://www.eurekalert.org/pub_releases/2013-01/jhm-gat011713.php

This is an old story for regular readers, but I'll restate it anyway: people are dying of aging at a rate of something more than a hundred thousand lives a day. It is a mark of our inventive ongoing engagement with ways and means of death that despite this vast toll, aging still only manages to kill two thirds of us - and that in this era of comparatively advanced medicine, comparative peace, and comparative risk aversion.

Biotechnology is today's revolutionary industry in the making. Costs are falling, capabilities increasing just as dramatically as happened for computers two decades ago. We could be well on the way to removing aging as a cause of death at this point. A detailed plan is in hand, the way forward to achieve the goal of rejuvenation biotechnology is as clear as life science research ever gets, and the cost of an initial demonstration of rejuvenation in mice is ten years and a sum of money that's a rounding error in comparison what is spent on developing new and better ways to kill people.

Here's the thing, though, the point that's enough to make bitter old folk of us all: we're not actually well on the way to removing aging as a cause of death. We could be, but we're not - we're only just getting started at a time when we could be far further ahead, and we're moving slowly when we could be moving far faster. The hard-won funding and solid research programs for SENS and related initiatives are a trickle where a river is needed. You have to start at the start, of course, and every flood of effort started with a few drops back at the beginning. Nonetheless the flood does not yet exist, despite every reason for it to do so: a hundred thousand lives a day, the suffering of hundreds of millions more, and yet it's hard to get anyone to care enough to even think much about the topic, let alone do anything to help stop it from happening.

Where is rationality in all this? It's that the world is an asylum, run by the inmates, that makes people bitter before their time. To a first approximation those with resources build wars and circuses, and sometimes throw a crust to to the few who work on making the human condition better than it was yesterday. Those without resources heartily support this strategy, even while they owe pretty much every affordable comfort to work accomplished by a few centuries of researchers and developers - the tiny crust-fed minorities of their time.

Over at Edge, you'll find a commentary from Aubrey de Grey on the topic of human rationality and the high cost of its absence in matters relating to support of medical research aimed at human rejuvenation:

Visionary topics are of necessity long-term, hence high risk, and of almost equal necessity high gain. In the area of medical research, for example, the question must be raised: are we benefiting the most people, to the greatest extent, with the highest probability, by the current distribution of research funding? In all such areas that I can think of, the fundamental bias apparent in public opinion and public policy is in favour of approaches that might, arguably (often very arguably), deliver modest short-term benefits but which offer pretty much no prospect of leading to more effective, second-generation approaches down the road. The routes to those second-generation approaches that show the best chance of success are, by contrast, marginalised as a result of their lack of "intermediate results".

We should be very, very worried about this. I would go so far as to say that it is already costing masses - masses - of lives, by slowing down life-saving research. And how hard is it to address, really? How hard is Bayes' Theorem, really? I would assert that the single most significant thing that those who understand the issue I have highlighted here can do to benefit humanity is to agitate for better understanding of probabilistic reasoning among policy-makers, opinion-formers and thence the public.

As might be expected, older people with a greater loss of muscle mass and strength - the condition known as sarcopenia - also tend to exhibit a higher risk of death:

Sarcopenia has been indicated as a reliable marker of frailty and poor prognosis among the oldest individuals. We evaluated the impact of sarcopenia on the risk of all-cause death in a population of frail older persons living in community. We analysed data from the Aging and Longevity Study, a prospective cohort study that collected data on all subjects aged 80 years and older residing in the Sirente geographic area (n = 364). The present analysis was conducted among those subjects who were between 80 and 85 years of age at the time of the baseline assessment (n = 197). The main outcome measure was all-cause mortality over 7-year follow-up.

According to the European Working Group on Sarcopenia in Older People (EWGSOP) criteria, the diagnosis of sarcopenia required the documentation of low muscle mass and the documentation of either low muscle strength or low physical performance. [Using] the EWGSOP-suggested criteria, 43 subjects with sarcopenia (21.8%) were identified. During the 7-year follow-up, 29 (67.4%) participants died among subjects with sarcopenia compared with 63 subjects (41.2%) without sarcopenia. After adjusting for potential confounders including age, gender, education, activities of daily living (ADL) impairment, body mass index, hypertension, congestive heart failure, chronic obstructive pulmonary disease, number of diseases, TNF-α, participants with sarcopenia had a higher risk of death for all causes compared with non-sarcopenic subjects.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23321202

Here is news of a research tool for those developing ways to target and destroy senescent cells. A successful method should minimize the contribution of cellular senescence to degenerative aging and thus extend healthy life - this is one of the necessary biotechnologies for human rejuvenation that is closest to actual implementation:

Researchers have long known that the gene, p16INK4a (p16), plays a role in aging and cancer suppression by activating an important tumor defense mechanism called 'cellular senescence'. The [team] has developed a strain of mice that turns on a gene from fireflies when the normal p16 gene is activated. In cells undergoing senescence, the p16 gene is switched on, activating the firefly gene and causing the affected tissue to glow.

Throughout the entire lifespan of these mice, the researchers followed p16 activation by simply tracking the brightness of each animal. They found that old mice are brighter than young mice, and that sites of cancer formation become extremely bright, allowing for the early identification of developing cancers. "With these mice, we can visualize in real-time the activation of cellular senescence, which prevents cancer but causes aging. We can literally see the earliest molecular stages of cancer and aging in living mice."

The researchers used these mice to make several unexpected discoveries. First, the group was able to track the accumulation of senescent cells in aging mice by assessing how brightly each mouse glowed. Surprisingly, the brightest animals were no more likely to die from spontaneous cancer than dimmer animals of the same age. That is, the number of senescent cells in the mouse did not predict its risk of dying.

Another surprise came from the disparities in p16 levels among the mice. The authors studied a large group of genetically identical animals that were all housed in the same way and fed the same diet. However, despite identical genetic and environmental conditions, the brightness of individual mice at any given age was highly variable, suggesting that factors beyond genetics and diet influence aging.

Link: http://www.eurekalert.org/pub_releases/2013-01/uonc-uru011713.php

Since we're on the subject of cryonics today, I thought I'd point you to a review of the Alcor-40 conference published in Alcor's house magazine. The conference was held a few months back; you might compare this review with another conference report that was published in October.

This is a fairly long piece, so look through at your own pace:

Alcor-40 Conference Review

In honor of its 40th anniversary, Alcor held its first conference in 5 years on October 19-21, 2012, in Scottsdale, Arizona. The program featured a wide variety of topics for presentation, with themes regarding how to improve the odds of a successful cryopreservation and theories of aging and their implications for stopping or reversing aging (as argued by their primary scientific proponents).

...

The Chief Scientific Officer of 21st Century Medicine, Inc. (21CM), Greg Fahy, kicked off the event with an overview of the work being carried out at 21CM in his talk "Progress Toward Reversible Cryopreservation of Complex Systems." Because cryonics is reliant upon technologies that do not yet exist, it is sometimes likened to religion. "Unlike religion, cryonics must be based on evidence," Fahy began, emphasizing that reversibility is the key component of successful suspended animation.

Fahy rounded things out with an update on 21CM's "20 year plan." Begun in 2010, their work in whole body vitrification has marched forward with the ultimate goal of reversibility by 2030. Precision perfusion control systems have allowed for unprecedented data collection during whole body vitrification experiments. Currently, the company is focusing on studies of cryoprotectant toxicity to make the next advance toward reversible cryoprotection of the most complex system of all, the whole organism.

The cryonics movement is perhaps the oldest continuous portion of the modern community of advocates and supporters interested in radical life extension and the defeat of aging. This is a community distinguished from all those that came before it by the fact that is members are in a position to actually do something about the issues of death and aging. Technology is far enough along for people to work on preserving the minds of those who die too early, and we now have a shot at building working rejuvenation therapies over the next twenty to thirty years. All it needs is money. Present efforts are foundation work or crude first attempts in comparison to what lies ahead, but they exist, which is more than could be said just a few decades ago.

Plastination seems to have the potential to become a viable alternative to cryonics as a long-term storage method for the brains of those who die before the advent of rejuvenation biotechnology. If the fine structure that encodes the data of the mind is preserved, then these individuals can wait indefinitely for the arrival of molecular nanotechnology needed to restore them to life. Cryonics has been around for decades, and has had its challenges, while plastination remains a comparatively new idea - and thus we should expect there to be hurdles to overcome.

One of my concerns with room temperature storage of plastinated individuals is the potential for bacteria and bugs than might like to consume the fixative compounds, something that isn't a concern in low-temperature storage. Here is another:

I have always been interested in chemical fixation as a (low cost) alternative for cryonics. In fact, years before all the talk about the "connectome" and "plastination" I spent considerable time exchanging messages with Michael Perry at Alcor about the technical and practical feasibility of chemical brain preservation. But no matter how open minded I tried to be about this approach, I kept running into the same challenges over and over again.

The challenge that has concerned me the most is whether a delayed start of chemical brain fixation will produce incomplete distribution of the chemical fixative in the brain because of ischemia-induced perfusion impairment. Thinking about the technical problem of "no-reflow" is not the first thing on the mind of someone who first hears about the idea of using chemical fixatives to preserve the brain. In my case, this concern was not just "theoretical." In my lab I have spent many years looking at the effects of cerebral ischemia on cryopreservation and chemical fixation. Last year we decided to broaden our investigations to delayed chemical fixation and we have not been pleased at what we have observed so far. After 1.5 years of room temperature storage the delayed aldehyde fixed brains are falling apart and continue to decompose. In small animals one might imagine that such perfusion impairment could be overcome by immersing the brains in the fixative instead but human brains are simply too large. By the time that the fixative would have reached the core of the brain, extensive autolysis will have occurred.

Link: http://www.evidencebasedcryonics.org/2013/01/14/in-praise-of-cold/

Sestrins have been linked to life span in flies, and here researchers look at the analogs in nematode worms. I've yet to notice similar work for mice, however:

Aging is a process of gradual functional decline leading to death. Reactive oxygen species (ROS) contribute to oxidative stress and cell damage that lead to aging but also serve as signaling molecules. Sestrins are evolutionarily conserved in all multicellular organisms and are required for regenerating hyperoxidized forms of peroxiredoxins and ROS clearance. However, whether sestrins regulate longevity in metazoans is still unclear.

Here, we demonstrated that SESN-1, the only sestrin ortholog in Caenorhabditis elegans, is a positive regulator of lifespan. sesn-1 gene mutant worms had significantly shorter lifespans compared to wild-type animals, and overexpression of sesn-1 prolonged lifespan. Moreover, sesn-1 was found to a play key role in defense against several life stressors, including heat, hydrogen peroxide and the heavy metal copper; and sesn-1 mutants expressed higher levels of ROS and showed a decline in body muscle function. [These] results suggest that SESN-1 is required for normal lifespan and its function in muscle cells prevents muscle degeneration over a lifetime.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23318476

The costs of life science research are falling rapidly. What was expensive is now cheap: a few bright graduate studies and a small lab can accomplish in six months what would have required an entire institution and the better part of a decade in 1990. This means that, setting aside the incredible burden of regulation, prototyping a major new medical procedure or taking a therapy from theory to working result in laboratory animals has become cheap in comparison to many endeavors. It can cost considerably less to build a focused therapy given a strategy to work with than to construct the laboratory building in which the researchers work, for example - though it is true that the building will not take as long to assemble.

Degenerative aging in particular does not lack for a plan that can lead to effective therapies: the Strategies for Engineered Negligible Senescence (SENS). The likely cost of following through from where we are now to demonstrating the collection of seven to ten different therapies needed to rejuvenate old mice is a billion dollars and a decade or two in which to spend it well. Today funding for these various lines of research runs at a bare few million a year, and a great deal of work and advocacy was required to reach that far.

A billion dollars at a rate of fifty to a hundred million a year is a large sum of money in one sense, but smaller than countless organized projects that take place in the wealthier regions of the world. How much longer can the earnest pursuit of rejuvenation continue to be within the easy grasp of an alliance of any dozen of the world's twelve hundred billionaires and yet not funded to any great level? If shared between such a group, the individual costs wouldn't come close to what these figures invest in order to achieve far less beneficial end goals.

Some similar sentiments can be found in a recent article:

If you make it real hot, real fast, the frog will jump out of the pot. But if you turn up the heat slowly, before the frog realizes it, it will be too late, and the frog slowly dies. As aging humans, we are all slowly (and some not so slowly) being boiled alive by the ravages of time. The world's 1,226 billionaires, like that ill-fated frog in the story above, are [also] slowly being boiled alive.

Why, then, aren't they, or at least several of them, stepping up to the plate and getting out of the slowly heating pot that will put an end to all that they now enjoy and have worked so successfully to achieve? After all, at least 215 of them have $5 billion or more, and we estimate we might solve aging for less than $5 billion total spread over the next 16-20 years.

Some billionaires actually get it and in fact have offered some funding. But none has made a major commitment as far as I know. And that's tragic - for them and for you.

For how long can a brass ring remain hanging unclaimed? The opportunity to build the basis for human rejuvenation biotechnology exists, yet there is no massively funded effort underway to reach that goal. For how long can this state of affairs continue?

This is one of a number of approaches in recent years that has significantly reduced the levels of amyloid beta in the brain in the mouse version of Alzheimer's disease used for research. As for the others, it remains to be seen whether it is a suitable basis for a human therapy. Even if so, like much of the approach of modern medicine for age-related conditions, it isn't addressing causes, only trying to patch over consequences:

One of the main characteristics of Alzheimer's disease is the production in the brain of a toxic molecule known as amyloid beta. Microglial cells, the nervous system's defenders, are unable to eliminate this substance, which forms deposits called senile plaques.

[Researchers] identified a molecule that stimulates the activity of the brain's immune cells. The molecule, known as MPL (monophosphoryl lipid A), has been used extensively as a vaccine adjuvant [for] many years, and its safety is well established.

In mice with Alzheimer's symptoms, weekly injections of MPL over a twelve-week period eliminated up to 80% of senile plaques. In addition, tests measuring the mice's ability to learn new tasks showed significant improvement in cognitive function over the same period.

The researchers see two potential uses for MPL. It could be administered by intramuscular injection to people with Alzheimer's disease to slow the progression of the illness. It could also be incorporated into a vaccine designed to stimulate the production of antibodies against amyloid beta. "The vaccine could be given to people who already have the disease to stimulate their natural immunity. It could also be administered as a preventive measure to people with risk factors for Alzheimer's disease."

Link: http://www.eurekalert.org/pub_releases/2013-01/ul-mst011513.php

This result is reminiscent of the demonstration that ethanol produces significant life extension in nematodes - and similarly, one wonders whether it will be confirmed, and if so why it wasn't noted a long time ago. If it is accurate, it casts doubt on a range of life span studies that used the solvents in question.

Lifespan extension through pharmacological intervention may provide valuable tools to understanding the mechanisms of aging and could uncover new therapeutic approaches for the treatment of age-related disease. Although the nematode C. elegans is well known as a particularly suitable model for genetic manipulations, it has been recently used in a number of pharmacological studies searching for compounds with anti-aging activity. These compound screens are regularly performed in amphipathic solvents like dimethyl sulfoxide (DMSO), the solvent of choice for high-throughput drug screening experiments performed throughout the world.

In this work, we report that exposing C. elegans to DMSO in liquid extends lifespan up to 20%. Interestingly, another popular amphipathic solvent, dimethyl formamide (DMF), produces a robust 50% increase in lifespan. These compounds work through a mechanism independent of insulin-like signaling and dietary restriction (DR). Additionally, the mechanism does not involve an increased resistance to free radicals or heat shock suggesting that stress resistance does not play a major role in the lifespan extension elicited by these compounds. Interestingly, we found that DMSO and DMF are able to decrease the paralysis associated with amyloid-β(3-42) aggregation, suggesting a role of protein homeostasis for the mechanism elicited by these molecules to increase lifespan.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23313473

The Russian end of the longevity science advocacy community seems to include a majority of its graphic design folk; certainly they've published a range of attractive, glossy materials in past years. Not that there's anything stopping the rest of us raiding 99 Designs or similar, other than the nagging feel that we should have donated those funds to the SENS Foundation to go towards research. But the point stands: it's not as though a lack of local design talent these days is any barrier to having professional quality work created at a good price.

Via Maria Konovalenko, here are a couple more items to add to the stack - click through for the full size PDF versions.

Political Action - Call to Fight Aging

Roadmap to Immortality

We have created the Roadmap to Immortality - a timeline of events that will lead to indefinite human lifespan extension. Some of these evens can happen simultaneously, some separately, some even already happened.

People are always willing to argue over the role for referencing immortality, in the modern diluted sense of agelessness achieved through medical technology, in the course of advocacy for research funding and public awareness of longevity science. I think it has its place: if no-one is pushing out the bounds of what is accepted as reasonable in public discourse, then "reasonable" will forever be a rejection of any talk of improving human life span. Indeed, that is exactly where things stood in the scientific community only a decade or two ago, and largely because researchers remained silent. Only by talking about and working towards ambitious goals like SENS and the complete defeat of degenerative aging does the average position in public debate become something like "well, maybe we could work on extending human life."

There is much work left to do, of course, and the path to moderation always sets in once real money arrives and people start to focus on achieving the next incremental advance - but it's still the case that you don't raise the average by cutting back the highest and most ambitious points.