Lifespan.io Officially Launches, Crowdfunding the Development of a Cure for Aging
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Philanthropy has an important role in funding medical research, and thus crowdfunding will have an equally important role in the years ahead: it is collaborative philanthropy, the diverse will of the public, organized and made real. The falling cost of early stage biotechnology research means that the suite of prototype technologies needed to arrest degenerative aging in mammals, preventing all age-related disease through periodic repair of the cell and tissue damage that causes aging, might be as little as a billion dollars and ten years of work away from where we stand today. If we all get our act together.

Many hands make light work, and getting our act together is the point of Lifespan.io. This new non-profit crowdfunding initiative officially launched last week, showcasing a SENS mitochondrial research project that is a third of the way towards being funded as of today. Lifespan.io is an outgrowth of the Life Extension Advocacy Foundation (LEAF), and the staff and volunteers seek to attract funding for the most important of early staging longevity research, speeding the advent of prototype rejuvenation therapies. This is certainly the time for it: today is still early in a great transformation in aging research, leaving behind the look but don't touch approaches and the palliative treatment of late stage symptoms without any hope of lasting cures. The near future is brightened by the promise of direct intervention in the underlying causes of aging and age-related disease, and thus the prospect of being able to cure not just age-related disease but the very process of aging itself.

The LEAF and Lifespan.io president, Keith Comito, was kind enough to send me his thoughts on where this initiative comes from and where it is going. We're all of us on our own journeys through this space of development and potential in medicine; more traveling companions are always welcome:

My team and I created Lifespan.io because we strongly believe that centralizing crowdfunding efforts in this field will help to create a powerful grassroots movement for the extension of healthy human lifespan. It can do this by not only building a focused community of passionate serial donors who can fund research directly, but also by providing an accessible gateway for the public at large to be introduced to the idea of life extension.

Lifespan.io can also be a powerful tool in positively shaping the dialogue surrounding life extending technologies going forward. The argument against life extension used to be that it was impossible and a waste of time, but now the critique is changing to one that takes on shades of income inequality: this technology might be possible, but it will be available only for the rich. Lifespan.io can serve as a counter-force to this; giving the everyday person agency in the progression of this technology - democratizing relevant research and making the results open to the public.

In the near future we also plan to support Lifespan.io with various forms of content, such as thought-provoking videos focused on engaging the broader public. Through this we can help reframe certain aspects of the ongoing conversation about transhumanist ideals such as life extension, which at times can be divisive, to a more positive one by genuinely inviting dialogue on the science and the societal issues relating to life extension, as well as providing a path for those who wish to become informed and involved. Personally I believe that many people can be reached on the issue if we speak with compassion and intelligence. Extending healthy life is not just for scientists or transhumanists - it is human; it is what we have always done since the very first poultices and medicines.

Realizing our work sits within a continuum of human development and thought both connects us to the past and empowers the drive to keep reaching for an even greater future. Ever since The Epic of Gilgamesh humanity has dreamed of this goal - it is exciting that right now we are in this unique moment of history where literally anyone can carry the torch forward, and help find the flower of rejuvenation Gilgamesh sought. You get the chance to be part of the first Hero's Journey, and that's pretty awesome. Call me optimistic, but I think we can inspire others to feel that excitement too.

Personally, I've always been interested in self-enhancement, and slowly that led me to seek out information on the concept of life extension. This eventually led me to Aubrey de Grey's book Ending Aging which made me aware that meaningful progress in this area was feasible in our lifetime. I reached out to him and we bounced some emails back and forth about creating a New York based organization to further this research. This started out as a discussion group that met once a month for about a year, the remnants of which coalesced into LEAF.

I believe a little reframing could go a long way towards reaching the everyman, instead of alienating him. As one example, I think "Do you want to live forever?" is the wrong question to ask, because of how cognitive biases affect the way we think of aging. Better to ask "Do you want to be alive tomorrow? And, do you expect the answer to that question to change tomorrow?" It is in essence the same question, but phrased in a way that mitigates the inherent cognitive bias. I think that if we can illustrate how combating aging is really about affording greater choice to everyone, we can reach more people than we think. Even if an individual doesn't want to live longer or be free from terrible age-related diseases, the odds are that someone they know, someone they love, would like the freedom to have that choice - I believe most people could be convinced that giving their loved ones that choice is a good thing.

A Few Recent Papers on Alzheimer's Disease
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Here you'll find links to a selection of recent papers on Alzheimer's disease with no particular central thesis: merely a sampling of representative research results. Alzheimer's research is as much investigation of cellular metabolism and the biochemistry of the brain as it is research into the disease itself. Scientists strive to understand everything that might put the mechanisms of disease development into context. Our neural biochemistry is enormously complex, and thus so is any form of dysfunction in the many interacting systems of the brain. Since there is still so much blank space still left on the comprehensive map of human biochemistry, there are many competing theories to explain the development and pathology of Alzheimer's disease (AD), in part or in whole. Theories proliferate in times of uncertainty, and since therapies emerging from the dominant branch of theories based on amyloid accumulation are still in search of meaningful results, there is plenty of room for heresy, hypothesis, and debate.

It is perhaps ironic that aging has such simple and well-cataloged roots, a few forms of cell and tissue damage that occur as a result of the normal operation of metabolism, and yet the research community spends all of its time working backwards from enormously complicated end states of diseases, where a great deal of time and money are required to make even modest advances in understanding. This makes more sense if one assumes that the goal is less one of treatment and more one of understanding human biochemistry: Alzheimer's disease is the narrow end of the wedge to obtain funding to develop that understanding. That may be part of the problem, that the incentives and the goals for much of the research establishment are not necessarily aligned with rapid progress towards effective treatments. The output of traditional investigation followed by drug discovery is almost entirely marginal treatments that tinker with some aspect of cellular behavior in the late-stage disease process, a far cry from the most effective approach of tackling root causes.

Yet at the same time Alzheimer's research is actually one of the few fields where it is possible to say that at least some within the community work on ways to attack fundamental forms of damage, in the form of amyloid clearance. With enough money and enough different competing research groups, someone somewhere will be close to doing the right thing. Clearance of amyloid is a capability that will be needed for rejuvenation therapies, since the presence of amyloid is a distinguishing difference between old tissues and young tissues. A robust way to clear amyloid in Alzheimer's should require little work to adapt to other forms of amyloid in the body, at which point we might start to see a greater understanding developed as to exactly how and why these deposits contribute to degenerative aging. The fastest way to enlightenment and practical results is often to remove the potential cause of a problem, rather than to keep analyzing the system as it is.

The papers below are illustrative of these points, being representative of several types of output generated by the Alzheimer's research community. Theories abound, as do suggested forms of compensatory treatment, and books can be written to provide an overview of even just aspects of Alzheimer's development in the full context of how the brain works. It is a very complicated business, and some of the approaches to treating Alzheimer's patients are now more than a decade old, still gathering data in search of any benefit.

Nerve Growth Factor Gene Therapy - Activation of Neuronal Responses in Alzheimer Disease

In 2001, we initiated a clinical trial of nerve growth factor (NGF) gene therapy in AD, the first effort at gene delivery in an adult neurodegenerative disorder. This program aimed to determine whether a nervous system growth factor prevents or reduces cholinergic neuronal degeneration in patients with AD. We present postmortem findings in 10 patients with survival times ranging from 1 to 10 years after treatment.

Among 10 patients, degenerating neurons in the AD brain responded to NGF. All patients exhibited a trophic response to NGF in the form of axonal sprouting toward the NGF source. Comparing treated and nontreated sides of the brain in 3 patients who underwent unilateral gene transfer, cholinergic neuronal hypertrophy occurred on the NGF-treated side. Activation of cellular signaling and functional markers was present in 2 patients who underwent adeno-associated viral vectors-mediated NGF gene transfer. Neurons exhibiting tau pathology and neurons free of tau expressed NGF, indicating that degenerating cells can be infected with therapeutic genes, with resultant activation of cell signaling. No adverse pathological effects related to NGF were observed.

These findings indicate that neurons of the degenerating brain retain the ability to respond to growth factors with axonal sprouting, cell hypertrophy, and activation of functional markers. Sprouting induced by NGF persists for 10 years after gene transfer. Growth factor therapy appears safe over extended periods and merits continued testing as a means of treating neurodegenerative disorders.

Aberrant Lipid Metabolism in the Forebrain Niche Suppresses Adult Neural Stem Cell Proliferation in an Animal Model of Alzheimer's Disease

Lipid metabolism is fundamental for brain development and function, but its roles in normal and pathological neural stem cell (NSC) regulation remain largely unexplored. Here, we uncover a fatty acid-mediated mechanism suppressing endogenous NSC activity in Alzheimer's disease (AD). We found that postmortem AD brains and triple-transgenic Alzheimer's disease (3xTg-AD) mice accumulate neutral lipids within ependymal cells, the main support cell of the forebrain NSC niche. Mass spectrometry and microarray analyses identified these lipids as oleic acid-enriched triglycerides that originate from niche-derived rather than peripheral lipid metabolism defects.

In wild-type mice, locally increasing oleic acid was sufficient to recapitulate the AD-associated ependymal triglyceride phenotype and inhibit NSC proliferation. Moreover, inhibiting the rate-limiting enzyme of oleic acid synthesis rescued proliferative defects in both adult neurogenic niches of 3xTg-AD mice. These studies support a pathogenic mechanism whereby AD-induced perturbation of niche fatty acid metabolism suppresses the homeostatic and regenerative functions of NSCs.

Vascular dysfunction in the pathogenesis of Alzheimer's disease - A review of endothelium-mediated mechanisms and ensuing vicious circles

Despite considerable research effort, the pathogenesis of late-onset AD remains unclear. Substantial evidence suggests that the neurodegenerative process is initiated by chronic cerebral hypoperfusion (CCH) caused by aging and cardiovascular conditions. CCH causes reduced oxygen, glucose and other nutrient supply to the brain, with direct damage not only to parenchymal cells, but also to the blood-brain barrier (BBB), a key mediator of cerebral homeostasis. BBB dysfunction mediates the indirect neurotoxic effects of CCH by promoting oxidative stress, inflammation, paracellular permeability, and dysregulation of nitric oxide, a key regulator of regional blood flow. As such, BBB dysfunction mediates a vicious circle in which cerebral perfusion is reduced further and the neurodegenerative process is accelerated. Endothelial interaction with pericytes and astrocytes could also play a role in the process. Reciprocal interactions between vascular dysfunction and neurodegeneration could further contribute to the development of the disease.

The Role of Oxidative Damage in the Pathogenesis and Progression of Alzheimer's Disease and Vascular Dementia

Oxidative stress (OS) has been demonstrated to be involved in the pathogenesis of the two major types of dementia: Alzheimer's disease (AD) and vascular dementia (VaD). Evidence of OS and OS-related damage in AD is largely reported in the literature. Moreover, OS is not only linked to VaD, but also to all its risk factors. Several researches have been conducted in order to investigate whether antioxidant therapy exerts a role in the prevention and treatment of AD and VaD. Another research field is that pertaining to the heat shock proteins (Hsps), that has provided promising findings. However, the role of OS antioxidant defence system and more generally stress responses is very complex. Hence, research on this topic should be improved in order to reach further knowledge and discover new therapeutic strategies to face a disorder with such a high burden which is dementia.

Relationships Between Mitochondria and Neuroinflammation: Implications for Alzheimer's Disease

Mitochondrial dysfunction and neuroinflammation occur in Alzheimer's disease (AD). The causes of these pathologic lesions remain uncertain, but links between these phenomena are increasingly recognized. In this review, we discuss data that indicate mitochondria or mitochondrial components may contribute to neuroinflammation. While, mitochondrial dysfunction could cause neuroinflammation, neuroinflammation could also cause mitochondrial dysfunction. However, based on the systemic nature of AD mitochondrial dysfunction as well as data from experiments we discuss, the former possibility is perhaps more likely. If correct, then manipulation of mitochondria, either directly or through manipulations of bioenergetic pathways, could prove effective in reducing metabolic dysfunction and neuroinflammation in AD patients. We also review some potential approaches through which such manipulations may be achieved.
More Life, Less Severe Illness, but More Years of Illness
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Global trends in life expectancy, at birth, at 30, and at 60, continue onward and upward at a fairly slow but steady pace: approximately two years every decade for life expectancy at birth and a year every decade for remaining life expectancy at 60. The research linked below crunches the numbers for the much of the world from 1990 to 2013, an extension of similar past studies to include more recent data. The authors show that lives are longer and age-related illness less severe, but the period of time spent in disability or illness has grown.

We are machines. Very complex machines, but nonetheless collections of matter subject to the same physical and statistical laws regarding component failure and damage as a car or an electronic device. Aging is damage, and a substantial portion of the trend in life extension is caused by an incidental, unintentional slowing of the pace at which that damage accrues. This slowing results from diverse causes, including control of infectious disease and reduction of the life-long burden imposed by infection, increased wealth and consequently greater access to medical care of all types, and an improved capacity to treat age-related medical conditions as they emerge. None of this is aimed at aging per se, and the historical trend in rising life expectancy has been slow precisely because there has been neither the ability nor the attempt to meaningfully intervene in the aging process.

What happens when you slow down the pace at which damage accumulates in a machine? You extend all the phases of its life span, both fully functional and in decline. At a given age its average level of dysfunction is lower than it would otherwise have been and it lasts longer as a result - but that also means it is spending more time with at least some dsyfunction before finally failing. The story should be little different for us, which is why I've long been fairly skeptical of the concept of compression of morbidity, wherein some factions of the research community suggest it should be possible to engineer a long period of good health followed by a rapid decline. In their defense, there are species, such as naked mole rats and salmon, that have exactly this shape to their lives, so it is clearly possible in principle. But in humans, with the way we work, intervention in aging means slowing down or repairing the damage, and slowing it down has this outcome of a longer period of a slower decline.

The future of health and longevity will look nothing like the past, however. The trend will not continue: it will leap to the upside in a much faster gain in longevity. This is because are now entering a transitional period in which researchers aim at the deliberate treatment of the mechanisms of aging, the underlying cause of age-related disease, rather than continuing expensive and ultimately futile efforts to patch over disease symptoms and proximate mechanisms. This is a night and day change in the entire approach to medicine, and upsets many regulatory frameworks and established business models, which means it has taken time and a lot of effort to get to the point at which enough people are on board to make it happen. We are close to the tipping point these days, but the vast majority of the money and the research community remains stuck in the past, working on strategies in medicine for age-related conditions that are now outmoded. Change is painfully slow in heavily regulated fields like medicine, and I expect that this transitional period will continue well past the point at which the first partial rejuvenation treatments are proven in the clinic, such as senescent cell clearance.

If we want to see the trends change, and the slowly lengthening period of slowly lessening disability be replaced by sudden leaps in life expectancy, accompanied by outright cures for many age-related conditions, then we have to make repair of the damage of aging a priority. Not merely slowing down the pace at which that damage accumulates as a side-effect of the operation of normal metabolism, but creating targeted biotechnologies capable of deliberate repair of the points of failure. More than enough is known today in order to do this, it is just a matter of finding the money and the will to proceed.

Life expectancy climbs worldwide but people spend more years living with illness and disability

Global life expectancy has risen by more than six years since 1990 as healthy life expectancy grows; ischemic heart disease, lower respiratory infections, and stroke cause the most health loss around the world. People around the world are living longer, even in some of the poorest countries, but a complex mix of fatal and nonfatal ailments causes a tremendous amount of health loss, according to a new analysis of all major diseases and injuries in 188 countries. Global life expectancy at birth for both sexes rose by 6.2 years (from 65.3 in 1990 to 71.5 in 2013), while healthy life expectancy, or HALE, at birth rose by 5.4 years (from 56.9 in 1990 to 62.3 in 2013).

The study's researchers use DALYs, or disability-adjusted life years, to compare the health of different populations and health conditions across time. One DALY equals one lost year of healthy life and is measured by the sum of years of life lost to early death and years lived with disability. The leading global causes of health loss, as measured by DALYs, in 2013 were ischemic heart disease, lower respiratory infections, stroke, low back and neck pain, and road injuries. For communicable, maternal, neonatal, and nutritional disorders, global DALY numbers and age-standardized rates declined between 1990 and 2013. While the number of DALYs for non-communicable diseases have increased during this period, age-standardized rates have declined. The number of DALYs due to communicable, maternal, neonatal, and nutritional disorders has declined steadily, from 1.19 billion in 1990 to 769.3 million in 2013, while DALYs from non-communicable diseases have increased steadily, rising from 1.08 billion to 1.43 billion over the same period.

Global, regional, and national disability-adjusted life years (DALYs) for 306 diseases and injuries and healthy life expectancy (HALE) for 188 countries, 1990-2013: quantifying the epidemiological transition

The Global Burden of Disease Study 2013 (GBD 2013) aims to bring together all available epidemiological data using a coherent measurement framework, standardised estimation methods, and transparent data sources to enable comparisons of health loss over time and across causes, age-sex groups, and countries. The GBD can be used to generate summary measures such as disability-adjusted life-years (DALYs) and healthy life expectancy (HALE) that make possible comparative assessments of broad epidemiological patterns across countries and time. We used the published GBD 2013 data for age-specific mortality, years of life lost due to premature mortality (YLLs), and years lived with disability (YLDs) to calculate DALYs and HALE for 1990, 1995, 2000, 2005, 2010, and 2013 for 188 countries.

Sociodemographic status explained more than 50% of the variance between countries and over time for diarrhoea, lower respiratory infections, and other common infectious diseases; maternal disorders; neonatal disorders; nutritional deficiencies; other communicable, maternal, neonatal, and nutritional diseases; musculoskeletal disorders; and other non-communicable diseases. However, sociodemographic status explained less than 10% of the variance in DALY rates for cardiovascular diseases; chronic respiratory diseases; cirrhosis; diabetes, urogenital, blood, and endocrine diseases; unintentional injuries; and self-harm and interpersonal violence. Predictably, increased sociodemographic status was associated with a shift in burden from YLLs to YLDs, driven by declines in YLLs and increases in YLDs from musculoskeletal disorders, neurological disorders, and mental and substance use disorders. In most country-specific estimates, the increase in life expectancy was greater than that in HALE. Leading causes of DALYs are highly variable across countries.

An Audio Interview with Aubrey de Grey and Brian Kennedy
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Here I'll point out a twenty minute podcast interview with Aubrey de Grey of the SENS Research Foundation and Brian Kennedy of the Buck Institute for Research on Aging. This was recorded at the recent Rejuvenation Biotechnology 2015 conference, hosted by the SENS Research Foundation in the Bay Area, where both institutions are based. The SENS Research Foundation remains perhaps the world's only organization focused wholly on developing the fundamental biotechnologies needed for near future rejuvenation therapies capable of actually reversing the course of aging. A little of the work taking place at the Buck Institute is funded in part by the SENS Research Foundation, such as the research programs in the Campisi Lab aiming at the end goal of senescent cell clearance therapies, but for the most part the Buck Institute funds much more modest and mainstream goals in aging research, meaning attempts to slightly slow the aging process through traditional approaches of investigating cellular metabolism and drug discovery.

Brian Kennedy and Aubrey de Grey on their Converging Approaches to Aging Research

Last week we attended the 2015 Rejuvenation Biotechnology Conference where we heard about the latest developments in aging research. We were fortunate enough to sit down with two of the major figures in the field of aging research, Aubrey de Grey, CSO of the SENS Research Foundation and Brian Kennedy, CEO of the Buck Institute for Research on Aging. Brian and Aubrey gone about their work in different ways but say that their approaches are now converging as the momentum behind aging research increases. How do the two see the field since Calico and Human Longevity emerged? What developments in the past year stand out to them? Join us for an exclusive interview with two of the aging field's visionary leaders.

I put in a fair attempt to extract coherent text from the audio via software, but it wasn't on the cards today, or at least not via the standard recourse of feeding it to CMU Sphinx. If anyone else has better luck, let me know. In the meanwhile, here is a transcription of the middle of the interview, which might be of more interest to those of you who have followed the evolution of SENS since the early days.

Moderator: Let's try to hone in on the difference between you two and your view of aging, and what should be done. I mean, you know each other, so maybe you could just speak up.

AdG: Ok, well, so the big thing, the big innovation that I introduced fifteen years ago was the idea that we might actually find it easier in the long run to postpone substantially the ill-health of old age in human beings by not slowing down the rate at which the body creates damage to itself as a side-effect of normal metabolic processes, but rather by periodically repairing that damage after it has been created - but of course before it gets to a level that is so bad for us that we start going downhill.

Moderator: Ok, so one focused on repair...

Aubrey: That's right, that was the idea I brought forward. And the basis for that idea came, in large part, from areas of biology that had never previously been associated with the biology of aging. So that meant of course that the people who were working in the biology of aging were completely unfamiliar with those areas. It took a long time for me to actually make that case, and only because I had to bring together a lot of scientists who had never talked to one another before, and generally get people to pay attention to areas of biology that they had previously thought were not relevant to their work.

Brian: I think there has been some convergence on our end from the point of view that we've been following the genetics of aging, and have identified a lot of genes that impact the aging process. It seems clear that while some of them may prevent the onset of damage, a lot of them can actually induce repair mechanisms to clean up the damage that exists. So I think that at least superficially there was a significant difference in what we were saying ten years ago - and in reality there was some difference too - but there has been a lot of convergence on both sides so that I doubt that our messages are all that much different now.

Aubrey: Right, I think that a lot of the differences were more perceived and not so real, and I think the mutual education that has gone on in the meantime has clarified that, and besides there isn't all that much difference in terms of the emphasis that goes on. But I think it is also very important to note that one thing where convergence has been extremely strong is not so much on the science, but on the communication of the science. I think that now that everybody in the field is comfortable with saying that aging is really actually quite bad for you and we ought to try and do something about it...

Moderator: And that it's modifiable.

Brian: Yes.

Aubrey: Yes, and that we can do something about it, that's right. Now we all really speaking from the same hymn sheet, even that actual sort of words we're using here are converging. Brian gave an example today, in that he's talking of longevity as a side-effect of good health, and that's exactly the same thing that I've been saying.

Moderator: There is a big difference in the accents. Now how did you two meet?

Brian: It was certainly at the aging meetings, and we met at one of them.

Aubrey: The biogerontology community is actually pretty small, even now, and it was smaller ten years, twenty years ago.

Moderator: So you met ten years ago?

Aubrey de Grey: At least fifteen, I would say.

Brian: Yes, probably right.

Moderator: So was that like, wow somebody else gets it, or?

Brian: I think that there was a period where we had to get comfortable with each other. Speaking my side from the field as a whole, I think that Aubrey's message was... there was a lot of insight, and also it was also more aggressive than we were used to, so at the time we had to figure out how to deal with each other.

Moderator: Did that make you kind of bolster up, get some more courage?

Brian: It created different responses in different people in the field, but what I think is that we need multiple voices - there's no reason that the field should be speaking with only one voice. When you have different ideas and you have some people that are more grounded in saying "this is what the data has already shown" and other people that are more visionary I think it is good.

Aubrey: All that is certainly true, I agree with all of that. I think one thing that made it difficult for me to find common ground, common rhetorical ground especially, with the community back then, was something that I have been calling longevity sticker shock. Specifically that if I'm right about the science, that actually the most promising approach to postponing the ill health of old age consists of periodic preventative repair, repairing damage rather than slowing down the creation of damage, then what that implies for longevity is rather dramatically different. Slowing down the accumulation of damage, you'll get a modest increase in longevity, and that increase will be less if you start later. But if you are repairing damage every so often then you are buying time much more effectively. I pointed out way back in 2003 or 2004 that this led to a concept I call longevity escape velocity, that via really very imperfect but improving treatments one might be able to stay indefinitely ahead of the process of aging by keeping damage below pathogenic levels. This of course implies that the longevity consequences would be very dramatic. I, perhaps slightly naively, pointed this out and said, look, it's perfectly reasonable to think that there are people alive today who will live to a thousand, because that's how long you would live if you just didn't have an increased risk of death per year as we do today. And a lot people ran away very rapidly, shall we say.

Brian: Yes, it was the number. I think that at the time, that message appealed to a very small segment of the population, of which there were prominent people who were good to appeal to, but the public didn't understand enough to get to the point of your message, I think.

Aubrey: That's right, yes.

Moderator: And that's changed?

Brian: I think, well, I still don't go around talking about escape velocity. I think it is an interesting concept, but I represent a very large institute conducting NIH-funded research, and what I saying is that I don't know what is possible in the future, but I know what is possible in the short term. If we can start extending healthspan using strategies that we are developing today, the benefits of that are huge. The long-term consequences we just don't know; it could be that you're right, but I want to get those first incremental steps so that we can really get everyone excited about the approach.

Aubrey: You touched on a really important point at the beginning of that answer, which was the funding sources. When I started talking in those terms, I started getting the attention of people who wouldn't dream of funding someone like Brian because Brian's too...he's not aiming high enough, in their view. People like Peter Thiel, for example, they just want to live forever and that's that. So when I come along and I explain longevity escape velocity, they'll say "that sounds like what I want to deal with," whereas conversely, as Brian points out, if he starts talking like that in grant applications to the NIH, it isn't going to be good for his chances.

Moderator: What response have both of you had to the entrance of Calico, the Google company, and Human Longevity, Craig Venter's new company?

Aubrey: It's a complicated question. I'll talk about Human Longevity first. In my opinion they are not really working on what we're working on. They are working on personalized medicine, trying to optimize therapies that essentially already exist using analysis of large amounts of genetic data.

Moderator: So a similar company to other companies that are out there, with a fancier name?

Aubrey: I would say that definitely their hearts are in the right place, but they are a regular, perfectly normal company. They want to make profits fairly soon. Calico have set themselves up as a completely unusual company with the goal of doing something very long-term, however long it takes, they want to actually fix aging. They said so - Larry Page was perfectly clear about that. The question is how are they going about it, and that's getting really interesting. The first thing that they've done, which I feel is an absolutely spectacularly good move, is to bifurcate their work into a relatively short-term track and a long-term track. The short term track involves drug discovery for age-related diseases, doing deals with big companies like Abbvie, and so on. That's all very wonderful and all very lucrative in the relatively short term, and has more or less nothing to do with the mission for which Calico was set up - but it is a fabulous way to insulate the stuff that they do that is to do with why Calico was set up from shareholder pressure. It gets a little more complicated though. So then on the long term side, the stuff being led by David Botstein and Cynthia Kenyon, the question is how are they going about their mission. Of course an awful lot of this unknown because they are a secretive company, but from the perspective of whom they are hiring, and what kinds of work those people have done in the past, one can certainly say that they are not just focusing on one approach. They are interested in diversity. My only real concern is that they may be emphasizing a curiosity-driven long term exploratory approach to an unnecessary degree. I'm all for finding out more and more about aging, but I'm also all for using what we've already found out to the best of our ability to try stuff and see what we can do. I should emphasize that this is only my impression from a very limited amount of information available, but my impression is that it is perhaps turning into an excessively curiosity-driven, excessively basic science, inadequately translational outfit. And that's kind of what I feared when Botstein came along in the first place, because he's on record as saying he doesn't have a translational bone in his body. Now Brian could obviously say a lot more if he wants to, as he's done a deal with Calico.

Brian: Let me start by saying that I think its great that these big companies are getting into the game. Almost no matter what happens that is going to help the field get more people, more private sector people involved, maybe get Big Pharma involved, and so I think it is a good thing. I can't say too much about Calico because we have a relationship with them, but I will say that I think it is an interesting challenge when all of a sudden a lot of money is on the table, and very good people are hired to say "go solve this problem," and they haven't been thinking about that problem until a month ago. So I think what we're going to see with Calico is that they're going to continue to evolve as they go forward, and I think it will be very interesting to see the kinds of stuff they choose to do, and it may be very different two years or three years from now.

Moderator: You were saying in the panel we were just at that you thought it was a game-changer.

Brian: I think it adds great momentum, and I think it will be equally important to really get Big Pharma to get into this game too. It is easy to say you've got a ton of money, but what is a ton of money? If you're going to start doing real clinical trials, phase III clinical trials, it takes more than a ton of money; Big Pharma has to come in. Getting Abbvie involved is a good step, but it would also be good if everyone else starts saying this is the place to be.

The DRACO Fundraiser Site: killingsickness
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This is a year of much grassroots fundraising for longevity science, it seems, with more new projects launched and more new faces joining the community of supporters. All of these developments are collectively, hopefully, yet another sign that faster growth and more publicity are yet to come: the tipping point for public acceptance of efforts to treat aging as a medical condition is somewhere near, just around the corner. Ten years from now, people will conveniently forget that they were ever opposed to the development of therapies for aging. How silly that would be, like opposing cancer research or heart disease treatments, like self-sabotage. Who would think such a thing?

Here at Fight Aging! we're preparing to launch our 2015 SENS rejuvenation research fundraiser on October 1st, which coincidentally is also Longevity Day and the International Day of Older Persons. The crowdfunding site Lifespan.io launched recently, and their first project is a part of the SENS research programs aimed at bypassing mitochondrial DNA damage so as to remove that contributing cause of degenerative aging. Drop by and give them a few dollars: it's just the starting point for that team of crowdfunding developers, and I expect to see interesting things from them in the years ahead.

Similarly, a fundraising effort is presently coming together with the aim of raising philanthropic donations for development of the anti-virus technology DRACO. This is an approach that can be applied to near any virus in mammals, as it targets cells in which viruses are replicating rather than the viral particles themselves. DRACO has been featured at SENS conferences in the past, and is an excellent example of a technology that is too radically different from the present status quo to have an easy time in fundraising, even when backed by studies that would be more than enough to raise money were the results produced by the output of the standard drug discovery process.

Hence the work of a small group of volunteers putting together initiatives like killingsickness, and aiming at starting a crowdfunding campaign starting on October 1st this year. It's a busy time.

killingsickness

As you already know, DRACOs research and development may lead to a cure for virtually all viruses. More importantly, DRACOs may end suffering and save millions of lives! Unfortunately, this has received only limited funding to date and so DRACOs research and development will only happen with your help! We will launch an IndieGoGo campaign October 1, 2015 and we hope you will donate. We do know you have a lot questions first, and we want to answer them! To that point, please comment with your key questions and we will develop and post an FAQ's here and on the IndieGoGo campaign page.

About DRACO

The DRACO approach and results have been called "visionary" by the White House and named one of the best inventions of the year by Time magazine. However, research on DRACO has entered the well-known "Valley of Death," in which a lack of funding prevents DRACO and many other promising new drugs from being developed further and advancing toward human medical trials. With your help, we would like to raise enough funding to help DRACO successfully pass through the Valley of Death and advance toward human trials.

In cell culture, DRACO is reported to have broad-spectrum efficacy against many infectious viruses, including Marburg marburgvirus and Zaire ebolavirus, dengue flavivirus, Amapari and Tacaribe arenavirus, Guama bunyavirus, H1N1 influenza and rhinovirus. Although DRACOs have not yet been tested against other viruses, their broad-spectrum activity may mean that they might also be effective against HIV, HSV (cold sores and genital herpes), herpes zoster virus (chickenpox/shingles), HTLV, Ebola, MERS, SARS, avian influenza (bird flu), and other major viruses. DRACOs might be effective against viruses that are currently untreatable, or that can currently only be controlled but not cured by existing drugs. Because of their broad-spectrum activity, DRACOs might be useful in treating viruses that have become resistant to existing antiviral drugs, or even in promptly treating outbreaks of newly emerged viruses (like MERS).

Looking beyond the consideration of this one technology, and this effort to bypass the issues afflicting funding of early stage research, I see this and other similar efforts as representative of an ongoing and important change in the research ecosystem. The falling cost of communication, still on its way down towards the vicinity of zero, is fundamentally changing all aspects of human interaction and collaboration. The need for organizations to act as middlemen in funding the least costly, most risky, and earliest stage research is evaporating: the people with the interest and incentive to fund this work can collaborate among themselves, talk to the researchers directly, and set up their own fundraising efforts.

All of this produces a much greater incentive to educate ourselves about research and medicine, so as to better pick the winners, and to be able to make a difference to our own futures. It is the same incentive as drives us to understand diet and exercise. That incentive will play out over the next decade or two to produce a funding landscape, a dynamic interaction between laboratory staff, researchers, and the public, that is very different from what we see today - at least in the areas that really matter to the pace of progress, which is to say the innovation that occurs in early stage research that is very hard to fund adequately through traditional channels.