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UNITY Biotechnology Raises $116M for Senescent Cell Clearance Development – Article by Reason

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Categories: Science, Transhumanism, Tags: , , , , , , , , , , , , , , , , ,

The New Renaissance HatReason
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The whispers of late have had it that UNITY Biotechnology was out raising a large round of venture funding, and their latest press release shows that this was indeed the case. The company, as you might recall, is arguably the more mainstream of the current batch of startups targeting the clearance of senescent cells as a rejuvenation therapy. The others include Oisin Biotechnologies, SIWA Therapeutics, and Everon Biosciences, all with different technical approaches to the challenge. UNITY Biotechnology is characterized by a set of high profile relationships with noted laboratories, venture groups, and big names in the field, and, based on the deals they are doing, appear to be focused on building a fairly standard drug development pipeline: repurposing of apoptosis-inducing drug candidates from the cancer research community to clear senescent cells, something that is being demonstrated with various drug classes by a range of research groups of late. Senescent cells are primed to apoptosis, so a nudge in that direction provided to all cells in the body will have little to no effect on normal cells, but tip a fair proportion of senescent cells into self-destruction. Thus the UNITY Biotechnology principals might be said to be following the standard playbook to build the profile of a hot new drug company chasing a hot new opportunity, and clearly they are doing it fairly well so far.

UNITY Biotechnology Announces $116 Million Series B Financing

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UNITY Biotechnology, Inc. (“UNITY”), a privately held biotechnology company creating therapeutics that prevent, halt, or reverse numerous diseases of aging, today announced the closing of a $116 million Series B financing. The UNITY Series B financing ranks among the largest private financings in biotech history and features new investments from longtime life science investors ARCH Venture Partners, Baillie Gifford, Fidelity Management and Research Company, Partner Fund Management, and Venrock. Other investors include Bezos Expeditions (the investment vehicle of Jeff Bezos) and existing investors WuXi PharmaTech and Mayo Clinic Ventures. Proceeds from this financing will be used to expand ongoing research programs in cellular senescence and advance the first preclinical programs into human trials.

The financing announcement follows the publication of research that further demonstrates the central role of senescent cells in disease. The paper, written by UNITY co-founders Judith Campisi and Jan van Deursen and published today, describes the central role of senescent cells in atherosclerotic disease and demonstrates that the selective elimination of senescent cells holds the promise of treating atherosclerosis in humans. In animal models of both early and late disease, the authors show that selective elimination of senescent cells inhibits the growth of atherosclerotic plaque, reduces inflammation, and alters the structural characteristics of plaque such that higher-risk “unstable” lesions take on the structural features of lower-risk “stable” lesions. “This newly published work adds to the growing body of evidence supporting the role of cellular senescence in aging and demonstrates that the selective elimination of senescent cells is a promising therapeutic paradigm to treat diseases of aging and extend healthspan. We believe that we have line of sight to slow, halt, or even reverse numerous diseases of aging, and we look forward to starting clinical trials with our first drug candidates in the near future.”

So this, I think, bodes very well for the next few years of rejuvenation research. It indicates that at least some of the biotechnology venture community understands the likely true size of the market for rejuvenation therapies, meaning every human being much over the age of 30. It also demonstrates that there is a lot of for-profit money out there for people with credible paths to therapies to treat the causes of aging. It remains frustrating, of course, that it is very challenging to raise sufficient non-profit funds to push existing research in progress to the point at which companies can launch. This is a problem throughout the medical research and development community, but it is especially pronrounced when it comes to aging. The SENS view of damage repair, which has long incorporated senescent cell clearance, is an even tinier and harder sell within the aging research portfolio – but one has to hope that funding events like this will go some way to turn that around.

From the perspective of being an investor in Oisin Biotechnologies, I have to say that this large and very visible flag planted out there by the UNITY team is very welcome. The Oisin team should be able to write their own ticket for their next round of fundraising, given that the gene therapy technology they are working on has every appearance of being a superior option in comparison to the use of apoptosis-inducing drugs: more powerful, more configurable, and more adaptable. When you are competing in a new marketplace, there is no such thing as too much validation. The existence of well-regarded, well-funded competitors is just about the best sort of validation possible. Well-funded competitors who put out peer-reviewed studies on a regular basis to show that the high-level approach you and they are both taking works really well is just icing on the cake. Everyone should have it so easy. So let the games commence! Competition always drives faster progress. Whether or not I had skin in this game, it would still be exciting news. The development of rejuvenation therapies is a game in which we all win together, when new treatments come to the clinic, or we all lose together, because that doesn’t happen fast enough. We can and should all of us be cheering on all of the competitors in this race. The quality and availability of the outcome is all that really matters in the long term. Money comes and goes, but life and health is something to be taken much more seriously.

Now with all of that said, one interesting item to ponder in connection to this round of funding for UNITY is the degree to which it reflects the prospects for cancer therapies rather than the prospects for rejuvenation in the eyes of the funding organizations. In other words, am I being overly optimistic in reading this as a greater understanding of the potential for rejuvenation research in the eyes of the venture community? It might be the case that the portions of the venture community involved here understand the market for working cancer drugs pretty well, and consider that worth investing in, with the possibility of human rejuvenation as an added bonus, but not one that is valued appropriately in their minds. Consider that UNITY Biotechnology has partnered with a noted cancer therapeutics company, and that the use of drugs to inducing apoptosis is a fairly well established approach to building cancer treatments. That is in fact why there even exists a range of apoptosis-inducing drugs and drug candidates for those interested in building senescent cell clearance therapies to pick through. Further, the presence of large numbers of senescent cells does in fact drive cancer, and modulating their effects (or removing them) to temper cancer progress is a topic under exploration in the cancer research community. So a wager on a new vision, or a wager on the present market? It is something to think about.

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries.
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This work is reproduced here in accord with a Creative Commons Attribution license. It was originally published on FightAging.org.

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An Example of the Glaring Lack of Ambition in Aging Research – Post by Reason

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The New Renaissance HatReason
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The mainstream of aging research, at least in public, is characterized by a profound lack of ambition when it comes to treating aging as a medical condition. Researchers talk about slightly altering the trajectory of aging as though that is the absolute most that is possible, the summit of the mountain, and are in many cases ambivalent when it comes to advocating for even that minimal goal. It is this state of affairs that drove Aubrey de Grey and others into taking up advocacy and research, given that there are clear paths ahead to rejuvenation, not just a slight slowing of aging, but halting and reversing the causes of aging. Arguably embracing rejuvenation research programs would in addition cost less and take a much shorter span of time to produce results, since these programs are far more comprehensively mapped out than are efforts to produce drugs to alter the complex operations of metabolism so as to slightly slow the pace at which aging progresses. It is most frustrating to live in a world in which this possibility exists, yet is still a minority concern in the research community. This article is an example of the problem, in which an eminent researcher in the field takes a look at a few recently published books on aging research, and along the way reveals much about his own views on aging as an aspect of the human condition that needs little in the way of a solution. It is a terrible thing that people of this ilk are running the institutes and the funding bodies: this is a field crying out for disruption and revolution in the name of faster progress towards an end to aging.

How can we overcome our niggling suspicion that there is something dubious, if not outright wrong, about wanting to live longer, healthier lives? And how might we pursue longer lives without at the same time falling prey to quasiscientific hype announcing imminent breakthroughs? In order to understand why aging is changing, and what this means for our futures, we need to learn more about the aging process itself. As a biologist who specializes in aging, I have spent more than four decades on a quest to do exactly this. Not only have I asked why aging should occur at all (my answer is encapsulated in a concept called disposability theory), but I have also sought to understand the fastest-growing segment of the population – those aged 85 and above. The challenges inherent in understanding and tackling the many dimensions of aging are reflected in a clutch of new books on the topic. Are these books worth reading? Yes and no. They take on questions like: Can we expect increases in human longevity to continue? Can we speed them up? And, on the personal level, what can we do to make our own lives longer and healthier? If nothing else, these books and their varied approaches reveal how little we actually know.

To find out more about factors that can influence our individual health trajectories across ever-lengthening lives, my colleagues and I began, in 2006, the remarkable adventure of the still ongoing Newcastle 85+ Study, an extremely detailed investigation of the complex medical, biological, and social factors that can affect a person’s journey into the outer reaches of longevity. For each individual, we determined whether they had any of 18 age-related conditions (e.g., arthritis, heart disease, and so on). Sadly, not one of our 85-year-olds was free of such illnesses. Indeed, three quarters of them had four or more diseases simultaneously. Yet, when asked to self-rate their health, an astonishing 78 percent – nearly four out of five – responded “good,” “very good,” or “excellent.” This was not what we had expected. The fact that these individuals had so many age-related illnesses fit, of course, with the popular perception of the very old as sadly compromised. But the corollary to this perception – that in advanced old age life becomes a burden, both to the individuals themselves and to others – was completely overturned. Here were hundreds of old people, of all social classes and backgrounds, enjoying life to the fullest, and apparently not oppressed by their many ailments.

As for my stake in the enterprise, I began investigating aging when I was in my early 20s – well before I had any sense of my own body aging. Quite simply, I was curious. What is this mysterious process, and why does it occur? Everything else in biology seems to be about making things work as well as they can, so how is it that aging destroys us? Now that I am growing older myself, my research helps me understand my own body and reinforces the drive to live healthily – to eat lightly and take exercise – though not at the cost of eliminating life’s pleasures. For all that I have learned about aging, my curiosity remains unabated. Indeed, it has grown stronger, partly because as science discovers more about the process, it reveals that there is ever more to learn, ever greater complexity to unravel, and partly because I am now my own subject: through new physical and psychological experiences in myself, I learn more about what older age is really like. I know all too well that the next phase of my life will bring unwelcome changes, and of course it must end badly. But the participants of the Newcastle 85+ Study have shown me that the journey will not be without interest.

Link: https://lareviewofbooks.org/article/want-live-longer-complicated-relationship-longevity/

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries.
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This work is reproduced here in accord with a Creative Commons Attribution license. It was originally published on FightAging.org.

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Criticizing Programmed Theories of Aging – Article by Reason

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The New Renaissance HatReason
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Today I’ll point out an open-access critique of programmed aging theories by the originator of the disposable soma theory of aging, one of the modern views of aging as accumulated damage rather than programming. The question of how and why we age is wrapped in a lot of competing theory, but of great practical importance. Our biochemistry is enormously complex and incompletely mapped, and thus the processes of aging, which is to how exactly our biochemistry changes over time, and all of the relationships that drive that change, are also enormously complex and incompletely mapped. Nonetheless, there are shortcuts that can be taken in the face of ignorance: the fundamental differences between young and old tissue are in fact well cataloged, and thus we can attempt to reverse aging by treating these changes as damage and repairing them. If you’ve read through the SENS rejuvenation research proposals, well, that is the list. The research community may not yet be able to explain and model how exactly this damage progresses, interacts, and spreads from moment to moment, but that effort isn’t necessary to build repair therapies capable of rejuvenation. You don’t need to build a full model of the way in which paint cracks and peels in order to scrub down and repaint a wall, and building that model is a lot most costly than just forging ahead with the painting equipment.

The engineering point of view described above, simply getting on with the job when there is a good expectation of success, is somewhat antithetical to the ethos and culture of the sciences, which instead guides researchers to the primary goal of obtaining full understanding of the systems they study. In practice, of course, every practical application of the life sciences is created in a state of partial ignorance, but the majority of research groups are nonetheless oriented towards improving the grand map of the biochemistry of metabolism and aging rather than doing what can be done today to create rejuvenation therapies. Knowledge over action. If we had all the time in the world this would be a fine and golden ideal. Unfortunately we do not, which places somewhat more weight on making material progress towards the effective treatment of aging as a medical condition – ideally by repairing its causes.

But what are the causes of aging? The majority view in the research community is that aging is a process of damage accumulation. The normal operation of metabolism produces forms of molecular damage in cells and tissues, a sort of biological wear and tear – though of course the concept of wear and tear is somewhat more nuanced and complex in a self-repairing system. This damage includes such things as resilient cross-links that alter the structural properties of the extracellular matrix and toxic metabolic waste that clutters and harms long-lived cells. As damage accumulates, our cells respond in ways that are a mix of helpful and harmful, secondary and later changes that grow into a long chain of consequences and a dysfunctional metabolism that is a long way removed from the well-cataloged fundamental differences between old and young tissues. An old body is a complicated mess of interacting downstream problems. In recent years, however, a growing minority have suggested and theorized that aging is not caused by damage, but is rather a programmed phenomenon – that some portion of the what I just described as the chain of consequences, in particular epigenetic changes, are in fact the root cause of aging. In the programmed view of aging, epigenetic change causes dysfunction and damage, not the other way around. That these two entirely opposite views can exist is only possible because there is no good map of the detailed progression of aging – only disconnected snapshots and puzzle pieces. There is a lot of room to arrange the pieces in any way that can’t be immediately refuted on the basis of well-known past studies.

There are two ways to settle the debate of aging as damage versus aging as evolved program. The first is to produce that grand map of metabolism and aging, something that I suspect is at the least decades and major advances in life science automation removed from where we stand now. The other is to build therapies that produce large degrees of rejuvenation, enough of a difference to put it far beyond argument that the approach taken is the right one. That is not so far away, I believe, as the first SENS rejuvenation therapies are presently in the early stages of commercial development. I think that, even with the comparative lack of funding for this line of development, ten to twenty years from now the question will be settled beyond reasonable doubt. Meanwhile, the programmed-aging faction has become large enough and their positions coherent enough that the mainstream is beginning to respond substantially to their positions; I expect that this sort of debate will continue all the way up to and well past the advent of the first meaningful rejuvenation therapies, which at this point look to be some form of senescent cell clearance.

Can aging be programmed? A critical literature review – by Axel Kowald and Thomas B. L. Kirkwood

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Many people, coming new to the question of why and how aging occurs, are attracted naturally to the idea of a genetic programme. Aging is necessary, it is suggested, either as a means to prevent overcrowding of the species’ environment or to promote evolutionary change by accelerating the turnover of generations. Instead of programmed aging, however, the explanation for why aging occurs is thought to be found among three ideas all based on the principle that within iteroparous species (those that reproduce repeatedly, as opposed to semelparous species, where reproduction occurs in a single bout soon followed by death), the force of natural selection declines throughout the adult lifespan. This decline occurs because at progressively older ages, the fraction of the total expected reproductive output that remains in future, on which selection can act to discriminate between fitter and less-fit genotypes, becomes progressively smaller. Natural selection generally favours the elimination of deleterious genes, but if its force is weakened by age, and because fresh mutations are continuously generated, a mutation-selection balance results. The antagonistic pleiotropy theory suggests that a gene that has a benefit early in life, but is detrimental at later stages of the lifespan, can overall have a net positive effect and will be actively selected. The disposable soma theory is concerned with optimizing the allocation of resources between maintenance on the one hand and other processes such as growth and reproduction on the other hand. An organism that invests a larger fraction of its energy budget in preventing accumulation of damage to its proteins, cells and organs will have a slower rate of aging, but it will also have fewer resources available for growth and reproduction, and vice versa. Mathematical models of this concept show that the optimal investment in maintenance (which maximizes fitness) is always below the fraction that is necessary to prevent aging.

In recent years, there have been a number of publications claiming that the aging process is a genetically programmed trait that has some form of benefit in its own right. If this view were correct, it would be possible experimentally to identify the responsible genes and inhibit or block their action. This idea is, however, diametrically opposed to the mainstream view that aging has no benefit by its own and is therefore not genetically programmed. Because experimental strategies to understand and manipulate the aging process are strongly influenced by which of the two opinions is correct, we have undertaken here a comprehensive analysis of the specific proposals of programmed aging. On the principle that any challenge to the current orthodoxy should be taken seriously, our intention has been to see just how far the various hypotheses could go in building a convincing case for programmed aging.

This debate is not only of theoretical interest but has practical implications for the types of experiments that are performed to examine the mechanistic basis of aging. If there is a genetic programme for aging, there would be genes with the specific function to impair the functioning of the organism, that is to make it old. Under those circumstances, experiments could be designed to identify and inhibit these genes, and hence to modify or even abolish the aging process. However, if aging is nonprogrammed, the situation would be different; the search for genes that actively cause aging would be a waste of effort and it would be too easy to misinterpret the changes in gene expression that occur with aging as primary drivers of the senescent phenotype rather than secondary responses (e.g. responses to molecular and cellular defects). It is evident, of course, that genes influence longevity, but the nature of the relevant genes will be very different according to whether aging is itself programmed or not.

For various programmed theories of aging, we re-implemented computational models, developed new computational models, and analysed mathematical equations. The results fall into three classes. Either the ideas did not work because they are mathematically or conceptually wrong, or programmed death did evolve in the models but only because it granted individuals the ability to move, or programmed death did evolve because it shortened the generation time and thus accelerated the spread of beneficial mutations. The last case is the most interesting, but it is, nevertheless, flawed. It only works if an unrealistically fast-changing environment or an unrealistically high number of beneficial mutations are assumed. Furthermore and most importantly, it only works for an asexual mode of reproduction. If sexual reproduction is introduced into the models, the idea that programmed aging speeds up the spread of advantageous mutations by shortening the generation time does not work at all. The reason is that sexual reproduction enables the generation of offspring that combine the nonaging genotype of one parent with the beneficial mutation(s) found in the other parent. The presence of such ‘cheater’ offspring does not allow the evolution of agents with programmed aging.

In summary, all of the studied proposals for the evolution of programmed aging are flawed. Indeed, an even stronger objection to the idea that aging is driven by a genetic programme is the empirical fact that among the many thousands of individual animals that have been subjected to mutational screens in the search for genes that confer increased lifespan, none has yet been found that abolishes aging altogether. If such aging genes existed as would be implied by programmed aging, they would be susceptible to inactivation by mutation. This strengthens the case to put the emphasis firmly on the logically valid explanations for the evolution of aging based on the declining force of natural selection with chronological age, as recognized more than 60 years ago. The three nonprogrammed theories that are based on this insight (mutation accumulation, antagonistic pleiotropy, and disposable soma) are not mutually exclusive. There is much yet to be understood about the details of why and how the diverse life histories of extant species have evolved, and there are plenty of theoretical and experimental challenges to be met. As we observed earlier, there is a natural attraction to the idea that aging is programmed, because developmental programming underpins so much else in life. Yet aging truly is different from development, even though developmental factors can influence the trajectory of events that play out during the aging process. To interpret the full complexity of the molecular regulation of aging via the nonprogrammed theories of its evolution may be difficult, but to do it using demonstrably flawed concepts of programmed aging will be impossible.

Given that the author here has in the past been among those who dismissed the SENS initiative as an approach to treating aging by repairing damage, it is perhaps a little amusing to see him putting forward points such as this one: “despite the cogent arguments that aging is not programmed, efforts continue to be made to establish the case for programmed aging, with apparent backing from quantitative models. It is important to take such claims seriously, because challenge to the existing orthodoxy is the path by which science often makes progress.” Where was this version of the fellow ten years ago?

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries.
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This work is reproduced here in accord with a Creative Commons Attribution license. It was originally published on FightAging.org.

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An Interview with Kelsey Moody of Ichor Therapeutics, Bringing a SENS Therapy for Macular Degeneration to the Clinic – Article by Reason

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The New Renaissance HatReason
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As I mentioned last week, earlier this year Fight Aging! invested a modest amount in the Ichor Therapeutics initiative to develop a treatment for macular degeneration, joining a number of other amateur and professional investors in helping to get this venture started. The approach taken here is based on the results of research carried out at the Methuselah Foundation and SENS Research Foundation over much of the past decade, funded by philanthropists and the support of our community of longevity science enthusiasts. This is how we succeed in building the future: medical science in the laboratory leads to medical development in startup companies, each new stage bringing treatments capable of repairing specific forms of age-related molecular damage that much closer to the clinic.

Ichor Therapeutics is one of a growing number of success stories to emerge from the SENS rejuvenation research community. Young scientists, advocates, and donors involved in earlier projects – years ago now – have gone on to build their own ventures, while retaining an interest in stepping up to do something meaningful to help bring an end to aging. Back in 2010, Kelsey Moody worked on the LysoSENS project to find ways to break down damaging metabolic waste in old tissues; fast-forward six years, and he is the now the CEO of a successful small biotechnology company with a great team, taking that very same technology and putting it to good use. I recently had the chance to ask Kelsey a few questions about the future of SENS rejuvenation research, as well as how the Ichor scientists intend to construct a new class of therapy for macular degeneration, one based on removing one of the root causes of the condition.

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Who are the people behind Ichor Therapeutics? How did you meet and decide that this was the thing to do? Why macular degeneration as a target?

People have always been the focus of Ichor. Since day one we have worked to create a positive environment that cultivates a product-oriented research focus and emphasizes autonomy and personal accountability for work. As a result, ambitious self-starters tend to find their way to Ichor and remain here. However, we recognized early on that just filling a lab with a bunch of blue-eyed bushy tailed young up-and-comers is not sufficient to develop a robust, mature, translational pipeline. We have augmented our team with a number of critical staff members who are seasoned pharma operators, including our Quality Assurance Director and General Counsel.

Age-related macular degeneration (AMD) was chosen as a target because we believe it is the closest SENS therapy to the clinic. While we obviously have an interest in providing cures for the patients suffering from AMD and are attracted to the large market opportunities such a treatment could bring, our broader interest is in validating the entire SENS paradigm. We believe that Aubrey de Grey continues to receive excessive criticism because nothing spun out of SENS has ever made it into a legitimate pre-clinical pipeline, much less to the bedside. However, this does not mean he is wrong. Our goal is to be the first group to bring a SENS inspired therapy into the clinic and in doing so, silence critics and generate new energy and capital for this cause.

I understand there’s a lengthy origin story for the approach you are taking to treat AMD; it’d be great to hear some of it.

Our approach to treating AMD is based on the hypothesis that cellular junk that accumulates over the lifespan significantly contributes to the onset and progression of AMD. Our goal is to periodically reduce the burden of the junk so it never accumulates to levels sufficient to induce pathology. The strategy to accomplish this calls for the identification of enzymes that can break down the junk in a physiological setting, and the engineering of these enzymes such that they can break down the target in the correct organelle of the correct cell without appreciable collateral damage to healthy cells or tissue.

Methuselah Foundation and SENS Research Foundation did excellent work in establishing this program nearly a decade ago. They successfully identified a number of candidate enzymes that could break down the molecular junk, but reported that the targeting systems evaluated failed to deliver these enzymes to the appropriate organelles and cells. My group reevaluated these findings, and discovered that these findings were flawed. The delivery failure could be entirely attributed to a subtle, yet highly significant difference between how the target cells behave outside of the body as compared to inside the body. It turned out that the approach was in fact valid, it was the cell based assay that had been used that was flawed. This discovery was striking enough that SENS Research Foundation provided Ichor with funding and a material and technology transfer agreement to reassess the technology, and over $700,000 in directed program investments and grants have been received in the last year or two.

You recently completed a round of funding for the AMD work; what is the plan for the next year or so?

The new funds will allow us to develop a portfolio of enzyme therapy candidates to treat AMD. We will obtain critical data necessary to secure follow-on investment including in vitro studies (cell culture studies to confirm mechanism of action and cytotoxicity) and pivotal proof-of-concept in vivo studies, such as toxicity, PK/PD (how long the enzyme stays in the body and where), and efficacy. We will also be restructuring the company (reincorporating an IP holding company in Delaware, ensuring all contracts are up to date and audited) and ensuring our IP position is on solid footing (licensing in several related patents from existing collaborators, and filing several provisional patents from our intramural work). Collectively, we believe these efforts will position us to obtain series A for investigational new drug (IND) enabling pre-clinical studies.

You’ve been involved in the rejuvenation research community for quite some time now. What is your take on the bigger picture of SENS and the goal of ending aging?

This is a loaded question. What I can say is that the medical establishment has made great progress in the treatment of infectious disease through the development of antibiotics, vaccines, and hygiene programs. However, similar progress has not been realized for the diseases of old age, despite exorbitant expenditures. I have chosen to work in this space because I think a different approach is necessary, and it is here that I believe my companies and I can be the most impactful. I think SENS provides a good framework within which to ask and answer questions.

What do you see as the best approach to getting nascent SENS technologies like this one out of the laboratory and into the clinic?

We need more people who fully understand, in a highly detailed way, what a real translational path looks like. To take on projects like this, being a good scientist is not enough. We need people who can speak business, science, medicine, and legal, and apply these diverse disciplines to a well articulated, focused product or problem. There is no shortage of people who partially understand some of these, but the details are not somewhat important – they are all that matter for success in this space.

Another area is for investors. Some of the projects that come across my desk for review are truly abysmal, yet I have seen projects that are clearly elaborate hoaxes or outright scams (to anyone who has stepped foot in a laboratory) get funded to the tune of hundreds of thousands of dollars or more. While it is perfectly reasonable for high net worth individuals to gamble on moon shots in the anti-aging space (and I am ever grateful for the investors who have taken such a gamble on us) even aggressive development strategies should have some basis in reality. This is especially true as more and more high tech and internet investors move into the space.

If this works stupendously well, what comes next for Ichor Therapeutics?

I really want to get back into stem-cell research, but I basically need a blank check and a strong knowledge of the regulatory path to clinic before I feel comfortable moving into the space. A successful AMD exit would accomplish both of these goals, and position us to pivot to cell-based therapies.

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries.
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Aubrey de Grey at the Launching Longevity Panel, and Announcing Acceptance of the First Paper to be Published on MitoSENS Research – Article by Reason

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The New Renaissance HatReason
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Today I’ll direct your attention to a couple of videos, thematically linked by the presence of Aubrey de Grey, cofounder of the SENS Research Foundation and tireless advocate for progress towards working rejuvenation therapies. For the first of the videos, de Grey recently took part in a panel discussion involving representatives of the biotechnology industry, the research establishment, and venture capital community, with the topic being the coming development of a new industry that will develop therapies to extend healthy life and turn back aging. That industry has barely started to form its earliest and smallest stage today, as the first lines of rejuvenation research reach the point of commercial viability. There are a few startups and a lot of deep pockets yet to be convinced that this is going somewhere – though the commentary in the panel is encouraged, considering those involved.

The recent Rejuvenation Biotechnology 2016 conference hosted by the SENS Research Foundation was more along the same lines, focused on creating a foundation for the near future industry that will build and provide rejuvenation therapies. The purpose of the conference series is to help smooth the way for these treatments to move rapidly from the laboratory to the clinic, to build the necessary relationships, manage expectations, and pull in the additional support needed to make best possible progress. The conference was livestreamed over the past couple of days, and at one point Aubrey de Grey announced the just-then-and-there acceptance of the first scientific publication for the MitoSENS team at the SENS Research Foundation. They are presently in the lead, at the cutting edge, among the few groups working on the project of copying mitochondrial genes into the cell nucleus to protect them from the damage of aging. Ultimately, copying all thirteen genes should completely remove the contribution of mitochondrial damage to degenerative aging, as mitochondria will no longer become dysfunctional as their local DNA is damaged. They will get the proteins they need from the cell nucleus instead. It is a worthy project, and it is always welcome to see progress on this front.

Launching Longevity: Funding the Fountain of Youth

 

Can technology make human longevity a reality? As the pace of discovery accelerates, scientists and entrepreneurs are closing in on the Fountain of Youth. Disrupting the aging process by hacking the code of life, promises better health and longer maximum lifespans. With many layers of complexity from science to ethics, there are still skeptics placing odds against human longevity. Venture capitalists are betting on success; putting big money on the table to fund longevity startups. Google/Alphabet and drugmaker AbbVie have invested $1.5 billion on Calico, while Human Longevity Inc. recently raised $220 million from their Series B funding round. Complementing traditional venture investment, VCs like Peter Thiel and Joon Yun have established foundations and prizes to accelerate the end of aging. Why are VCs suddenly investing heavily in longevity startups? Will extended lifespan be a privilege of the wealthy or will the benefits be accessible to all? How long before these well-funded startups bring viable products to market?

 

Aubrey de Grey Announces Progress in MitoSENS

 

Ok everybody, before I introduce the next session I just wanted to make a very small, brief, but very welcome announcement. Literally half an hour ago we received some extremely good scientific news. Those of you who have been following SENS research since before the SENS Research Foundation itself even existed will know that, about a decade ago, the very first project, the very first research program that we were able to initiate – with the help of, especially, the initial donation of Peter Thiel – was to make mitochondrial mutations harmless by essentially putting backup copies of the mitochondrial DNA into the nuclear genome, modified in such way of course that the encoded proteins would be colocated back into the mitochondria to do their job. This is an idea that was first put forward more than 30 years ago, but it is an idea that despite quite a bit of initial effort, nobody was able to make work. When I first came across this concept, in fact I’d thought of it myself, it’s a pretty obvious idea really, I came to the conclusion that a lot of the despair and despondency and pessimism about this approach was premature, and that it was worth having another go, and so that was the very first project we decided to fund.

Suffice to say that it has not been quite as easy as I was hoping to make progress in that space, but progress has now been made, step by step, over the past several years, with the help especially of the absolutely amazing team we have at the research center, who work on this, headed by Matthew O’Connor. Amutha Boominathan is the number two on the team, and is absolutely indispensable, I’ve no idea where we’d be without her. So, what’s happened half an hour ago is that for the very first time in the entire history of this project, we have got far enough to have a paper accepted in a very nice journal, Nucleic Acids Research, which reports on our progress in this area. The headline result in this paper is that we are the first team ever to get two of the proteins encoded by genes in the mitochondrial DNA simultaneously functioning in the same cell line, and of course – two is equivalent to infinity for mathematicians, you know that, right? – this is extremely heartening news, and I just wanted to let you all know, thank you.

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries.
This work is reproduced here in accord with a Creative Commons Attribution license. It was originally published on FightAging.org.

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A Most Interesting Data Set Covering the Longevity of Polish Elite Athletes Across Much of the 20th Century – Article by Reason

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The New Renaissance HatReason
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Today I noticed an open access paper in which the authors examine mortality data for Polish Olympic athletes over the past 90 years or so, and compare it with established historical data for the general population. This blends two topics that are occasionally covered here at Fight Aging!: firstly, the growth in human life expectancy in recent history and its causes, and secondly the topic of how regular exercise and life expectancy interact. It is the present consensus that elite athletes, those at the top of their profession, live longer than the rest of us, but it remains open to debate as to whether this is because more exercise is better, or because very robust people who would have lived longer anyway are more likely to enter the world of professional athletics. Researchers want to map the dose-response curve for exercise, in other words. Even though there is very good, very solid evidence for the benefits of regular moderate exercise versus being sedentary, going beyond that to a more nuanced view of what more or less exercise does for health is a challenging goal given the starting point of statistical snapshots of data from various study populations.

Studying the history of life expectancy isn’t much easier, though there the challenges tend to revolve around the ever-decreasing quality of data as you look further back in time. The 20th century marked transitions from hopeful aspiration to solid accomplishment in all fields of medicine, too many profound advances in the capabilities of medical science and practice to list here. As the decades passed, this important progress focused ever more on treatments for age-related conditions. An individual born in the US in 1900 suffered through the end of the era of poor control of infectious disease, prior to modern antibiotics and antiviral drugs, and likely benefited little from later progress towards better control of heart disease and other common age-related diseases. An individual born in the US in 1950, on the other hand, enjoyed a youth with comparatively little fear of disease, and is probably still alive today, with access to far more capable therapies than existed even a couple of decades ago.

Given all of this, one of the interesting things to note in the analysis of the Polish data is that the elite athletes born in the early 20th century appear to have a lower rate of aging than the general population, as determined by a slower rise in mortality over time, but that this difference between athletes and the average individual is greatly diminished for people born in the latter half of the 20th century. This suggests, roughly, that advances in medicine from 1900 to 1950 had a leveling effect, bringing up the average, preventing early deaths, but doing little to address age-related disease. That said, there is a large variation in results across the range of similar studies, both those that look at the history of longevity, and those that look at populations of athletes at a given time. It is wise to consider epidemiological studies in groups rather than one by one, and look for common themes. Still, this one is a fascinating data set for the way in which it combines historical trends and exercise in the study of aging.

Examining mortality risk and rate of ageing among Polish Olympic athletes: a survival follow-up from 1924 to 2012 – by Yuhui Lin, Antoni Gajewski, and Anna Poznańska

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A sedentary lifestyle is associated with the onset of chronic diseases including ischaemic heart disease, type-II diabetes and neurodegenerative diseases. Frequent exercise is perceived as a major behavioural determinant for improved life expectancy and a slower rate of ageing. There is little doubt that frequent exercise is beneficial for individuals’ well-being, and an active lifestyle reduces the risk for chronic diseases. However, it is still uncertain whether the rate of ageing decelerates in response to frequent and intense physical exercise. Our attempt is the first empirical study to show the application of a parametric frailty survival model to gain insights into the rate of ageing and mortality risk for Olympic athletes.

Our participants for this parametric frailty survival analysis were Polish athletes who had participated in the Olympic Games from 1924 to 2010. We assumed that these athletes were elite in their preferred sports expertise, and that they were engaged in frequent, if not intense, physical exercise. The earliest recorded year of birth was 1875, and the latest was in 1982; total N=2305; male=1828, female=477. For reliable estimates, mortality improvements by calendar events and birth cohort had to be taken into consideration to account for the advancements made in medicine and technology. After the consideration of mortality improvements and the statistical power for parametric survival analysis, we restricted our analysis to male athletes born from 1890 to 1959 (M=1273). For reliable estimates, we preassigned recruited athletes into two categorical cohorts: 1890-1919 (Cohort I); 1920-1959 (Cohort II).

Our findings suggest that Polish elite athletes in Cohort I born from 1890-1919 experienced a slower rate of ageing, and had a lower risk for mortality and a longer life-expectancy than the general population from the same birth cohort. It is very unlikely that these survival benefits were gained within a short observational time. Therefore, we argue that participation in frequent sports from young adulthood reduces mortality risk, increases life-expectancy and slows the rate of ageing. The age-specific mortality trajectories of Cohort I elite athletes also suggest frequent exercise can decelerate the rate of ageing by 1% with an achievement of threefold risk reduction in mortality. In comparison with those of the general population, the differences in energy expenditure, behavioural habits, body mass and sports expertise were likely to be the contributing factors to the higher variance in lifespan among elite athletes.

In Cohort II, the estimated rate of ageing is highly similar between elite athletes and the general population, which contradicts our estimates for Cohort I. This may be attributed to mortality improvements from year 1920 onwards in Poland. These mortality improvements have changed individuals’ susceptibilities for different causes of death, which has resulted in an increased variation in lifespan both in the general population and for elite athletes. Interestingly, the comparison of the rate of ageing of elite athletes in Cohort I and II shows a similar rate of ageing. Among the elite athletes, the estimates suggest that Cohort II individuals benefited from a 50% mortality risk reduction as compared with individuals born in Cohort I. The estimated overall mortality risk of the Polish general population is 29% lower in Cohort II than in I.

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries.
This work is reproduced here in accord with a Creative Commons Attribution license. It was originally published on FightAging.org.

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25% Median Life Extension in Mice via Senescent Cell Clearance, Unity Biotechnology Founded to Develop Therapies – Article by Reason

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The New Renaissance HatReason
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With today’s news, it certainly seems that senescent cell clearance has come of age as an approach to treating aging and age-related conditions. Some of the leading folk in the cellular senescence research community today published the results from a very encouraging life span study, extending life in mice via a method of removing senescent cells. This is much the same approach employed in one of the first tests of senescent cell clearance, carried out in accelerated aging mice a few years ago, but in this case normal mice were used, leaving no room to doubt the relevance of the results. The researchers have founded a new company, Unity Biotechnology, to develop therapies for the clinic based on this technology. Clearance of senescent cells has been advocated as a part of the SENS vision for the medical control of aging for more than a decade now, and it is very encouraging to see the research and development community at last coming round to this view and making tangible progress.

Senescent cells have removed themselves from the cycle of replication in reaction to cell and tissue damage, or a local tissue environment that seems likely to result in cancer. Their numbers accumulate with age. Most are destroyed by the immune system or their own programmed cell death mechanisms, but enough linger for the long term for their growing presence to be one of the contributing causes of the aging process. These cells behave badly, secreting harmful signals that degrade tissue function, generate inflammation, and alter the behavior of surrounding cells as well. Near every common age-related condition is accelerated and made worse by the presence of large numbers of senescent cells. We would be better off without them, aging would be slowed by the regular removal of these errant cells, and the therapies to make that possible are on the near horizon.

The mouse lifespan study is the important news here, as it demonstrates meaningful extension of median life span through removal of senescent cells, the first such study carried out in normal mice for this SENS-style rejuvenation technology. This sort of very direct and easily understood result has a way of waking up far more of the public than the other very convincing evidence of past years. So it looks like Oisin Biotechnology, seed funded last year by the Methuselah Foundation and SENS Research Foundation to bring a senescent cell clearance therapy to market, now has earnest competition. Insofar as the competitive urge in business and biotechnology speeds progress and produces better results, let the games begin, I say.

Scientists Can Now Radically Expand the Lifespan of Mice – and Humans May Be Next

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Researchers have made this decade’s biggest breakthrough in understanding the complex world of physical aging. The researchers found that systematically removing a category of living, stagnant cells (ones which can no longer reproduce) extends the lives of otherwise normal mice by 25 percent. Better yet, scouring these cells actually pushed back the process of aging, slowing the onset of various age-related illnesses like cataracts, heart and kidney deterioration, and even tumor formation. “It’s not just that we’re making these mice live longer; they’re actually stay healthier longer too. That’s important, because if you were going to equate this to people, well, you don’t want to just extend the years of life that people are miserable or hospitalized.” By rewriting a tiny portion of the mouse genetic code, the team developed a genetic line of mice with cells that could, under the right circumstances, produce a powerful protein called caspase when they start secreting p16. Caspase acts essentially as a self-destruct button; when it’s manufactured in a cell, that cell rapidly dies. So what exactly are these circumstances where the p16 secreting cells start to create caspase and self-destruct? Well, only in the presence of a specific medicine the scientists could give the mice. With their highly-specific genetic tweak, the scientists had created a drug-initiated killswitch for senescent cells. In today’s paper, the team reported what happened when the researchers turned on that killswitch in middle-aged mice, effectively scrubbing clean the mice of senescent cells.

Naturally occurring p16Ink4a-positive cells shorten healthy lifespan

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Senescent cells accumulate in various tissues and organs over time, and have been speculated to have a role in ageing. To explore the physiological relevance and consequences of naturally occurring senescent cells, here we use a previously established transgene, INK-ATTAC, to induce apoptosis in p16Ink4a-expressing cells of wild-type mice by injection of AP20187 twice a week starting at one year of age. We show that AP20187 treatment extended median lifespan in both male and female mice of two distinct genetic backgrounds. The clearance of p16Ink4a-positive cells delayed tumorigenesis and attenuated age-related deterioration of several organs without apparent side effects, including kidney, heart and fat, where clearance preserved the functionality of glomeruli, cardio-protective KATP channels and adipocytes, respectively. Thus, p16Ink4a-positive cells that accumulate during adulthood negatively influence lifespan and promote age-dependent changes in several organs, and their therapeutic removal may be an attractive approach to extend healthy lifespan.

Unity Biotechnology Launches with a Focus on Preventing and Reversing Diseases of Aging

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Unity will initially focus on cellular senescence, a biological mechanism theorized to be a key driver of many age-related diseases, including osteoarthritis, glaucoma and atherosclerosis. “Imagine drugs that could prevent, maybe even cure, arthritis or heart disease or loss of eyesight. It’s an incredible aspiration. If we can translate this biology into medicines, our children might grow up in significantly better health as they age. There will be many obstacles to overcome, but our team is committed and inspired to achieve our mission. This has been a long journey, and we’re at the point now where we can start making medicines to achieve in humans what we’ve achieved in mice. I can’t wait to see what happens as we move into the clinic.”

To close this post, and once again, I think it well worth remembering that SENS rejuvenation biotechnology advocates and supporters have been calling for exactly this approach to treating aging for more than a decade. That call was made based on the evidence arising from many fields of medical research, and from a considered perspective of aging as a process of damage accumulation, one that can be most effectively treated by repair of that damage. The presence of senescent cells is a form of damage. SENS was not so long ago derided and considered out on the fringe for putting forward that position, but for several years now it has been very clear that the SENS viewpoint was right all along. I strongly encourage anyone who remains on the fence about the validity of the SENS proposals for the treatment of aging to reexamine his or her position on the science.

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries.
This work is reproduced here in accord with a Creative Commons Attribution license. It was originally published on FightAging.org.

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Zero-Gravity Orbital Habitation Causes Changes That Are at Least Superficially Similar to Accelerated Aging – Article by Reason

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The New Renaissance HatReason
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That old people will go into orbit to escape the rigors of gravity and thus live longer in their declining years was a staple of golden age and later science fiction. These works were written at a time in which our knowledge of human biochemistry – and the application of that knowledge to medicine – was crude in comparison to today. It is fascinating that we can say that for such a short span of years, a mere short lifetime past, but the differences between the medicine of the 1950s and the medicine of today are profound indeed. The writers of that time largely envisaged a future incorporating great gains in energy generation, and a consequent diaspora from Earth, while computation, medicine and the human condition remained much unchanged; older spacemen in the outer reaches struggling with heart disease in their fifties. Instead we found that expanding the generation, storage, transmission, and application of energy is very hard, and the largely unanticipated information revolution occurred instead. We lost the near future of cheap heavy lift to orbit and the solar system at our beck and call, but gained Moore’s Law, biotechnology, nanotechnology, a pervasive internet, and medical progress that is in the early stages of conquering heart disease and may yet save us from all of degenerative aging.

As it turns out, retreating from the rigors of gravity may well have the opposite effect to that imagined by the authors of the last century. Among the alterations produced by orbital habitation in zero gravity are those that appear, at least superficially, much like accelerated aging of the cardiovascular system. The root causes have yet to be pinned down, since very few people are actually researching this topic, but since the onset of these symptoms is fairly rapid, I’d guess at the cause being more a matter of regulatory dysfunction than increased tissue damage, such as the presence of cross-links related to arterial stiffening in aging. Here I’ll point out a few links to the work of one research group on this topic in recent years:

Waterloo to lead new experiment aboard International Space Station

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The experiment will link changes in astronauts’ hearts and blood vessels with specific molecules in the blood to determine why astronauts experience conditions that mimic aging-related problems and chronic diseases on earth. The findings will help identify important indicators for chronic disease and assist with the development of early interventions for people on earth. “We know that astronauts return from space with stiffer arteries and resistance to insulin, conditions affecting many adults as they age. For the first time, we will be able to track exactly how – and why – the body’s blood vessels change, and use these findings to potentially improve quality of life and the burden of chronic disease.” “In space, astronauts’ bodies show aging-like changes much faster than on Earth. The International Space Station provides a unique platform to study aging-related conditions providing insights that can be used to help understand some of the biggest health issues affecting society. Our research to date suggests that even though astronauts exercise every day, the actual physical demands of tasks of daily living are greatly reduced due to the lack of gravity. This lifestyle seems to cause changes in the vascular system and in the body’s ability to regulate blood glucose that would normally take years to develop on earth.”

U.Waterloo – Vascular Aging and Space Research Program

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We study factors related to cardiovascular health with aging. One focus is on blood pressure regulation and its impact on brain blood flow to help us understand some of the factors that could contribute to falls in the elderly, especially those that occur on rising from bed. Another focus is on aging blood vessels. We have reported a strong link between peripheral arterial stiffness and a reduction in brain blood flow. Our space research program is very active. We recently completed the study Cardiovascular and Cerebrovascular Control on Return from the International Space Station (CCISS). We are currently collecting data for the project Cardiovascular Health Consequences of Long-Duration Space Flight (Vascular).

Cardiovascular Health Consequences of Long-Duration Space Flight (Vascular)

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Cardiovascular Health Consequences of Long-Duration Space Flight (Vascular) investigates the impact of long-duration space flight on the blood vessels of astronauts. Space flight accelerates the aging process, and it is important to understand this process to develop specific countermeasures. Data is collected before, during, and after space flight to assess inflammation of the artery walls, changes in blood vessel properties, and cardiovascular fitness. Spaceflight can cause stiffening of the arteries, affecting the body’s ability to control blood pressure. This investigation assessed the blood vessels of astronauts and found decreased flexibility of the carotid artery during flight. Researchers found no relationship between the level of physical fitness and this decrease. The experiment also provided data on the mechanisms behind increased arterial stiffness from spaceflight. Further research is needed to establish effective ways to counter the cardiovascular consequences of spaceflight and ultimately help treat increased arterial stiffness from aging on Earth, which can cause high blood pressure and organ damage.

Impaired cerebrovascular autoregulation and reduced CO2 reactivity after long duration spaceflight

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Long duration habitation on the International Space Station (ISS) is associated with chronic elevations in arterial blood pressure in the brain compared with normal upright posture on Earth and elevated inspired carbon dioxide. Although results from short-duration spaceflights suggested possibly improved cerebrovascular autoregulation, animal models provided evidence of structural and functional changes in cerebral vessels that might negatively impact autoregulation with longer periods in microgravity. Seven astronauts (1 woman) spent 147 ± 49 days on ISS. Preflight testing (30-60 days before launch) was compared with postflight testing on landing day or the morning 1 or 2 days after return to Earth. The results indicate that long duration missions on the ISS impaired dynamic cerebrovascular autoregulation and reduced cerebrovascular carbon dioxide reactivity.

Recent findings in cardiovascular physiology with space travel

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The cardiovascular system undergoes major changes in stress with space flight primarily related to the elimination of the head-to-foot gravitational force. A major observation has been that the central venous pressure is not elevated early in space flight yet stroke volume is increased at least early in flight. Recent observations demonstrate that heart rate remains lower during the normal daily activities of space flight compared to Earth-based conditions. Structural and functional adaptations occur in the vascular system that could result in impaired response with demands of physical exertion and return to Earth. Cardiac muscle mass is reduced after flight and contractile function may be altered. Regular and specific countermeasures are essential to maintain cardiovascular health during long-duration space flight.

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries.
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Jason Hope on Philanthropy – Article by Reason

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The New Renaissance Hat
Reason
November 30, 2015
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Jason Hope, you might recall, has provided half a million dollars in research funding to the SENS Research Foundation, used to establish a SENS laboratory at Cambridge in order to push forward with the Foundation’s AGE-breaker program. AGE-breakers are drugs or other treatments capable of breaking down advanced glycation end-products (AGEs). These are a class of metabolic waste product that accumulate in our tissues to cause significant harm that includes the progressive loss of elasticity in skin and blood vessels.

There is, on the whole, far too little work undertaken today on AGE-breaker treatments in comparison to the benefits that a treatment could bring. What little research has taken place over the past twenty years unfortunately produced no effective therapies. As it turned out the AGEs that are important in short-lived laboratory animals are not the same at all as those that are important in humans – something that would have been challenging to identify until comparatively recently, and which resulted in promising animal studies that then went nowhere in commercial trials.

Now, however, researchers know that the vast majority of all AGEs in human tissues consist of just one type, called glucosepane – so the way is open for bold philanthropists and forward-looking researchers to build therapies that will be effective in removing this contribution to degenerative aging. Glucospane removal is one of the areas in which the SENS Research Foundation and its backers pick up the slack, undertaking important rejuvenation research that is neglected by the mainstream, even though it was exactly the mainstream research community that produced all of the studies and evidence that demonstrate the important role of glucospane in aging.

In any case, I should point out that Jason Hope runs a website and blog in which he discusses his take on philanthropy and his support for research aimed at extending healthy human life and rejuvenating the old. This makes for an interesting follow-on from yesterday’s post on big philanthropy. More folk of this ilk would certainly be a good thing, and I’m always pleased to see more of the better connected people in this world of ours speaking openly of their support for rejuvenation biotechnology.

Philanthropy

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Philanthropy has become a big focus for me. The organizations I have chosen to stand behind have come from many facets of my life. One of my passions has become the research done at the SENS Research Foundation. Their involvement in anti aging is not just about wanting to live forever. It’s about creating a longer, better quality of life.

Foundations like SENS are taking a different approach to anti-aging. They are focused on finding cures for disease that break down the body and thus cause us to age faster than we should. Disease like Alzheimer’s and heart and lung disease affect all functions of the body. Traditional medicine looks at treating these diseases after they happen. We want to focus on stopping these diseases from ever happening. We have spent so much time focused on medication for treating disease and not enough time on preventing that disease from ever happening.

By supporting scientific research that thrives through innovation and is not afraid to challenge the modern school of thought we will continue to break down walls.

A 21st-Century Philanthropic Model For Philanthropy

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Can you conceive of a world without age-related disease, disability and suffering? What about a world in which it’s possible for the average person to live 120 healthy years? While it may sound like a utopian dream, such a world is the exact goal of some of society’s most brilliant scientists and visionary leaders. At this very minute, groundbreaking work is underway at universities across the globe as researchers attempt to apply regenerative medicine to age-related disease through the repair of damage to tissue, cells and molecules within the body. While this research couldn’t be possible without the leadership of the world’s wealthiest philanthropists, it also relies upon the collective power of everyday people who have joined forces in their commitment to a better quality of life for all.

Traditionally, big ticket donors have been the primary target for fundraising programs. Research has consistently shown that the bulk of donor funds come from a small percentage of the wealthiest donors: in fact, a full 75 percent of funds raised come from gifts of over $1 million.

Instead of resigning themselves solely to the influence of the individual, non-profits are turning to the collective power of a group. The MFoundation’s “The 300 Pledge” fundraising campaign is an exciting example of this method in practice. The 300 Pledge asks 300 funders to commit $1,000 a year for 25 years toward critical research aimed at ending age-related diseases. When broken down, this goal is manageable for many households: just $3 a day or $85 a month – less than your daily tab at Starbucks. Obviously, the model is working: to date, 291 people have taken up the challenge, with nine spots remaining.

As evidenced by the magnificent philanthropy of people like Peter Thiel, Bill Gates and others like them, it’s obvious that one person can make a difference. However, fundraising challenges, like MFoundation’s “The 300,” also demonstrate the power of a dedicated group of people to foster real world change for the billions of people living in the world today as well as the generations that follow. In doing so, those who take up the challenge create a unique and world-altering legacy for themselves.

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries. 
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SENS Research Foundation Joins the Global #GivingTuesday Movement – Press Release by SENS Research Foundation

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The New Renaissance Hat
SENS Research Foundation
November 28, 2015
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Every Dollar Contributed Up to the First $5,000 Will Be Quadrupled, Turning into $20,000.
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MOUNTAIN VIEW, Calif. — November 24, 2015 — The SENS Research Foundation (SRF), a non-profit organization focused on transforming the way the world researches and treats age-related disease, has joined #GivingTuesday, a global day of giving that harnesses the collective power of individuals, communities and organizations to encourage philanthropy and celebrate generosity worldwide. Every dollar donated to SRF up to the first $5,000 will be quadrupled, making every dollar raised turn into $20,000.

Occurring this year on December 1, #GivingTuesday is held annually on the Tuesday after Thanksgiving (in the U.S.) and the widely recognized shopping events Black Friday and Cyber Monday to kick-off the holiday giving season and inspire people to collaborate in improving their local communities and to give back in impactful ways to the charities and causes they support.

SENS Research Foundation is aiming to reach a goal of $20,000 with the help of contributors who have pledged to match each dollar raised up to the first $5,000. The Croeni Foundation, a philanthropic organization dedicated to giving, the environment and health, has pledged to match the first $5,000 raised dollar for dollar. The foundation gave SRF an unrestricted $5,000 earlier this year, as well. Aubrey de Grey, CSO of SENS Research Foundation, has offered a dollar for dollar matching challenge up to $5,000. And Fight Aging! will match every dollar up to $125,000 through December 31, 2015. Fight Aging! encourages the development of medical technologies, lifestyles, and other means to help people live comfortably, healthily, and capably for as long as they desire.

“We are looking forward to participating in #GivingTuesday for a second year, and offer our thanks to Jan Croeni and the Croeni Foundation, as well as Aubrey de Grey and Fight Aging! for their support,” said Jerri Barrett, vice president of outreach, SENS Research Foundation. “Today’s cost for the treatment and care of chronic diseases of aging costs around $40,000 per second and will only continue to go up, as we spend more money per patient, while the number of patients is increasing. As a society, we need to change our ways and start treating age-related diseases more intelligently. The funds we raise on #GivingTuesday will help facilitate our efforts to do just that, as we work to continue learning how to prevent or reverse age-related diseases.”

Those who are interested in joining SENS Research Foundation’s #GivingTuesday initiative can donate at www.sens.org/donate. To learn more about #GivingTuesday participants and activities or to join the celebration of giving, please visit: http://www.givingtuesday.org/

About SENS Research Foundation (SRF)

SENS Research Foundation is a 501(c)(3) nonprofit that works to research, develop, and promote comprehensive regenerative medicine solutions for the diseases of aging. SRF is focused on a damage repair paradigm for treating the diseases of aging, which it advances through scientific research, advocacy, and education. SENS Research Foundation supports research projects at universities and institutes around the world with the goal of curing such age-related diseases as heart disease, cancer, diabetes and Alzheimer’s disease. Educating the public and training researchers to support a growing regenerative medicine field are also major endeavors of the organization that are being accomplished though advocacy campaigns and educational programs. For more information, visit www.sens.org.

Media Contact:
Jerri Barrett
408-204-7229
jerri.barrett@sens.org

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