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MOUNTAIN VIEW, CA--(Marketwired - May 15, 2017) - SENS Research Foundation (SRF) has launched a new research program focused on somatic gene therapy in collaboration with the Buck Institute for Research on Aging. Brian Kennedy, PhD, a leading expert on the biology of aging, will be running the project in his lab at the Buck. Many potential treatments of age-related diseases require the addition of new genes to the genome of cells in the body, a technology known as somatic gene therapy. The technology has been hampered, up until now, by the inability to control where the gene is inserted. That lack of control resulted in a significant risk of insertion in a location that encourages the cell to become malignant. SRF has devised a new method for inserting genes into a pre-defined location. In this program, this will be done as a two-step process, in which first CRISPR is used to create a "landing pad" for the gene, and then the gene is inserted using an enzyme that only recognizes the landing pad. SRF has created "maximally modifiable mice" that already have the landing pad, and this project will evaluate how well the insertion step works in different tissues. "Somatic gene therapy has been a goal of medicine for decades. Being able to add new healthy genes will enable us to address treatments of such age-related diseases as atherosclerosis and macular degeneration. Our collaboration with SRF will substantially move us toward finding effective treatments to genetically based age-related diseases," said Dr. Kennedy. "Partnering with Brian Kennedy and the Buck enables SRF to continue towards our goal of achieving human clinical trials on rejuvenation biotechnologies in the next five years. Brian's leadership in moving this technology into mammals is a huge step forward," said Dr. Aubrey de Grey, CSO, SENS Research Foundation. This research has been made possible through the generous support of the Forever Healthy Foundation and its founder Michael Greve, as well as the support of our other donors. The Forever Healthy Foundation is a private nonprofit initiative whose mission is to enable people to vastly extend their healthy lifespans and be part of the first generation to cure aging. In order to accelerate the development of therapies to bring aging under full medical control, the Forever Healthy Foundation directly supports cutting-edge research aimed at the molecular and cellular repair of damage caused by the aging process. 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 macular degeneration, heart disease, cancer, 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. About Buck Institute for Research on Aging Buck Institute is the U.S.'s first independent research organization devoted to Geroscience -- focused on the connection between normal aging and chronic disease. Based in Novato, California, the Buck is dedicated to extending "healthspan," the healthy years of human life, and does so by utilizing a unique interdisciplinary approach involving laboratories studying the mechanisms of aging and others focused on specific diseases. Buck scientists strive to discover new ways of detecting, preventing and treating age-related diseases such as Alzheimer's and Parkinson's, cancer, cardiovascular disease, macular degeneration, osteoporosis, diabetes and stroke. In their collaborative research, they are supported by the most recent developments in genomics, proteomics, bioinformatics and stem cell technologies. For more information: www.thebuck.org.


News Article | December 15, 2016
Site: www.technologyreview.com

Why does a mole rat live 30 years but a mouse only three? With $1.5 billion in the bank, Google’s anti-aging spinout Calico is rich enough to find out. At a laboratory outside San Francisco, money from the founders of Google maintains a large number of naked mole rats. The hairless rodents require exacting, expensive conditions to thrive: they live in coöperative colonies like ants, led by a queen rat. But what is truly extraordinary is that they can live about 30 years—10 times longer than a mouse. The rodents belong to Calico Labs, short for the California Life Company. In 2013, the cofounder of Google, Larry Page, announced that his company would form Calico and fund it lavishly to carry out a long-term project, trying to sort out the causes of aging and do something about them. The company’s mission: to build a Bell Labs of aging research. It hoped to extend the human life span by coming up with a breakthrough as important, and as useful to humanity, as the transistor has been. There are reasons to think aging can be slowed in fundamental ways. Among Calico’s first hires was Cynthia Kenyon, now its vice president of aging research, who 20 years ago showed that altering a single DNA letter in a laboratory roundworm made it live six weeks instead of three. There is something hair-raising about Kenyon’s videos of old, should-be-dead worms wriggling vigorously across a petri dish. So Google’s founders created an academic-­biotech hybrid they call an R&D company to follow up on such clues, providing nearly unlimited funding to a group of top researchers. Calico has hired stars like artificial-intelligence specialist Daphne Koller. With equal contributions from Google’s parent company, Alphabet, and the drug company AbbVie, it has $1.5 billion in the bank. But despite the hype around its launch—Time magazine asked, “Can Google Solve Death?”—Calico has remained a riddle, a super-­secretive company that three years in hasn’t published anything of note, rebuffs journalists, and asks visiting scientists to sign nondisclosure agreements. In fact, Calico has other researchers “a little miffed,” says Felipe Sierra, director of the division of aging biology at the National Institute on Aging. “We want to know what they are doing so we can focus on other things, or collaborate. They are a research company, so what are they researching?” MIT Technology Review has learned that Calico is, in effect, an elite university research group housed within a corporate bunker, doing mostly basic science. It has more than 100 employees and has assembled a Noah’s ark of yeast, worms, and more exotic creatures like the naked mole rats, which are kept at the Buck Institute for Research on Aging, about 30 miles from Calico’s South San Francisco headquarters. What’s different about a mole rat? That is the sort of costly, open-ended question Calico can afford to ask. And then there’s the seven-year study Calico is financing that will follow 1,000 mice from birth to death to search for biomarkers of aging. Right now, there’s no proven test for a person’s “biological” age; finding one would be scientifically useful and possibly lucrative. “They don’t open the kimono much,” says Brian ­Kennedy, a Buck Institute scientist who interacts with Calico. “I think they believe we need a broader grasp on the biology of aging. They recognize it can’t possibly be ­simple.” The Google founders aren’t the first billionaires to decide that aging is the “most fundamental unsolved problem in biology,” as Calico’s press releases put it. Larry Ellison, the cofounder of Oracle, gave away $335 million to scientists studying aging before redirecting his foundation’s grants toward eliminating polio in 2013. The investor Peter Thiel has also donated to the anti-aging cause, and there’s even a $500,000 Palo Alto Longevity Prize to anyone who can radically extend the life of a mammal. The difficulty is that scientists don’t know enough about why animals age. Calico’s Hal Barron, hired from Roche to lead its drug development efforts, told the National Academy of Medicine in 2015 that there would be no short-term payoff. “We believe you have to take a very long view,” he said, “and not rush into the clinic until you really know what you are doing.” A hundred and seventy five years ago most people died from infections, not from old age. Thanks to vaccines, better nutrition, and all-around improvements in public health and medicine, life expectancy at birth in wealthy nations has doubled from 40 to around 80 years, an average gain of 2.5 years per decade. But now that we live longer, we have traded up to a new set of killers that are harder to beat: cancer, heart disease, stroke, and dementia. For all these diseases, aging is the single biggest risk factor. An 80-year-old is 40 times as likely to die from cancer as someone middle-aged. The risk for Alzheimer’s rises by 600 times. But what if it were possible to postpone all these deaths by treating aging itself? “I think we have failed in our effort to attack chronic disease when we attack them one by one,” Sierra says. “And the reason is that they have one major risk factor, which is the biology of aging.” Overarching theory David Botstein is Calico’s chief scientific officer. He is 74, with a grizzled shadow of beard reaching up from his collar. In November, I found him at a lecture hall at MIT, where he offered a rare window onto experiments under way at Calico. Botstein, a well-known Princeton geneticist whom Calico recruited out of near retirement, was in town to celebrate the birthday of a successful former student, now a sexagenarian. “The pleasure is coming to see old friends,” he says. “The not-so-­pleasure is if these guys are 60, what am I?” In his lecture, Botstein described several technologies—four, in fact—that Calico has for isolating old yeast cells from the daughter cells that bud off them. (One project has the institutional-sounding name Mother Enrichment Program.) These old cells are tracked and subjected to a comprehensive analysis of which genes are turned up or turned down, a technique that is Botstein’s specialty. Botstein told me Calico is exactly what Google intended: a Bell Labs working on fundamental questions, with the best people, the best technology, and the most money. “Instead of ideas chasing the money, they have given us a very handsome sum of money and want us to do something about the fact that we know so little about aging,” says Botstein. “It’s a hard problem; it’s an unmet need; it is exactly what Larry Page thinks it is. It’s something to which no one is really in a position to pay enough attention, until maybe us.” Botstein says no one is going to live forever—that would be perpetuum mobile, or perpetual motion, which defies the laws of thermodynamics. But he says ­Kenyon’s experiments on worms are a “perfectly good” example of the life span’s malleability. So is the fact that rats fed near-starvation diets can live as much as 45 percent longer. The studies Botstein described in yeast cells concerned a fundamental trade-off that cells make. In good times, with lots of food, they grow fast. Under stresses like heat, starvation, or aging, they hunker down to survive, grow slowly, and often live longer than normal. “Shields down or shields up,” as ­Botstein puts it. Such trade-offs are handled through biochemical pathways that respond to nutrients; one is called TOR, and another involves insulin. These pathways have already been well explored by other scientists, but Calico is revisiting them using the newest technology. “A lot of our effort is in trying to verify or falsify some of the theories,” Botstein says, adding that he thinks much of the science on aging so far is best consumed “with a dose of sodium chloride.” Some molecules touted as youth elixirs that can act through such pathways—like resveratrol, a compound in red wine—never lived up to their early hype. According to Botstein, aging research is still seeking a truly big insight. Imagine, he says, doctors fighting infections without knowing what a virus is. Or think back to cancer research in the 1960s. There were plenty of theories then. But it was the discovery of oncogenes—specific genes able to turn cells cancerous—that provided scientists with their first real understanding of what causes tumors. “What we are looking for, I think above everything else, is to be able to contribute to a transformation like that,” he says. “We’d like to find ways for people to have a longer and healthier life. But by how much, and how—well, I don’t know.” Botstein says a “best case” scenario is that Calico will have something profound to offer the world in 10 years. That time line explains why the company declines media interviews. “There will be nothing to say for a very long time, except for some incremental scientific things. That is the problem.” To get there, Calico is ratcheting up its expertise and skills. Botstein says it has demonstrated it could decode a human genome from scratch, without peeking at the official genome map. That’s a difficult task requiring significant investment in computing and know-how. But Calico got the right answer, so it’s confident of accurately mapping the genome of the naked mole rat—a job he says is half done. And a precise understanding of how the mole rat’s genes are organized may hold clues to its long life. “A lot of what we do is technology development,” says Botstein. “It’s not interesting, and it’s not supposed to be interesting. It’s how you put one foot in front of the other so you don’t trip on yourself.” Big disappointment To some, Calico’s heavy bet on basic biology is a wrong turn. The company is “my biggest disappointment right now,” says Aubrey de Grey, an influential proponent of attempts to intervene in the aging process and chief science officer of the SENS Research Foundation, a charity an hour’s drive from Calico that promotes rejuvenation technology. It is being driven, he complains, “by the assumption that we still do not understand aging well enough to have a chance to develop therapies.” Indeed, some competitors are far more aggressive in pursuing interventions than Calico is. “They are very committed to these fundamental mechanisms, and bless them for doing that. But we are committed to putting drugs into the clinic and we might do it first,” says Nathaniel David, president and cofounder of Unity Biotechnology. This year, Jeff Bezos joined investors who put $127 million behind Unity, a startup in San Francisco that’s developing drugs to zap older, “senescent” cells that have stopped dividing. These cells are suspected of releasing cocktails of unhelpful old-age signals, and by killing them, Unity’s drugs could act to rejuvenate tissues. The company plans to start with a modestly ambitious test in arthritic knees. De Grey’s SENS Foundation, for its part, has funded Oisin Biotechnologies, a startup aiming to rid bodies of senescent cells using gene therapy. Other scientists say it is time to begin large human studies of “geroprotectors”—drugs that could decelerate aging altogether. One such effort is being spearheaded by gerontologists at Albert ­Einstein College of Medicine, in New York. The medication they hope to test, metformin, is used to treat diabetes. It cropped up as an anti-aging prospect after scientists reviewing medical records found that people taking it not only were much less likely to die than other diabetics but died at a 15 percent lower rate than all other patients. Metformin lowers blood sugar levels, one clue it may have something in common with a low-calorie diet. But getting a study off the ground hasn’t been easy. To convince the U.S. Food and Drug Administration to approve the trial, doctors decided to measure metformin’s effectiveness in preventing three separate diseases: heart attack, dementia, and cancer. “They do not recognize aging as a disease, so what we have done is choose diseases of aging with minimal overlap in their causes,” says Steven Austad, a biologist at the University of Alabama at Birmingham and scientific director of the American Federation for Aging Research, which has endorsed the metformin study. “If it simultaneously delays them, that would indicate a slowed rate of aging.” The trial is designed to involve 6,000 people and would last six years. It would be the first large study of a geroprotector in volunteers, according to S. Jay ­Olshansky, a public health researcher at the University of Illinois at Chicago. He therefore rates the trial as significant no matter whether it flops or, as he hopes, sets off “the most groundbreaking events in public health in this century.” The only problem is who will pay for the trial, expected to cost $65 million. The chance the NIH will pay for the entire study is “remote,” says Austad, and since metformin is an old drug not covered by patents, drug companies aren’t interested either. Instead, Olshansky and Austad are going with what’s become a favorite play in research on aging: they plan to hit up billionaires for the money. Funding a groundbreaking advance, Olshansky promises potential investors, could be their “ticket to immortality.” Playing the long game The science of aging is easy to disregard, given its long historical connection to alchemy, quacks, and vitamin pushers. Even now, many scientists do their utmost to avoid the phrase “anti-aging research”—sounding as it does like a promise made on a tin of skin cream. “There are a lot of charlatans in aging research. I should be careful in what I say, but it attracts pretty quirky people,” says Gary Churchill, a mouse geneticist at the Jackson Laboratory, in Bar Harbor, Maine. It can’t help, either, that the people who bankroll this science keep saying they hope to live forever. Bill Maris, the former head of Google Ventures who hatched the idea for Calico, has said he thinks it is possible people could live “for 500 years.” That’s pretty unlikely. In that sense, Calico’s creation of a strictly controlled research fortress staffed by recognized leaders makes sense as an inoculum against hokum, maybe even from the people paying the bills. “They are playing the long game,” Churchill says. “It’s a good strategy. It could leave them positioned a decade from now to have something.” Churchill’s work with Calico gives some idea of how long it could take. In April 2016, the company agreed to pay for a large experiment at Jackson Labs to search for a “biomarker” of aging—a molecule, which they hope to find in the blood, whose quantity or properties change with “biological” age, not just with the hands on the clock. Such a diagnostic could be extraordinarily useful, and profitable. But searching for such a marker is not cheap. At Jackson Labs, Churchill’s team plans to follow 1,000 mice, drawing blood and placing them inside special cages where food and water intake can be precisely measured and the rodents’ droppings and urine collected. Half the mice will be on a calorie-restricted diet to extend their lives—necessary to confirm whether a biomarker really tags them as biologically younger. The experiment will generate millions of readings—for levels of growth hormones and glucose, among other things. Churchill wouldn’t say how much Calico is paying, but simply feeding that many mice could cost $3 million. “We’ve mapped it out, planned it. It’s immense, and we’d never be able to do this with the NIH,” he says. “The willingness to invest in the long term is the most appealing thing about Calico.” Churchill says the ideal biomarker of aging would actually estimate how much longer you have left to live, barring any unforeseen events. And the readout would change if you took a drug or adopted a diet that somehow rescheduled your appointment with the Grim Reaper. With a test like that, companies could see whether their drugs actually influenced aging without waiting many, many years for the answer. Finding such a blood marker would be the kind of breakthrough that aging research so desperately needs—and that Calico was created to discover.


Wiley C.D.,Buck Institute for Research on Aging | Velarde M.C.,Buck Institute for Research on Aging | Lecot P.,Buck Institute for Research on Aging | Liu S.,Buck Institute for Research on Aging | And 11 more authors.
Cell Metabolism | Year: 2016

Cellular senescence permanently arrests cell proliferation, often accompanied by a multi-faceted senescence-associated secretory phenotype (SASP). Loss of mitochondrial function can drive age-related declines in the function of many post-mitotic tissues, but little is known about how mitochondrial dysfunction affects mitotic tissues. We show here that several manipulations that compromise mitochondrial function in proliferating human cells induce a senescence growth arrest with a modified SASP that lacks the IL-1-dependent inflammatory arm. Cells that underwent mitochondrial dysfunction-associated senescence (MiDAS) had lower NAD+/NADH ratios, which caused both the growth arrest and prevented the IL-1-associated SASP through AMPK-mediated p53 activation. Progeroid mice that rapidly accrue mtDNA mutations accumulated senescent cells with a MiDAS SASP in vivo, which suppressed adipogenesis and stimulated keratinocyte differentiation in cell culture. Our data identify a distinct senescence response and provide a mechanism by which mitochondrial dysfunction can drive aging phenotypes. © 2016 Elsevier Inc.


News Article | November 22, 2016
Site: www.eurekalert.org

A new study from UC Berkeley found that tissue health and repair dramatically decline in young mice when half of their blood is replaced with blood from old mice. The study argues against the rejuvenating properties of young blood and points to old blood, or molecules within, as driving the aging process. "Our study suggests that young blood by itself will not work as effective medicine," said Irina Conboy, associate professor in the Department of Bioengineering at UC Berkeley. "It's more accurate to say that there are inhibitors in old blood that we need to target to reverse aging." The study will be published Nov. 22 in the journal Nature Communications. The research was supported by funding from the National Institutes of Health, SENS Research Foundation, Rogers' Family and Calico. In 2005, Conboy and colleagues published a study in Nature that found evidence for tissue rejuvenation in older mice when they are surgically joined to younger mice so that blood is exchanged between the two. Despite remaining questions about the mechanism underlying this rejuvenation, media coverage of the study fixated on the potential of young blood to reverse the aging process, and on comparisons to vampires, which was not the takeaway from the study, Conboy said. In the years since the 2005 study, scientists have spent millions to investigate the potential medical properties of youthful blood with enterprises emerging to infuse old people with young blood. "What we showed in 2005 was evidence that aging is reversible and is not set in stone," Conboy said. "Under no circumstances were we saying that infusions of young blood into elderly is medicine." Blood exchange in humans is FDA-approved for a few devastating illnesses (auto-immunity, for example, where self-reacting antibodies are removed), but high volume or repeated additions of blood or its components to genetically different people is known to have side effects of immune rejection, leading to organ failure. While the experimental model used in the 2005 study found evidence that some aspects of aging may be reversed, the techniques used in the study do not allow scientists to precisely control the exchange of blood, which is necessary to dig deeper into blood's effect on aging. When two mice are sutured together, a technique called parabiosis, blood is not the only thing that is exchanged in this setup; organs are also shared, so old mice get access to younger lungs, thymus-immune system, heart, liver and kidneys. In surgical suturing it takes weeks to a month for the effects of blood to take place and the precise timing is not actually known. Nor is the precise amount of the exchanged blood. In the new study, Conboy and colleagues developed an experimental technique to exchange blood between mice without joining them so that scientists can control blood circulation and conduct precise measurements on how old mice respond to young blood, and vice versa. In the new system, mice are connected and disconnected at will, removing the influence of shared organs or of any adaptation to being joined. One of the more surprising discoveries of this study was the very quick onset of the effects of blood on the health and repair of multiple tissues, including muscle, liver and brain. The effects were seen around 24 hours after exchange. With the new experimental setup, the research team repeated the experiments from 2005. In each test, blood was exchanged between an old mouse and a young mouse until each mouse had half its blood from the other. The researchers then tested various indicators of aging in each mouse, such as liver cell growth as well as liver fibrosis and adiposity (fat), brain cell development in the region that is needed for learning and memory, muscle strength and muscle tissue repair. In many of these experiments, older mice that received younger blood saw either slight or no significant improvements compared to old mice with old blood. Young mice that received older blood, however, saw large declines in most of these tissues or organs. The most telling data was found when researchers tested blood's impact on new neuron production in the area of the brain where memory and learning are formed. In these experiments, older mice showed no significant improvement in brain neuron stem cells after receiving younger blood, but younger mice that received older blood saw a more than twofold drop in brain cell development compared to normal young mice. The researchers think that many benefits seen in old mice after receiving young blood might be due to the young blood diluting the concentration of inhibitors in the old blood. "Under no circumstances did young blood improve brain neurogenesis in our experiments," Conboy said. "Old blood appears to have inhibitors of brain cell health and growth, which we need to identify and remove if we want to improve memory." The research team has begun to investigate specific molecules in old blood that might cause inhibition of cell development, but future experiments are needed for a clear picture of why young animals are worse off with old blood.


News Article | April 11, 2016
Site: motherboard.vice.com

Easter celebrations. The swearing in of President Obama with a bible. The Pledge of Allegiance’s “One nation under God.” Ted Cruz’s freakish evangelism. Even when we sneeze, many Americans still reflexively say: God bless you. American society exists in an engulfing religious framework—and that inescapable Abrahamic point of view leads to one ultimate goal: an eternal afterlife with the maker. For the majority of Americans—about 70 percent—that is what they believe and how they live in this world. Whether you like it not, America is a culture mired in deathism—the idea that human death is natural, inescapable, and ultimately desirable because it unites one with God. Lately, though, the burgeoning transhumanism movement is challenging all that. Gerontologists, crynocists, singularitarians, biohackers, roboticists, geneticists, futurists, and anti-aging activists—all considered part of the transhumanist platform—are standing up and demanding humans conquer biological death. Once seen as fringe, but now increasingly seen as potentially visionary, transhumanists are challenging the very nature of what it means to be a human being. Motherboard recently featured a part of the transhumanism movement in an exciting and informative short documentary called Forever Young. The show focuses on the eclectic Church of Perpetual Life—a nonprofit transhumanist organization in south Florida aiming to combine spirituality, community, and hard science research. I recently spoke at the Church of Perpetual Life while on tour with my Immortality Bus. The church is a unique place, to say the least. Forever Young explores the transhumanist and spiritual beliefs of some of the church parishioners, including businessman Bill Faloon, who co-founded the church in 2013. Faloon and the parishioners—nearly all who doubt the existence of an afterlife—are people bent on using the latest anti-aging science to live indefinitely. In my mind, the 21-minute show is not really about the Church of Perpetual Life or even any of its members. It’s about the quest to achieve indefinite lifespans—and how one community within the much larger transhumanist movement is attempting that. Some of the best parts of the video are the appearances of famous transhumanists: Dr. Aubrey de Grey, Chief Scientist at SENS Research Foundation and Transhumanist Party anti-aging advisor; Martine Rothblatt, transgender entrepreneur and CEO of United Therapeutics; and Bernadeane Brown, co-founder at People Unlimited. The documentary also briefly features cryonics, mind uploading, robotics, and oncology. The appearances of the celebrity transhumanists and the technology people want to use to live indefinitely are my favorite parts of the show—and they also hint at how large and diversified the transhumanism movement has become. Near the end, the film focuses on Bill Faloon and examines complexities he’s had with the FDA and IRS regarding his life extension pursuits. With tough investigative journalism, the Forever Young host Claire Evans challengingly questions some of his methods. I feel compelled to rush to Faloon’s defense—and to all transhumanists whose methods are potentially unconventional. Viewers need to understand that transhumanists like myself and Faloon believe we are fighting for our lives. Similar to how the HIV-stricken community and its citizen scientists battled the AIDS epidemic in the 1980s when the US government and big pharma companies wouldn’t help—made famous by the documentary How to Survive a Plague—transhumanists are literally battling death right now. I speak for most transhumanists when I say we don’t have time to follow all the damn laws and regulations of the bloated government when 150,000 people a day are dying in the world—and many science experts in the world believe we will conquer death in this century. We are in a desperate race to find those life extension technologies and save hundreds of millions of lives. And if transhumanists appear to sometimes make decisions as if they were living in the Wild West—both in the documentary and in the real world—it’s because we are involved in the most important crusade humanity has ever faced. There’s no time to lose. We are in a war against death. The difference between humanity overcoming death in 2030 versus the year 2050 is the difference of saving 1 billion human lives. Chew on that for a moment. This is a race. If I weren’t an atheist and believed in afterlives like most people in America, I’d be a very different person. I wouldn’t need to be a transhumanist, because death would just be a transition into another living realm. But transhumanists don’t feel that way. Death means the loss of consciousness forever and the physical cellular breakdown of the body. It means never ever having another thought, and becoming dirt and food for bugs. Ask nearly any transhumanist what they most want out of life, and they will tell you they want to escape the expiration date of their existence. And they’ll also tell you that government regulations, the US military, and the FDA are simply part of an overarching culture that indirectly facilitates the death of human beings—especially since the US Congress, the President, and all Supreme Court members believe in an afterlife. If America is not a culture of monopolistic fundamental religiosity and fatalism, than I don’t know what is. Realizing you don’t want to die, and that you also don’t believe in an afterlife, usually takes a personal epiphany. Every transhumanist has a conversion moment—an instant when they make a Transhumanist Wager and decide dying is not acceptable. Mine happened when I almost stepped on a landmine in Vietnam while working for National Geographic. Afterward, I thought: What the hell? I almost died and had my body blown in half. Death is the stupidest and most tragic experience ever. Something must be done about it. Cofounder Bill Faloon in front of the Church of Perpetual Life in Hollywood, Florida. Photo: Motherboard Sadly, it’s almost impossible to tell people the follies of dying—even if they love life. Every single person must arrive at this understanding for themselves. It’s a very personal revelation, and not one that can be taught or forced. Becoming a transhumanist—becoming dedicated to overcoming death with science and technology—must be experienced personally in a heartfelt and deeply philosophical way. That said, an entire international science movement has now sprung up to help this process along of wanting to live indefinitely—to defy the culture of death we are all surrounded by. Cryogenic facilities are out there like Alcor and the Cryonics Institute. Nonprofits like SENS Research Foundation do amazing work. Singularity University educates young science and life extension entrepreneurs. Private companies like Insilico Medicine which uses big data to figure out how live longer now exist. And of course, communities like the Church of Perpetual Life have recently sprung up. Even what is being billed as the largest life extension gathering of its kind, the RAAD Festival, is happening this August in San Diego—with a hoped-for 2,000 participants. To wage war against death, transhumanists are starting new life extension enterprises more quickly than ever before. Some of these projects and organizations are brilliant and some are wacky—and some surely will fail and disappear. But the more partners and allies transhumanism has, the better. And greater chances of overall success will come from putting our hopes into visionaries like Bill Falloon and the many other controversial and colorful figures in the life extension movement. The alternative is putting our hope into someone like the Pope, who maintains that condoms are sinful—and the result is that millions of people in Africa will likely die from AIDS as a result because they contract HIV. Or in George W. Bush, who stopped life-saving stem cell research for seven years in America because of religious beliefs. Or in presidential candidate Ted Cruz, who makes decisions about science and medical policy based on a 3,000-year-old book that says Jesus needs to forgive us our sins so we can live with him forever in bliss. Pure insanity. (But very useful for the power hungry conservatives who use religion to control America’s moral, cultural, and philosophical outlook.) Sometimes I think we ought to have glass coffins for our loved ones who die, and keep them in viewing rooms, so we can watch them decompose—so we can see all that we loved about people close to us slowly disappear into nothingness. It would force us to realize something quintessential—that if we’re wrong about the afterlife, we forever lose this precious miracle called life. If America cares about the health of its people, it needs to join the war on conquering aging and death. Many gerontologists believe we could stop or reverse aging within 25 years if enough funding is put into it. With that in mind, America needs to recognize that in the twenty-first century, dying is a public safety issue—that people deserve a universal right to indefinite lifespans, as put forth in the Transhumanist Bill of Rights. And the government must take a leading role in establishing the science and forming the culture to offer people their maximum longevity—in the same way it offers vaccinations to avoid disease. Thankfully, hundreds of thousands of people around America are starting to get it. Google’s life extension company Calico was recently formed to battle aging. Facebook’s Mark Zuckerberg’s recently made positive statements about trying to cure disease and live much longer. Billionaire Peter Thiel generously supports life extension research. And Ray Kurzweil’s dedication to overcoming involuntary death is in the media all the time. It’s all proof that some of the best minds of the world are joining the battle to conquer death. When people look back in 50 years—and we all hopefully have the choice to live indefinitely because of modern technology—the world will understand that things that seem strange and fringe now, were done to fight a system of anti-science culture bent on dying. Thankfully, transhumanists saw it didn't have to be that way, and pushed back against those that believed the grave was our destiny. Zoltan Istvan is a futurist, author of The Transhumanist Wager, and US presidential candidate for the Transhumanist Party. He writes an occasional column for Motherboard in which he ruminates on the future beyond natural human ability.


Aflaki E.,U.S. National Institutes of Health | Stubblefield B.K.,U.S. National Institutes of Health | Maniwang E.,U.S. National Institutes of Health | Lopez G.,U.S. National Institutes of Health | And 10 more authors.
Science Translational Medicine | Year: 2014

Gaucher disease is caused by an inherited deficiency of glucocerebrosidase that manifests with storage of glycolipids in lysosomes, particularly in macrophages. Available cell lines modeling Gaucher disease do not demonstrate lysosomal storage of glycolipids; therefore, we set out to develop two macrophage models of Gaucher disease that exhibit appropriate substrate accumulation. We used these cellular models both to investigate altered macrophage biology in Gaucher disease and to evaluate candidate drugs for its treatment. We generated and characterized monocyte-derived macrophages from 20 patients carrying different Gaucher disease mutations. In addition, we created induced pluripotent stem cell (iPSC)-derived macrophages from five fibroblast lines taken from patients with type 1 or type 2 Gaucher disease. Macrophages derived from patient monocytes or iPSCs showed reduced glucocerebrosidase activity and increased storage of glucocerebroside and glucosylsphingosine in lysosomes. These macrophages showed efficient phagocytosis of bacteria but reduced production of intracellular reactive oxygen species and impaired chemotaxis. The disease phenotype was reversed with a noninhibitory small-molecule chaperone drug that enhanced glucocerebrosidase activity in the macrophages, reduced glycolipid storage, and normalized chemotaxis and production of reactive oxygen species. Macrophages differentiated from patient monocytes or patient-derived iPSCs provide cellular models that can be used to investigate disease pathogenesis and facilitate drug development.


De Grey A.D.N.J.,SENS Research Foundation
Rejuvenation Research | Year: 2014

Elsewhere in this issue, Marios Kyriazis articulates a sharply skeptical assessment of the feasibility of medical rejuvenation, otherwise known as the "damage repair" approach to postponing the ill health of old age. His critique incorporates many errors of fact and/or interpretation and/or logic, which I enumerate here. I recognize that many of these errors are by no means Kyriazis's alone but are shared by numerous observers across the full range of biological expertise. It is for that reason above all that I hope this exchange will be of value to readers. Additionally, Kyriazis raises a number of valid concerns that have not been systematically addressed, by myself or by others, in past publications; I will attempt to remedy that here. For clarity, I will not structure this response as an essay, but instead as a simple point-by-point list of comments concerning individual statements and inferences that Kyriazis makes. © 2014 Mary Ann Liebert, Inc.


De Grey A.D.,SENS Research Foundation
Current Aging Science | Year: 2015

In the 60 years since Medawar questioned the assumption that aging is a selected trait with a fitness benefit, mainstream biogerontology has overwhelmingly adopted the view that aging is a product of evolutionary neglect rather than evolutionary intent. Recently, however, this question has come to merit further scrutiny, for three reasons: a variety of new ways in which aging could indeed be “programmed” have been proposed, several phenomena with superficial similarities to programmed aging have been suggested to offer evidence for it and against the mainstream consensus, and above all it has become appreciated that the existence or otherwise of “pro-aging genes” has enormous implications for determining our optimal strategy for the medical postponement of age-related ill-health. Accordingly, it is timely to revisit the arguments and data on this topic. In this article I discuss difficulties in reconciling the programmed-aging concept with existing data, flaws in various arguments given by others that existing data prove aging to be programmed, and extensions of these considerations to various phenomena that in one or another way resemble programmed aging. I conclude that, however much we might wish that aging were programmed and thus that the ill-health of old age could be greatly postponed just by disabling some aspect of our genetic makeup, the unfortunate truth is that no such program exists, and thus that our only option for substantial extension of healthspan is a divide-and-conquer panel of interventions to repair the damage that the body inflicts upon itself throughout life as side-effects of its normal operation. I explicitly avoid arguments that rely on unnecessarily abstruse evolutionary theory, in order to render my line of reasoning accessible to the broadest possible audience. © 2015 Bentham Science Publishers.


Vijg J.,Yeshiva University | De Grey A.D.N.J.,SENS Research Foundation
Gerontology | Year: 2014

One of the main benefits of the dramatic technological progress over the last two centuries is the enormous increase in human life expectancy, which has now reached record highs. After conquering most childhood diseases and a fair fraction of the diseases that plague adulthood, medical technology is now mainly preoccupied by age-related disorders. Further progress is dependent on circumventing the traditional medical focus on individual diseases and instead targeting aging as a whole as the ultimate cause of the health problems that affect humankind at old age. In principle, a major effort to control the gradual accumulation of molecular and cellular damage - considered by many as the ultimate cause of intrinsic aging - may rapidly lead to interventions for regenerating aged and worn-out tissues and organs. While considered impossible by many, there really is no reason to reject this as scientifically implausible. However, as we posit, it is not only scientific progress that is currently a limiting factor, but societal factors that hinder and may ultimately prevent further progress in testing and adopting the many possible interventions to cure aging. © 2014 S. Karger AG, Basel.


PubMed | SENS Research Foundation
Type: | Journal: Rejuvenation research | Year: 2016

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