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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 | October 26, 2016
Site: www.biosciencetechnology.com

A simple Google search for "what does vitamin D do?" highlights the widely used dietary supplement's role in regulating calcium absorption and promoting bone growth. But now it appears that vitamin D has much wider effects -- at least in the nematode worm, C. elegans. Research at the Buck Institute shows that vitamin D works through genes known to influence longevity and impacts processes associated with many human age-related diseases. The study, published in Cell Reports, may explain why vitamin D deficiency has been linked to breast, colon and prostate cancer, as well as obesity, heart disease and depression. "Vitamin D engaged with known longevity genes - it extended median lifespan by 33 percent and slowed the aging-related misfolding of hundreds of proteins in the worm," said Gordon Lithgow, PhD, senior author and Buck Institute professor. "Our findings provide a real connection between aging and disease and give clinicians and other researchers an opportunity to look at vitamin D in a much larger context." The study shines a light on protein homeostasis, the ability of proteins to maintain their shape and function over time. It's a balancing act that goes haywire with normal aging -- often resulting in the accumulation of toxic insoluble protein aggregates implicated in a number of conditions, including Alzheimer's, Parkinson's and Huntington's diseases, as well as type 2 diabetes and some forms of heart disease. "Vitamin D3, which is converted into the active form of vitamin D, suppressed protein insolubility in the worm and prevented the toxicity caused by human beta-amyloid which is associated with Alzheimer's disease," said Lithgow. "Given that aging processes are thought to be similar between the worm and mammals, including humans, it makes sense that the action of vitamin D would be conserved across species as well." Postdoctoral fellow Karla Mark, PhD, led the team doing the experiments. She says the pathways and the molecular network targeted in the work (IRE-1/XBP-1/SKN-1) are involved in stress response and cellular detoxification. "Vitamin D3 reduced the age-dependent formation of insoluble proteins across a wide range of predicted functions and cellular compartments, supporting our hypothesis that decreasing protein insolubility can prolong lifespan." "We've been looking for a disease to associate with vitamin D other than rickets for many years and we haven't come up with any strong evidence," said Clifford Rosen, MD, the director of the Center for Clinical and Translational Research and a senior scientist at the Maine Medical Center Research Institute studying osteoporosis and obesity. "But if it's a more global marker of health or longevity as this paper suggests, that's a paradigm shift. Now we're talking about something very different and exciting." "This work is really appealing and challenging to the field," said Janice M. Schwartz, MD, a professor of medicine and bioengineering and therapeutic sciences the University of California, San Francisco, and a visiting research scientist at the Jewish Home in San Francisco. She has studied vitamin D supplementation in the elderly. "We focus on vitamin D and the bones because that's where we can measure its impact. I believe that vitamin D is as crucial for total body function and the muscles as it is for bones. Vitamin D influences hundreds of genes - most cells have vitamin D receptors, so it must be very important." How much vitamin D do humans need and how do they best get it? The issue is confusing with disagreement rampant among experts. The Institute of Medicine's (IOM) latest recommendations (from 2011) pertain only to vitamin D's role in bone health and fracture reduction. Experts concluded that evidence for other proposed benefits of vitamin D was inconsistent, inconclusive, or insufficient to set recommended intakes. The IOM recommends a daily intake of 600 International Units (IU) for people between 1 and 70 years old, and 800 IU daily for those older. The upper limit -- the levels above which health risks are thought to increase -- was set at 4,000 IU per day for adults. Excess vitamin D can raise blood levels of calcium which leads to vascular and tissue calcification, with subsequent damage to the heart, blood vessels and kidneys. Many vitamin D researchers and some health organizations, including the Endocrine Society and the International Osteoporosis Foundation, disagreed with the IOM's recommendations for daily intake, instead recommending supplementation of 800 to 2,000 IU per day, at least for people known or likely to have low blood levels. The disagreement highlights another difficulty: measuring blood levels of vitamin D is problematic given a lack of standardization and reliability among labs. Blood levels of the precursor to the active vitamin D are measured in nanograms per milliliter (ng/mL) in the U.S. Many researchers and expert groups have argued that a blood level of at least 30 ng/mL is optimal; some call for optimum levels to be set at 40 or 50 ng/mL. But the IOM report concluded that blood levels starting at 20 ng/mL would be adequate for bone health in the vast majority of people. Based on problems with laboratory standards and a lack of agreed-upon meaning of results, both Rosen and Schwartz agree that the costs of universal testing for vitamin D levels would outweigh the benefits. Instead, both recommend universal supplementation of between 800 - 1000 IU of vitamin D daily for adults. "It's safe, there's no reason for anyone not to take it," said Schwartz, who has written about vitamin D for the popular press. Schwartz says older adults may be particularly prone to vitamin D deficiency because the skin's ability to manufacture vitamin D from sun or UV light exposure declines with age, adding that the elderly are less likely to spend time in the sun, are more likely to have diets lacking in sources of vitamin D, and may suffer from gastrointestinal disorders that make it harder to absorb vitamin D. Others prone to vitamin D deficiency include those with darker skin and those who live in higher latitudes where the sun's angle is low in the sky. Given adequate funding, senior author Lithgow plans to test vitamin D in mice to measure and determine how it affects aging, disease and function -- and he hopes that clinical trials in humans will go after the same measurements. "Maybe if you're deficient in vitamin D, you're aging faster. Maybe that's why you're more susceptible to cancer or Alzheimer's," he said. "Given that we had responses to vitamin D in an organism that has no bone suggests that there are other key roles, not related to bone, that it plays in living organisms." Lithgow gave a shout out to the tiny, short-lived nematode worms which populated this study. "Working in these simple animals allows us to identify novel molecular pathways that influence how animals age," he said. "This gives us a solid starting point to ask questions and seek definitive answers for how vitamin D could impact human health. We hope that this work will spur researchers and clinicians to look at vitamin D in a larger, whole-person context that includes the aging process."


News Article | October 26, 2016
Site: www.eurekalert.org

A simple Google search for "what does vitamin D do?" highlights the widely used dietary supplement's role in regulating calcium absorption and promoting bone growth. But now it appears that vitamin D has much wider effects -- at least in the nematode worm, C. elegans. Research at the Buck Institute shows that vitamin D works through genes known to influence longevity and impacts processes associated with many human age-related diseases. The study, published in Cell Reports, may explain why vitamin D deficiency has been linked to breast, colon and prostate cancer, as well as obesity, heart disease and depression. "Vitamin D engaged with known longevity genes - it extended median lifespan by 33 percent and slowed the aging-related misfolding of hundreds of proteins in the worm," said Gordon Lithgow, PhD, senior author and Buck Institute professor. "Our findings provide a real connection between aging and disease and give clinicians and other researchers an opportunity to look at vitamin D in a much larger context." The study shines a light on protein homeostasis, the ability of proteins to maintain their shape and function over time. It's a balancing act that goes haywire with normal aging -- often resulting in the accumulation of toxic insoluble protein aggregates implicated in a number of conditions, including Alzheimer's, Parkinson's and Huntington's diseases, as well as type 2 diabetes and some forms of heart disease. "Vitamin D3, which is converted into the active form of vitamin D, suppressed protein insolubility in the worm and prevented the toxicity caused by human beta-amyloid which is associated with Alzheimer's disease," said Lithgow. "Given that aging processes are thought to be similar between the worm and mammals, including humans, it makes sense that the action of vitamin D would be conserved across species as well." Postdoctoral fellow Karla Mark, PhD, led the team doing the experiments. She says the pathways and the molecular network targeted in the work (IRE-1/XBP-1/SKN-1) are involved in stress response and cellular detoxification. "Vitamin D3 reduced the age-dependent formation of insoluble proteins across a wide range of predicted functions and cellular compartments, supporting our hypothesis that decreasing protein insolubility can prolong lifespan." "We've been looking for a disease to associate with vitamin D other than rickets for many years and we haven't come up with any strong evidence," said Clifford Rosen, MD, the director of the Center for Clinical and Translational Research and a senior scientist at the Maine Medical Center Research Institute studying osteoporosis and obesity. "But if it's a more global marker of health or longevity as this paper suggests, that's a paradigm shift. Now we're talking about something very different and exciting." "This work is really appealing and challenging to the field," said Janice M. Schwartz, MD, a professor of medicine and bioengineering and therapeutic sciences the University of California, San Francisco, and a visiting research scientist at the Jewish Home in San Francisco. She has studied vitamin D supplementation in the elderly. "We focus on vitamin D and the bones because that's where we can measure its impact. I believe that vitamin D is as crucial for total body function and the muscles as it is for bones. Vitamin D influences hundreds of genes - most cells have vitamin D receptors, so it must be very important." How much vitamin D do humans need and how do they best get it? The issue is confusing with disagreement rampant among experts. The Institute of Medicine's (IOM) latest recommendations (from 2011) pertain only to vitamin D's role in bone health and fracture reduction. Experts concluded that evidence for other proposed benefits of vitamin D was inconsistent, inconclusive, or insufficient to set recommended intakes. The IOM recommends a daily intake of 600 International Units (IU) for people between 1 and 70 years old, and 800 IU daily for those older. The upper limit -- the levels above which health risks are thought to increase -- was set at 4,000 IU per day for adults. Excess vitamin D can raise blood levels of calcium which leads to vascular and tissue calcification, with subsequent damage to the heart, blood vessels and kidneys. Many vitamin D researchers and some health organizations, including the Endocrine Society and the International Osteoporosis Foundation, disagreed with the IOM's recommendations for daily intake, instead recommending supplementation of 800 to 2,000 IU per day, at least for people known or likely to have low blood levels. The disagreement highlights another difficulty: measuring blood levels of vitamin D is problematic given a lack of standardization and reliability among labs. Blood levels of the precursor to the active vitamin D are measured in nanograms per milliliter (ng/mL) in the U.S. Many researchers and expert groups have argued that a blood level of at least 30 ng/mL is optimal; some call for optimum levels to be set at 40 or 50 ng/mL. But the IOM report concluded that blood levels starting at 20 ng/mL would be adequate for bone health in the vast majority of people. Based on problems with laboratory standards and a lack of agreed-upon meaning of results, both Rosen and Schwartz agree that the costs of universal testing for vitamin D levels would outweigh the benefits. Instead, both recommend universal supplementation of between 800 - 1000 IU of vitamin D daily for adults. "It's safe, there's no reason for anyone not to take it," said Schwartz, who has written about vitamin D for the popular press. Schwartz says older adults may be particularly prone to vitamin D deficiency because the skin's ability to manufacture vitamin D from sun or UV light exposure declines with age, adding that the elderly are less likely to spend time in the sun, are more likely to have diets lacking in sources of vitamin D, and may suffer from gastrointestinal disorders that make it harder to absorb vitamin D. Others prone to vitamin D deficiency include those with darker skin and those who live in higher latitudes where the sun's angle is low in the sky. Given adequate funding, senior author Lithgow plans to test vitamin D in mice to measure and determine how it affects aging, disease and function -- and he hopes that clinical trials in humans will go after the same measurements. "Maybe if you're deficient in vitamin D, you're aging faster. Maybe that's why you're more susceptible to cancer or Alzheimer's," he said. "Given that we had responses to vitamin D in an organism that has no bone suggests that there are other key roles, not related to bone, that it plays in living organisms." Lithgow gave a shout out to the tiny, short-lived nematode worms which populated this study. "Working in these simple animals allows us to identify novel molecular pathways that influence how animals age," he said. "This gives us a solid starting point to ask questions and seek definitive answers for how vitamin D could impact human health. We hope that this work will spur researchers and clinicians to look at vitamin D in a larger, whole-person context that includes the aging process." Citation: Vitamin D Promotes Protein Homeostasis and Longevity via the Stress Response Pathway Genes SKN-1, IRE-1, and XBP-1 Other Buck researchers involved in the study are Kathleen J. Dumas, Dipa Bhaumik, Birgit Schilling, Sonnet Davis, Tal Ronnen Oron, Dylan Sorensen, Rachel B. Brem, Simon Melov, Arvind Ramanathan, Bradford W. Gibson and Mark Lucanic. Acknowledgements: The work was supported by funding from the Larry L. Hillblom Foundation, the Glenn Foundation for Medical Research and grants from the National Institutes of Health: UL102417, R01AG029631-01A1, R21AG048528, R01AG029631, PL1 AG032118, 1S10 OD016281. About the Buck Institute for Research on Aging The Buck Institute challenges the way we think about aging by approaching it as if it were a disease. We do not accept aging as inevitable decline. Our mission is to extend the healthy, vital years of life. Our research is aimed at rendering chronic diseases as preventable, deferrable, curable or, at the least, manageable. Whenever possible, we want to restore function. Buck scientists are pioneers. They work in a dynamic, collaborative environment to understand how normal aging contributes to conditions such as Alzheimer's and Parkinson's diseases, cancer, osteoporosis, arthritis, heart disease, diabetes, macular degeneration and glaucoma, among others. We are an independent nonprofit organization working in an architectural landmark located in northern Marin County, California. For more information: http://www.


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.


News Article | December 1, 2016
Site: www.eurekalert.org

December 1, 2016/Novato, California: A study from the Buck Institute offers for the first time an explanation for the benefits of fasting at the neuronal level, providing a possible mechanism for how fasting can afford health benefits. Publishing on December 1st in Neuron, researchers used fruit fly larvae to uncover the presence of a molecular pathway that responds to nutrient scarcity and lowers synapse activity at the junctions between neurons and muscle cells. Specific effects in response to changing nutrient availability at the level of the synapse has not been reported before. "On the one hand, our findings might sound counter-intuitive because we always think of fasting as being beneficial and here we have found blockage of a natural neuronal activity," said senior author and Buck Institute professor Pejmun Haghighi, PhD. "On the other hand, we think that we might actually be answering the question of why fasting is beneficial. Perhaps it's a good thing that when nutrients are unavailable, an organism reduces neurotransmitter release and thus saves a good proportion of its overall energy expenditure." Additionally, Haghighi added, neurotransmission requires continuous orchestration of signal transmission steps and this stress could lead to accumulated damage in neurons. "Our findings suggest that one of the reasons that fasting is beneficial is that it gives the nervous system a break and calms things down," he said. Dampening of synaptic activity occurred within three hours of removing nutrients from the larval food. The inhibition was pronounced, reducing activity by half. "It's really amazing that a change in nutrient intake can have such dramatic influences on neuron activity on such a short time scale," said the study's co-lead author Grant Kauwe, PhD, a postdoctoral research fellow in the Haghighi lab. "It demonstrates how quickly changes caused by fasting can occur." Researchers have long wondered exactly how caloric restriction extends lifespan and slows age-related disease in a range of species, but the impetus for the current study actually stemmed from Haghighi's decades-long interest in understanding the molecular mechanisms that regulate neurotransmitter release at synapses. In particular, he has focused on a phenomenon called synaptic homeostasis, which is a way that neuronal circuits maintain activity within a set range to ensure stable and reliable communication. In 2012, Haghighi's team published a paper showing synaptic homeostasis was controlled by an enzyme, the target of rapamycin (TOR), which plays a critical role in regulating lifespan in a wide range of organisms from yeast to mice. This finding connected on a molecular level how nervous system function and lifespan regulation are intertwined. TOR plays many roles, but one of its primary tasks is to function like a wrench loosening and tightening the control of protein synthesis in response to nutrients, specifically amino acid availability. While previous evidence had suggested that fasting influences neuronal activity and neurotransmitter release, Haghighi realized that no research had linked TOR's known ability to regulate nutrients and lifespan with TOR's role in synaptic homeostasis. To determine the molecular details about how nutrient reduction affects synapse function, Haghighi's team combined their genetic and molecular tools with imaging and electrophysiological techniques to see what happened when they changed the food composition of Drosophila larvae. At the basic level, their experiments were recording neuron activity in muscle, Kauwe explained. The synapse between a neuron and a muscle - the neuromuscular junction - of a fruit fly larva turns out to be a good model for studying how the nervous system works in general, which can be applied to other organisms, including humans. The team started by restricting protein in the larvae's diet, since protein restriction was already known to reduce TOR activity. Surprisingly, they discovered that synaptic homeostasis was unaffected by dietary restriction, despite lower TOR activity. However, transient removal of food, called acute fasting, completely suppressed synaptic homeostasis within a few hours. The team's further experiments delved into what else beyond TOR was involved to evoke the suppression. They showed genetically that there was an additional response coming from the transcription factor - Forkhead box O (Foxo) - which in turn enhances the transcription of one of the translational regulators: eukaryotic initiation factor 4E binding protein (4E-BP). Furthermore, it is the balance between TOR and 4E-BP that controls synapse stability. Stability is a hallmark of healthy neuronal circuits and disruption of this stability in the form of increased activity at the synapse may lead to neurodegenerative diseases, such as Parkinson's disease, Alzheimer's disease, schizophrenia or epilepsy. "We might have some real insight into the advantages of dampening of synaptic activity that is caused by fasting," said Haghighi, for example, how fasting can be beneficial for epileptic patients, who can experience reduced seizures when restricting calories. Kauwe and others in Haghighi's lab are exploring why such a change in the set point of synaptic transmission occurs so rapidly, and how dampening neuron activity might be beneficial in treating, or even preventing, neurodegenerative diseases. "I think uncovering this mechanism is an important basic discovery that could lead to tangible ways of thinking about design of therapeutic approaches for neurodegenerative diseases in the near future," said Haghighi. Other Buck researchers involved in the study are the study's co-lead author Kazuya Tsurudome, Megumi Mori, Lindsay Gray, Mario R. Calderon and Nicole Chicoine. Jay Penney and Fatima Elazouzzi were previously in the Haghighi lab and Nahum Sonenberg from McGill University collaborated with the group. Acknowledgements: This work was supported by grants from the National Institutes of Health (R01NS082793) to Haghighi and a T32 training grant (AG000266) to Kauwe. The Buck Institute challenges the way we think about aging by approaching it as if it were a disease. We do not accept aging as inevitable decline. Our mission is to extend the healthy, vital years of life. Our research is aimed at rendering chronic diseases as preventable, deferrable, curable or, at the least, manageable. Whenever possible, we want to restore function. Buck scientists are pioneers. They work in a dynamic, collaborative environment to understand how normal aging contributes to conditions such as Alzheimer's and Parkinson's diseases, cancer, osteoporosis, arthritis, heart disease, diabetes, macular degeneration and glaucoma, among others. We are an independent nonprofit organization working in an architectural landmark located in northern Marin County, California. For more information: http://www.


News Article | February 3, 2016
Site: www.fastcompany.com

The cells in our bodies are constantly under stress from all kinds of sources. In response, they can recover or die. But some cells experience a state of "cellular senescence," where the cells stop dividing altogether but remain in the body in a kind of purgatory. As the number of these cells increase, it's theorized that they will start to produce inflammatory by-products that result in aging. For decades, scientists have been fascinated with cellular senescence and its role in age-related diseases. But researchers have only shown in the past five years that clearing these cells might keep common ailments at bay that occur as we age, like osteoarthritis, glaucoma, and atherosclerosis. And now, investors are starting to see opportunities to bring new therapies to market. A startup called Unity Biotechnology, which is launching today, is building off of soon-to-be published research in the journal Nature. The research, which was led by a small team at the Mayo Clinic, explores how removing these senescent cells in naturally-aging mice can extend their life span and delay age-related decline. This paper follows recent research, published in Nature Medicine, which found that it's possible to clear these cells in mice by targeting an important pathway for their survival. In other words, by making it near-impossible for these retired cells to stay alive and wreak potential havoc in the body. "The researchers have shown that clearing these cells profoundly impacts quality of life of a mammal," says Nathaniel David, chief executive officer and cofounder of Unity Biotechnology in an interview. "It remains to be seen how it will work in humans, but we're betting that it will translate." These are still early days for Unity, but health care investors are jumping on opportunities to fund promising anti-aging research. The initial funding was led by ARCH Venture Partners, with contributions from the Mayo Clinic, and Venrock, a health-focused venture capital firm. The company says it is also working with top anti-aging researchers and lead investigators, including Mayo Clinic professor and biochemist Jan M. van Deursen, and Buck Institute of Research on Aging professor Judith Campisi. "This is the coolest biology I've seen in a while," said Camille Samuels, an investor at Venrock who joined Unity's board. "Finally legitimate science is coming to a space (anti-aging technology) that has seen a lot of snake oil." "There are a lot of researchers working on this, but not a lot of companies," says Sabah Oney, a geneticist formerly of Roche. "It's very interesting." But before it releases a magic anti-aging pill, the company will need to invest in further research as well as a clinical trial phase that involves humans and not mice. That process typically takes years. From there, the drugmakers would need to apply for approval from federal regulators. Unity says its leadership team has collectively moved more than 90 promising therapies to human clinical trials, and created more than 13 FDA-approved medicines. David says the company will initially focus on osteoarthritis and other conditions that "make it hurt to be old," before expanding the scope to cancer and other diseases. In the coming years, the company might compete with Calico, the mysterious anti-aging company that spun out of Alphabet (Google's parent company). Calico was announced in 2013, but it has revealed few details about its research objectives since then. However, the company did recruit some impressive names in the anti-aging community, including UC San Francisco's Cynthia Kenyon (watch her fascinating TED talk here). Kenyon's research has centered on the increasing the life span of microscopic roundworms by suppressing a single gene. Calico also scooped up Robert Cohen, a senior oncologist at Genentech; and David Botstein, the former director of the Lewis-Sigler Institute for Integrative Genomics at Princeton University. This story has been updated with quotes from Unity Biotechnology's CEO.


News Article | December 16, 2016
Site: www.eurekalert.org

The interaction between bacteria and worms can be used to understand host-microbiome signals in humans that contribute to diseases such as type 2 diabetes and obesity December 13, 2016/Novato, California: The billions of microorganisms living within the human digestive tract appear to play a significant role in health and disease, notably metabolic syndrome, autoimmune disorders and diabetes - but how these organisms do so is not well understood. Researchers at the Buck Institute have used worms to provide a framework for deciphering how specific bacterial signals from the microbiome influence the host, whether the host is a worm or a human. The work, done in the nematode worm C. elegans and detailed in Scientific Reports, an online open access journal from the publishers of Nature, reveals for the first time how different genes in bacteria - rather than metabolites produced by the bacteria - modify the biology of the worms that eat them. "The dynamic nature of the gut microbial community has proven hard to study in mice and even harder in human subjects," said Buck professor Pankaj Kapahi, PhD, senior scientist on the study. To start to untangle the complicated interactions, his team thought to use worms, which eat bacteria as part of their normal diet. "We have uncovered the effects of bacterial genetics on the physiology of a simple organism, which may serve as a model system to study the gut microbiome in mammals to identify novel therapeutics to treat diseases," he said. "Humans have a gut full of bacteria that are 'talking' with intestinal cells and ultimately affect the whole organism, so there has been a lot of research targeting bacterial metabolites associated with human disease. This study is the first one to explore how the bacteria themselves talk to the host," said Amit Khanna, PhD, a postdoctoral research fellow in Kapahi's lab. The foundations of this study began years ago not as a study of the microbiome, but as a contemplation of why worms that ate less lived longer. Kapahi wondered what in the worms' diet was responsible for this change in lifespan, and he thought the best way to answer that question would be to genetically mutate the bacteria they eat to see what caused any changes. To have an easy yes-or-no answer as to whether different mutations in bacteria affected the worms, the team took advantage of a phenomenon in the worm's life cycle called dauer, in which larvae shut down their functions to survive harsh environmental conditions. It is known that one of the factors causing worms to enter dauer are compounds produced by the bacteria they eat and that one of the pathways that controls this response is the insulin-like signaling pathway. Although humans and nematodes are of course quite different, Kapahi noted, many pathways are very similar, including insulin-like signaling, which plays a role in human diseases, such as type 2 diabetes and obesity. To ask the question about what genes in bacteria normally present at low levels in human gut flora would affect the insulin-like signaling pathway in worms, the team first systematically screened nearly 4,000 stains of E. coli bacteria that each had a single gene deactivated ("knocked out") to see which enhanced dauer formation. They found 56 mutants that did so. Some of these mutants also extended adult lifespan in control worms. The team picked one of the bacterial mutants that increased lifespan by the largest amount - called adenylate cyclase (cyaA) - to further explore. They found cyaA modulates dauer formation and lifespan by influencing TGF-β signaling, and they uncovered the entire molecular mechanism: they could see how the sensory neurons talk to the target cells and what were the molecular pathways involved that caused a worm to enter dauer. "The idea that a single gene mutation - in the bacteria that the worms normally eat - could throw off an entire animal and send it into a dauer state was certainly not a concept that we anticipated when we began this study," said Kapahi. The results demonstrate that the combination of bacterial and worm genetics can be a powerful tool to study the molecular signals by which bacteria modulate nutrient signaling and host physiological processes, such as development and aging. These processes are often very similar in higher organisms, so the significance of the study is not limited to C. elegans. Worms also allow questions to be answered rapidly, on the order of 10 to 15 days. "There a lot of studies showing that the microbiome influences this and that, but we have very little understanding of the mechanisms and how to make sense of the mounds of data," said Khanna. "We think our method might be the way forward: to be able to ask specific questions about what do individual bacterial components contribute and how do they do it." Citation: A genome-wide screen of bacterial mutants that enhance dauer formation in C. elegans [Scientific Reports 6, Article number: 38764 (2016)] DOI: 10.1038/srep38764 Other Buck researchers involved in the study include co-first authors Jitendra Kumar and Misha A. Vargas, LaKisha Barrett, Subhash Katewa, Patrick Li, Tom McCloskey, Amit Sharma, Nicole Naude?, Christopher Nelson and Rachel Brem. Other collaborators include David W. Killilea from Children's Hospital Oakland Research Institute, Sean Mooney from University of Washington and Matthew Gill from The Scripps Research Institute - Florida. Acknowledgements: The work was supported by grants from the American Federation for Aging Research and the NIH : R01AG038688 and RL1 AAG032113. About the Buck Institute for Research on Aging The Buck Institute challenges the way we think about aging by approaching it as if it were a disease. We do not accept aging as an inevitable decline. Our mission is to extend the healthy, vital years of life. Our research is aimed at rendering chronic diseases as preventable, deferrable, curable or, at the least, manageable. Whenever possible, we want to restore function. Buck scientists are pioneers. They work in a dynamic, collaborative environment to understand how normal aging contributes to conditions such as Alzheimer's and Parkinson's diseases, cancer, osteoporosis, arthritis, heart disease, diabetes, macular degeneration, and glaucoma, among others. We are an independent nonprofit organization working in an architectural landmark located in northern Marin County, California. For more information: http://www.


News Article | November 25, 2015
Site: phys.org

Dietary restriction enhances the expression of the circadian clock genes in the peripheral tissue of fruit flies, according to research from the Kapahi lab at the Buck Institute. Publishing in Cell Metabolism, the researchers show that dietary restriction, induced by reducing protein in the diet, increased the amplitude of circadian clocks and enhanced the cycles of fat breakdown and fat synthesis. This improvement in fat metabolism may be a key mechanism in explaining why dietary restriction extends lifespan in several species, including the flies in this study. The research also presents a tantalizing possibility for humans eager to take a drug that would allow them to reap the health benefits of dietary restriction without going on an extreme diet. When scientists genetically altered the flies to boost clock function the animals lived longer, even when they ate whatever they wanted to. On the other hand, disrupting the clocks, either genetically or by keeping the flies under constant light, made the animals irresponsive to the beneficial effects of dietary restriction. "More than 10-15% of the genome is under circadian control, especially genes which regulate processes involving cellular repair and metabolism," said senior scientist and Buck professor Pankaj Kapahi, PhD. "Every cell has a clock and the action of clocks in peripheral tissues, fat, intestines, kidneys—plays an important role in modulating metabolism and thereby mediating lifespan extension via dietary restriction." Previous work from the Kapahi lab showed that flies on a lifespan-extending Spartan diet exhibited an enhanced turnover of triglycerides. This new work, also led by Buck assistant research professor Subhash D. Katewa, PhD, suggests a role for timeless, a circadian clock gene, in the cycling of specific medium chain triglycerides under dietary restriction. "The role of medium chain triglycerides in aging and regulation of clock functions is not clear, however dietary medium chain triglycerides have been associated with weight loss and improved healthspan in both humans and mice," said Katewa, noting current consumer interest in coconut oil which is rich in medium chain triglycerides. "Our work demonstrates for the first time that medium chain triglyceride synthesis in animals is under nutritional and circadian control," he said. "If we want to modulate the effects of nutrient manipulation on fat metabolism and aging then targeting the activity of peripheral circadian clocks gives us a way to achieve that goal." "Circadian rhythms, which impact many behaviors like sleep or cellular processes like metabolism, tend to dampen with age," said Kapahi. "The metabolic rhythms of flies on dietary restriction maintain a remarkable robustness as they age, which we think helps them live longer. It is exciting to contemplate how this mechanism might be exploited for human health." Explore further: Key protein may explain the anti-aging and anti-cancer benefits of dietary restriction More information: Peripheral circadian clocks mediate dietary restriction dependent changes in lifespan and fat metabolism in Drosophila, Cell Metabolism, CELL-METABOLISM-D-15-00087R3


A cross section through a fly intestine depicting intestinal stem cells in green and enterocytes, functional gut cells, in red with large blue nuclei. Left: Under normal conditions, stem cells are distributed throughout the basal side of the epithelium and can be activated to regenerate enterocytes. Upon constitutive elevation of cytosolic Ca2+, intestinal stem cells become rapidly activated and can regenerate enterocytes. Right: Shown here is a condition in which Ca2+ was strongly and chronically elevated, resulting in excessive stem cell proliferation and causing tumors. Credit: Akos Gerencser, PhD, Buck Institute Adult stem cells ensure continuous regeneration of tissues throughout our entire life. But the activity of these stem cells has to be carefully controlled in order to support regeneration without cancer. How this balanced control is achieved and maintained as the organism ages remains a critical question in stem cell biology. Publishing in Nature, researchers at the Buck Institute have identified a new mode of stem cell regulation. Working in the fly gut, senior scientist Heinrich Jasper, PhD, and colleagues show that stem cells adjust their proliferative activity in response to a wide variety of signals via intracellular calcium (Ca2+) signaling. Mechanisms that control the intracellular Ca2+ concentration and proteins that respond to intracellular Ca2+ changes thus emerge as master regulators of stem cell activity. Adult stem cells in the gut exist in a very active environment, they are continually bombarded with signals - from diet, the microbiome, and from invading bacteria and other stressors. Should the cells spring into regenerative action and divide or remain poised for future needs? Jasper says a Ca2+ sensitive gene regulatory system integrates these stimuli to control intestinal proliferation by influencing the oscillation of Ca2+ levels within the cells. "These findings help explain how stem cells are able to respond to such a wide range of stimuli," said Jasper, who is also the Chief Scientific Officer at the Buck Institute. "The fact that one variable - Ca2+ - is integrating all of these signals was quite an exciting and surprising discovery in stem cell biology with implications for our understanding of various cancers and a range of degenerative diseases." Postdoctoral fellow Hansong Deng, PhD, determined the wide-ranging significance of Ca2+ signaling after discovering that intestinal stem cells have receptors that sense L-glutamate, and that dietary L-glutamate stimulated stem cell division and gut growth in the flies. Deng teamed up with Buck Research Professor Akos Gerencser, PhD, (co-director of the Institute's imaging core) who was able to image live stem cells in the fly gut. Surprisingly, they discovered that Ca2+ levels oscillate regularly in stem cells and that L-glutamate regulates stem cell activity by triggering a sustained increase of Ca2+ within the cell. Research showed that this change in Ca2+ levels in stem cells was not limited to the response to L-glutamate, but was also observed when these cells became activated in response to other stimuli, including infection and tissue damage. In addition, the scientists found that elevating Ca2+ by genetically perturbing Ca2+ pumps in the stem cells resulted in a strong, continuous proliferative response. A sustained elevated intracellular Ca2+ concentration thus emerged as a universal and required characteristic of activated stem cells, and Deng found that the activation of stem cells by Ca2+ was accomplished by Ca2+-sensitive protein phosphates and transcription factors. The researchers say this universal role of Ca2+ in stem cell activation suggests that these cells use the intracellular Ca2+ concentration as a gauge to respond dynamically to the multitude of signals vying for their attention. Jasper says that in the future, his lab plans to explore the role of this regulatory system in influencing stem cell based diseases and age-related dysfunctions in the gut and other high-turnover tissues, adding that the work has important implications for how environmental challenges influence such diseases. L-glutamate, for example, is the most abundant naturally-occurring amino acid in the body and is involved in many metabolic processes. Dietary sources of L-glutamate include beef, chicken, fish and eggs. Its sodium salt is also known as the flavor enhancer MSG, which was fed to the flies in this study. Jasper says this study provides an interesting new angle to our understanding of the effects of the widely-used ingredient. "We've shown in the fly that supplementing a protein-restricted diet with MSG stimulates the proliferation of stem cells. Supplementing the same diet with high concentrations of MSG, on the other hand, impaired stem cell activity, indicating that at these high concentrations MSG may cause stem cell toxicity. Whether the effect of MSG on stem cell proliferation is a good or bad thing is another story," he said. "Supplementing the diet with low levels of MSG might just be supporting regeneration or it might be causing stem cells to proliferate too much, facilitating the development of gastrointestinal cancers. It's an open question that needs more study, especially in vertebrates." Explore further: Complex signaling between blood and stem cells controls regeneration in fly gut More information: Hansong Deng et al. Signal integration by Ca2+ regulates intestinal stem-cell activity, Nature (2015). DOI: 10.1038/nature16170


News Article | October 28, 2016
Site: www.businesswire.com

NOVATO, Calif.--(BUSINESS WIRE)--The Buck Institute for Research on Aging (Buck Institute) today announced the appointment of Edward Lanphier as president and chief executive officer. He succeeds Brian Kennedy, Ph.D., who resigned his position in order to devote all of his time to leading his pioneering Geroscience research at the Buck. “The Buck Institute is indebted to Brian for his leadership over the last six years, during which time the Buck developed the nation’s first Ph.D. program in th

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