Latest news with #ScrippsResearch
Daily Mail
5 days ago
- Science
- Daily Mail
CEO's scientist best friend, 67, made unthinkable move as he came in to land small plane
A Georgian scientist has died after his plane inexplicably plunged into the Pacific Ocean moments after he was cleared to touch down in California. Tsotne Javakhishvili was operating a 2014 Cessna T240 Corvalis TTx owned by world-renowned American scientist Peter Schultz when it disappeared on Sunday. National Transportation Safety Board (NTSB) officials described the incident to the Daily Mail as a 'presumed crash' and confirmed that nobody else was on board. The single-engine plane departed Ramona Airport in San Diego County and headed for Montgomery-Gibbs Executive Airport, which is less than 30 miles away. Officials said Javakhishvili checked in with the destination runway's control tower for touchdown and was cleared to land at 1.55pm - but he never replied to controllers. Instead, the four-seater plane veered west for several minutes and plunged into the Pacific Ocean about 470 miles off the coast of San Diego. Javakhishvili is still missing and the plane has not yet been found. NTSB and Federal Aviation Authority (FAA) officials told the Daily Mail they are investigating the cause of the crash. FlightAware tracking website shows the path of the plane as it continued way off course before disappearing from the radar. Officials shared the plane's registration number, which matches the four-seater aircraft owned by scientist Peter Schultz. Schultz is a world-leading scientist and the CEO of Scripps Research, a medical and scientific institution based in La Jolla, California. 'Widely considered one of the top chemists in the world, he has made many seminal contributions to the field, including the development and application of methods to expand the genetic code of living organisms, the discovery of catalytic antibodies, and the development and application of molecular diversity technologies to address problems in chemistry, biology and medicine,' Schultz's biography reads. Javakhishvili was the founder and director of the Institute of Synthetic Biology at the University of Georgia in the European country's capital city of Tbilisi. He was also the director of Molecular Biology at California biotechnology company Ambrx, according to his LinkedIn page, which says he specialized in genomics. The University of Georgia confirmed Javakhishvili's death in a Facebook post. 'With a heavy heart, we are following the search works of our colleague, founder and director of the Institute of Synthetic Biology at the University of Georgia, Tsotne Javakhishvili, three days ago, in America,' the university said on Wednesday. 'Our full support goes out to his family, friends, students and colleagues during this uncertain and difficult time. 'We are closely following the ongoing investigation into the plane disappearance off San Diego coast, piloted by our colleague, Tsotne Javakhishvili, Founder and Director of the Institute of Synthetic Biology of the University of Georgia.' David Gvalia, a friend and former colleague of the pilot, said he was still in shock after hearing the news. 'I would call him my best friend,' he told ABC News affiliate KGTV. 'I'm numb, completely numb... it's devastating. I still can't believe it.' 'Everybody loved him. Everybody respected him. He was larger than life, extremely smart and extremely kind,' Gvalia added. 'His exit from his life is poetic for numerous reasons because, as hard as it is for me to accept it, he died doing the thing he loved doing,' Schultz confirmed that Javakhishvili was his friend and an experienced aviator. The duo worked on several scientific projects together.
Scientific American
14-07-2025
- Health
- Scientific American
A Longevity Expert Breaks Down the Science and Hype of Biological Aging Tests
How old are you really? Counting birthdays may be a common tally, but your 'age' isn't determined by time alone. New research increasingly shows the importance of considering chronological age as something very different from biological age—in which the body and its cells, tissues and organs all have separate 'clocks' that can tick at different speeds. 'Calculating biological age, I think, is core to the advances we've made in the science of aging,' says Eric Topol, a cardiologist and genomics professor at Scripps Research in California. 'It's a way you can tell if a person, organ, or any biological unit is at pace of aging—if it's normal, abnormal or supernormal.' In his new book Super Agers: An Evidence-Based Approach to Longevity, Topol delves into the recent surge in public interest in biological aging and the accelerating quest to refine ways to measure it—giving a more precise picture of a person's longevity prospects and of potential ailments that can be prevented or treated early. Scientific American spoke with Topol about the latest research in biological aging, factors that might speed it up or slow it down and what it can tell us about our health. On supporting science journalism If you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today. [ An edited transcript of the interview follows. ] How is biological age determined and how has the research evolved? The real beginning of this research started more than a decade ago by geneticist Steven Horvath with his 'clock' [test], with which, basically using saliva, you could look at specific genetic markers in a genome and predict a person's biological age. His clock is really known as an epigenetic clock, or methylation clock. As people age, DNA changes and gets methylated—this is when a methyl group [molecule] attaches to specific nucleotides of DNA. I kind of liken it to the body rusting out. Basically, you're getting marks at specific parts of the genome that track with aging in humans and every other species of mammal. In Horvath's initial test, there clearly was a detection of both alignment with the person's real age, or chronological age—and when it wasn't matching up. In other words, if a person's biological age was off by a few years from their real age, you'd wonder why that is. Then what's proliferated in the more than 10 years since has been all these other clocks: protein clocks, RNA clocks, immune system clocks—you name it. Using plasma proteins from a blood sample, we can also clock organs—whether it's the heart, brain, liver or kidney. So we have seen just enormous advances in these clocks, and they keep getting refined with added features. There's a race to get the best clocks to predict survival. What can biological age tests tell us clinically? We can detect in an individual if something's not right at different levels. For example, if your biological age is five years older than your real age, is there an organ that might be linked with that? Then you can use these clocks to see if lifestyle, prevention or treatment can slow down the pace of aging and get it into alignment with your actual age. The question is: When will doctors actually start using them? The medical community is very hard to change. So it hasn't happened yet, but I believe it will eventually. Tests are also made available by commercial companies, but they can be very expensive. You can run an epigenetic test in a very simple way for $10 or $20, while some of these companies are charging $200. I haven't seen their publications to be able to say with confidence that they are doing things right, and the lack of standards from one company to the next is disconcerting. They don't want to shock [customers by telling them] that they're 10 years older than their real chronological age. Eventually, I believe, we're going to have high-fidelity epigenetic clocks with no motivation for a provider to hold things back if a person's data are really bad. Why might someone biologically age 'faster' or 'slower' than their actual age? If you had to pick one mechanism behind why biological age and chronological age are misaligned, it would most likely be because there are some genes that are either protective or linked with accelerated aging—but that's such a small part of the story. Another root cause appears to be that our immune system gets weaker and less functional as we get older. In the average person, this starts around age 55 to 60. It drops its level of protection, or it gets dysregulated—off track—and it can have an untoward, hyperactive response. Now when you have that happen, you start to see inflammation in the organs, such as in the arteries of the heart or the brain—it's what I call 'inflammaging.' Obviously our lifestyle also has a big impact—eating a really healthy diet that's not proinflammatory and doesn't have a lot of ultraprocessed foods or red meat. Good sleep health helps reduce inflammation. There's only one thing that's been definitively shown to slow the epigenetic aging process, and that's exercise. I think these clocks ultimately are going to be very good incentives for people to adopt a healthy lifestyle. We can't get everybody to do all these things that we know help them, but if they get their own data and they see something's off track, the hope is that they'd [change their lifestyle]. That's, of course, just one of the ways to prevent diseases. There are also drugs and other treatments. What environmental factors are also important to consider? We have all kinds of food deserts in the U.S. We have air pollution and unmitigated accumulation in the air and water of microplastics and nanoplastics, which get into every part of our body and induce inflammation. And we have forever chemicals as well that are pervasive. These all play a factor in lifestyle, health and aging. Let's talk more about 'inflammaging.' We know some inflammation can be good for the body to fight infections, for instance, but a lot can be bad. How does chronic inflammation potentially accelerate aging? Inflammation and aging are so tightly intertwined. The immune system is really the driver for good [when it attacks pathogens] and for bad when it promotes too much inflammation in walls of arteries or the brain. That's heart disease and neurodegenerative disease, respectively. But what's so exciting is we can dial up or down the immune system now. For example, [there have been] natural, amazing experiments with the shingles vaccines, which reduce dementia and Alzheimer's disease 20 to 25 percent. So how does that work? Well, [the vaccine] amps up the immune system in people and older adults. That's going to be the critical thing in using these metrics: zooming in on the immune system and inflammation to keep people's immune system intact and stop it when it starts to go haywire. That's the future. In the last chapter of the book, I presented the first cut of my ' immunome '—an assay of every virus and pathogen I've been exposed to, every antibody I have. But that's just scratching the surface. The immune system clock could turn out to be the most useful of all; if I could pick one, that's the one I would want. But the immune system is very complex. Maybe we don't have to do a systematic, comprehensive assessment of our immunome [that would include checking antibody titers and] sequencing B cells, T cells and interferons. If we can use just a group of plasma proteins, that would be terrific. That remains to be seen. There's a human immunome project just getting started to try to compare things such as the proteins with the much more sophisticated and expensive ways to get at the health of an immune system. What are the downsides of slowing down biological aging, or extending lifespan? We feel really great if we get to age 85. 'Super agers' who don't get one of the big four age-related diseases [type 2 diabetes, cancer, or heart or neurodegenerative disease] say 'Well, I did it.' Of course, if you get up to age 98, you're really doing well. I think we're going to have a whole lot more super agers. But that's not going to get around the fact that eventually they're going to develop some problems—one of the big four or other conditions. It could be you get an infection because your immune system is just too weak. Or it could be you break your hip because your bone density is so low and you wind up with a pulmonary embolus [a clot that blocks blood flow to the lungs]. Eventually you die, and you may have a chronic illness between that point of extended health span and when you die. I don't want to put a sense out there that super agers won't see problems in the latter stages of their lives. But the point is, let's extend the health span—high-quality life without these big age-related diseases—as much as we can before getting into the downturn of a health arc.
Fox News
28-06-2025
- Health
- Fox News
Ingredient in common kitchen herbs could target Alzheimer's, but don't change any recipes just yet
Experts believe they've identified a chemical compound in certain herbs that could help mitigate or prevent Alzheimer's disease — but before anyone makes a run for the spice rack, there are a few catches. In a study published in the journal Antioxidants earlier this year, researchers from the Scripps Research Institute identified a compound called carnosic acid, which is prevalent in rosemary and sage. The compound could prove therapeutic for neurodegenerative disorders, including Alzheimer's disease, the experts concluded. Carnosic acid contains "striking antioxidant [and] anti-inflammatory properties," the researchers wrote in the findings. Scripps Research postdoctoral associate Piu Banerjee and board-certified neurologist Dr. Stuart Lipton, based in California, spoke with Fox News Digital about the results. "In this study, we observed that administering this drug to mice that had advanced Alzheimer's-like disease significantly improved the number of neurons, as well as the number of synapses or connections between the brain cells," the team said. The experts added, "It also reduced inflammation that is caused by the current anti-amyloid antibody therapies. We also observed an improvement in the learning and memory behavior of the mice that received the drug." "From the results of our animal studies, we are cautiously optimistic for its success in the human clinical trials." Banerjee and Lipton also noted that carnosic acid is a "prodrug," meaning it's inactive at first — but once it enters the body, it's activated by oxidative and inflammatory stress. "It specifically targets cells undergoing oxidative and inflammatory stress, without affecting the healthy, normal brain cells," Banerjee said. "This further makes it a safe option for therapeutics." The experts agreed that carnosic acid could potentially improve the inflammation that generally occurs in most aging brains. There are cautions, however. Courtney Kloske, director of scientific engagement for the Chicago-based Alzheimer's Association, told Fox News Digital that studies based on a mouse model of Alzheimer's can be helpful but are not conclusive. There is insufficient clinical evidence to recommend rosemary and sage as a standard therapy. "Models are important in helping us understand the basic biology of the disease, but we need human studies in representative populations for ideas to be fully validated," Kloske said. "Therefore, while these are intriguing findings, more research is needed to understand the impacts and outcomes of these compounds on people living with, or at risk for, Alzheimer's." Cooking sage and rosemary won't provide the full anti-inflammatory effects, Banerjee and Lipton stressed. "Critically, one cannot take sufficient herbs safely to produce the same effect as our new drug," Banerjee said. The study, funded in part by the National Institutes of Health, did have some limitations, the researchers acknowledged. Kloske advised that, at this point, "no one should consume these herbs (or carnosic acid) to prevent or treat Alzheimer's or other cognitive impairment." Dr. Lee Murray, a neurologist in Jackson, Tennessee, echoed Kloske's concerns. "Before patients start incorporating rosemary and sage in every dish they eat, we need to remember these studies are pre-clinical," Murray told Fox News Digital. "Currently, there is insufficient clinical evidence to recommend rosemary and sage as a standard therapy for Alzheimer's dementia." Murray, however, said the data "is encouraging" and opens the door to additional pathways for potential therapeutics. Banerjee said she hopes that "our drug will start human clinical trials soon." She added, "If it proves to be effective, it will be a great new drug for those suffering from Alzheimer's … From the results of our animal studies, we are cautiously optimistic for its success in human clinical trials."
New York Times
03-06-2025
- Business
- New York Times
The U.S. Lit a Beacon for Science. Under Trump, Scientists Fear It's Dimming
Ardem Patapoutian's story is not just the American dream, it is the dream of American science. He arrived in Los Angeles in 1986 at age 18 after fleeing war-torn Lebanon. He spent a year writing for an Armenian newspaper and delivering Domino's at night to become eligible for the University of California, where he earned his undergraduate degree and a postdoctoral fellowship in neuroscience. He started a lab at Scripps Research in San Diego with a grant from the National Institutes of Health, discovered the way humans sense touch, and in 2021 won the Nobel Prize. But with the Trump administration slashing spending on science, Dr. Patapoutian's federal grant to develop new approaches to treating pain has been frozen. In late February, he posted on Bluesky that such cuts would damage biomedical research and prompt an exodus of talent from the United States. Within hours, he had an email from China, offering to move his lab to 'any city, any university I want,' he said, with a guarantee of funding for the next 20 years. Dr. Patapoutian declined, because he loves his adopted country. Many scientists just setting out on their careers, however, fear there is no other option but to leave. Scientific leaders say that's risking the way American science has been done for years, and the pre-eminence of the United States in their fields. China and Europe are on hiring sprees. An analysis by the journal Nature captured the reversal: Applications from China and Europe for graduate student or postdoctoral positions in the United States have dropped sharply or dried up entirely since President Trump took office. The number of postdocs and graduate students in the United States applying for jobs abroad has spiked. Want all of The Times? Subscribe.
Daily Mail
31-05-2025
- Health
- Daily Mail
Devastating blow in race for vaccine against deadly disease that affects millions
A major US research program to develop a vaccine against HIV has been abruptly canceled by the Trump administration, sparking outrage as infections rise and global prevention efforts stall. The administration's termination of the promising $258million research program stunned scientists, whose years-long project had also benefited the development of treatments for COVID-19, autoimmune conditions, and even snakebite antivenom. Researchers at Duke University and the Scripps Research Institute were informed on Friday that their funding would be cut. 'The consortia for HIV/AIDS vaccine development and immunology was reviewed by NIH leadership, which does not support it moving forward,' a senior official, who asked not to be named, told the New York Times. 'NIH expects to be shifting its focus toward using currently available approaches to eliminate HIV/AIDS.' 'I find it very disappointing that, at this critical juncture, the funding for highly successful HIV vaccine research programs should be pulled,' Dennis Burton, an immunologist who led the program at Scripps, told the New York Times. For decades, the United States has led the world in HIV research, pouring billions into cutting-edge science that turned a once-fatal virus into a manageable condition for millions. American labs were the first to crack the genetic code of HIV, to develop life-saving antiretroviral drugs, and to pioneer global initiatives like PEPFAR that saved more than 25 million lives worldwide. The now-axed vaccine program was another shining example of US scientific leadership, bringing together top researchers from coast to coast and pushing the boundaries of immunology. The cancellation is part of a broader rollback of federal HIV efforts. The NIH has also paused funding for a separate clinical trial of an HIV vaccine developed by Moderna. HIV rates remain high. In 2023 alone, the World Health Organization reported 1.3 million new infections, including 120,000 children. More than 32,000 people in the US contracted the virus last year and there was another 4,000 new cases in the UK. 'This is just inconceivable,' Mitchell Warren, executive director of the HIV prevention organization AVAC, told the New York Times. In some parts of the US, the effects are already being felt. In Texas, the state's Department of Health Services told grantees to pause HIV prevention activities 'until further notice.' In Mecklenburg County, North Carolina, 10 health department staffers have been laid off. Across Africa, several countries are reporting major disruptions in prevention work after delays in US aid. 'The HIV pandemic will never be ended without a vaccine, so killing research on one will end up killing people,' John Moore, an HIV researcher at Weill Cornell Medical College, said. 'The NIH's multiyear investment in advanced vaccine technologies shouldn't be abandoned on a whim like this.' Trial after trial has failed to produce a traditional HIV vaccine, but the Duke and Scripps teams had been taking a new approach: studying broadly neutralizing antibodies shown in animals to protect against multiple strains of the virus. That promising pipeline may now run dry. 'Almost everything in the field is hinged on work that those two programs are doing,' said Warren. 'The pipeline just got clogged.' During his first term, President Trump had supported efforts to curb the HIV epidemic. But in his second term, his administration has slashed prevention efforts, terminated several PrEP-related grants, and shut down the HIV prevention division at the CDC. While officials say the work may be transferred to a yet-to-be-formed federal agency, no details have been shared.
