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Yahoo
17 hours ago
- Health
- Yahoo
Gov. Polis signs bill meant to help Colorado tackle sexual assault kit backlog
Police evidence bag containing DNA swabs. (Tek Image/Science Photo Library via Getty Images) Colorado Gov. Jared Polis signed a bill Tuesday intended to improve to the Colorado Bureau of Investigations' capacity to review sexual assault kits, which include DNA samples and other evidence from survivors. Senate Bill 25-304 establishes the Colorado Sexual Assault Forensic Medical Evidence Review Board, which will review the effectiveness of the state's medical, legal and criminal response to sexual assault and make victim-centered recommendations to the Colorado Legislature. The governor and attorney general have until Aug. 1 to appoint members of the board, including representatives from state agencies and various organizations that advocate for sexual assault victims. The board will need to submit a preliminary report to the Legislature by Dec. 15. SUBSCRIBE: GET THE MORNING HEADLINES DELIVERED TO YOUR INBOX Law enforcement agencies overseeing sexual assault criminal cases will be required to update victims on the status of their kit every 90 days. The bill also sets a 60-day turnaround goal for crime labs reviewing forensic medical evidence from sexual assault kits. The agency's current goal is 90 days, which it expects to achieve in 2027. The estimated turnaround time for kits at the end of April was about a year and a half, with 1,369 kits in the backlog, according to a recently implemented data dashboard. Colorado's forensic services are facing a historic backlog of sexual assault kits due to reduced staff capacity and ballooning fallout from the discovery that a former CBI forensic scientist manipulated more than 1,000 DNA test results over her career. The backlog means delayed justice for survivors, as DNA evidence can often be critical for a criminal conviction. The bill originally would have created a full-time position to oversee the state's work to improve the kit review process, but it was amended to reduce spending given the tight budget year. Sponsors include Rep. Jenny Willford, a Northglenn Democrat, Rep. Meg Froelich, an Englewood Democrat, and Sen. Mike Weissman, an Aurora Democrat. SUPPORT: YOU MAKE OUR WORK POSSIBLE
National Geographic
7 days ago
- Science
- National Geographic
9 celestial events this June's, from a strawberry moon to interstellar clouds
The Milky Way and its core region in constellations Sagittarius and Scorpius, as seen from Dinosaur Provincial Park in Alberta, Canada. Composite Photograph by Alan Dyer, VW Pics/Science Photo Library Whether you're waking up early to spot Venus in the pre-dawn sky, staying up late to peep the Lagoon Nebula, or spending the whole night on the hunt for meteors, June's night sky has something for every stargazer. Here's what to keep an eye out for when you look up this month. (9 must-see night sky events to look forward to in 2025.) Venus at greatest western elongation—June 1 On June 1, Venus will reach its farthest distance west of the sun from the perspective of Earth—a point known as greatest western elongation. This is a particularly good time to get a glimpse at Earth's neighboring planet, as it won't be drowned out by sunlight. In some time zones, the exact timing of this event occurs on May 31, while in others, it's on June 1. But the best time to view Venus is just before dawn, when it rises in the eastern sky in the Northern Hemisphere, or the northeastern sky if you're in the Southern Hemisphere. A "well-placed" globular cluster—June 2 Missed seeing the "well-placed" globular clusters in May? The Great Hercules Cluster, or Messier 13, reaches its highest point in the night sky on June 2, putting it in a prime viewing position. Discovered in 1714 by English astronomer Edmond Halley, for whom the iconic Halley's Comet is named, the Great Hercules Cluster is a collection of more than 100,000 stars densely packed into a glittering, spheroidic shape. While it can be hard to discern with the naked eye, it's easily visible through binoculars. Daytime Arietids meteor shower peak—June 7 As its name implies, the prolific daytime Arietid meteor shower doesn't peak at night, but during the day. That, of course, makes most of the meteors nearly impossible to see. But there's still a chance of spotting shooting stars in the predawn hours on June 7, just before the estimated peak during the daylight hours. And if you want to "see" the daytime activity, visit the NASA Meteor Shower Portal and look for colored dots—those indicate meteors associated with the active meteor shower. The June full moon, known as the Strawberry Moon, rises over St Paul's Cathedral and The Shard in central London on June 22, 2024. Photograph by Peter Macdiarmid, eyevine/Redux The full Strawberry Moon rises behind the Empire State Building in New York City on June 21, 2024. Photograph by Gary Hershorn, Getty Images This month's full moon, known as the "Strawberry Moon," won't take on the red hue of its namesake fruit, but it is lovely nonetheless. The nickname, popularized by the Farmers' Almanac, is derived from Indigenous traditions in North America that link full moons to annual harvesting and hunting events. In June, that's the ripening of wild strawberries. (Learn about the lunar cycle and the origins of each month's full moon name.) Old European nicknames for the June full moon include the Mead or Honey Moon. According to NASA, this might be tied to the honey harvesting that happens during this month—and it could be the inspiration for the modern honeymoon, as ancient traditions called for June weddings. Mars and Regulus meet, and a "well-placed" Butterfly Cluster—June 16 Mars and the bright star Regulus—known for its colorful twinkling—will have a close encounter on June 16, with peak viewing occurring around 90 minutes after sunset. Regulus is a four-star system, as opposed to a single star, but only three of those four individual stars will be visible during this event through the eye of a telescope. Then, around midnight, the Butterfly Cluster will be "well-placed" in the night sky, reaching its highest point above the horizon. To see this butterfly-shaped open cluster of stars, grab a pair of binoculars. The summer Milky Way filling the night sky at Waterton Lakes National Park in Alberta, Canada. The pink glow of the Lagoon Nebula can be seen above the horizon, in the Milky Way galaxy's core. Composite Photograph by Alan Dyer, VW Pics/UIG/Getty Images Star clusters aren't the only "well-placed" celestial objects this month. The Lagoon Nebula, or Messier 8, is a swirling cloud of interstellar gas where stars are born, located some 5,200 light years away. It reaches its highest point in the night sky around midnight on June 22. From mid-latitudes in the Northern Hemisphere, the Lagoon Nebula can sometimes be seen with the naked eye under ideal viewing conditions. Otherwise, binoculars or a telescope is the best way to spot them. Prime stargazing conditions—June 25 On this night, there's a new moon lunar cycle, which means the sky will be plenty dark for stargazing. While brighter celestial objects like planets and stars are typically visible through the moon's light pollution, dimmer ones like distant galaxies and nebulae will be easier to see during the new moon, particularly through a telescope. (These are the best stargazing sites in North America.) If you're a photographer, this is the perfect time to try your hand at astrophotography. In the Northern Hemisphere, the Milky Way's galactic core rises high in the night sky throughout the summer, making it a prime focal point. A Bootid meteor seen photographed in June 2018. Photograph by Steve Dudrow, Getty Images The Bootids are a notoriously variable meteor shower, producing astonishing displays of hundreds of shooting stars some years, and just a few other years. If you're willing to try your luck, the meteor shower is expected to peak on June 27. And luck is already on your side—the moon will be barely illuminated as a waxing crescent, so it won't impede your view of fainter shooting stars. Close approach of the moon and Mars—June 30 To close out the month, the waxing crescent moon and Mars will put on a little show. Our celestial neighbors will pass within 1°16' of each other; if you hold your arm out fully toward the moon and stick your pinky finger up, your finger's width is about the distance between the pair, so you'll be able to see them simultaneously through binoculars. Keep an eye out for the "earthshine" phenomenon, where light reflected from Earth makes the unlit part of the crescent moon glow faintly. This most commonly happens just after sunset or right before sunrise.
National Geographic
16-05-2025
- Health
- National Geographic
Colon cancer is rising in young people. Finally, scientists have a clue about why.
As scientists question the rise in early colon cancer cases, a new study is offering some potential answers. Colored scanning electron micrograph (SEM) of a macrophage white blood cell (center) that is being destroyed by toxins released by E. coli bacteria (red). Some strains of E. coli release colibactin, a toxin which damages the DNA of cells, and may contribute to the development of colorectal cancer. Micrograph by Steve Gschmeissner, Science Photo Library Colorectal cancer should be on your radar: Today, one in five people under the age of 54 is diagnosed with the disease, marking an 11 percent uptick in this age group over the past two decades. What, exactly, is fueling the surge in younger patients has perplexed scientists and medical professionals alike. (Colon cancer is rising among young adults. Here are signs to watch for.) For years, however, experts have suspected that colibactin, a toxin produced by E. coli and other bacteria that can damage DNA, could be involved. Now, a new study published in Nature has identified a strong link between childhood exposure to colibactin and colorectal cancer in patients under the age of 40. Here's how the study expands scientists' understanding of the microbiome's influence on colorectal cancer development, plus how a focus on colibactin could pave the way for earlier detection and new prevention strategies. What researchers discovered in colon cancer patients The researchers initially designed the study to broadly explore why people in different countries develop colorectal cancer at different rates, so the colibactin observation was 'somewhat incidental,' says lead study author Ludmil Alexandrov, a professor of cellular and molecular medicine at the University of California, San Diego. He and his team analyzed blood and tissue samples from the tumors of nearly 1,000 colorectal cancer patients across 11 countries, including Canada, Japan, Thailand, and Colombia. They used DNA sequencing technology to identify cellular mutations, or genetic changes that can help cancer form, grow, and spread. 'Different carcinogens leave this characteristic pattern of mutations, which we call mutational signatures,' Alexandrov explains. 'The simplest example is if you smoke cigarettes, you get a specific pattern of mutations across your lung cells.' Alexandrov and his team found that people diagnosed with colorectal cancer under the age of 50 had a 'striking enrichment' of mutations associated with colibactin. The younger the person was, on average, the higher the prevalence of these signatures. Those diagnosed with colorectal cancer under age 40 were about three times more likely to have colibactin-driven mutations than those diagnosed after age 70. 'When we sequence cancers, we see this archeological record of everything that happened in that person's lifetime,' Alexandrov says. Meaning, scientists can figure out the approximate timing of when specific mutations took hold in the gut. The study's results suggest that the participants' colibactin exposure happened before they turned 10. This early 'hit' to the gut microbiome seemed to put people 20 to 30 years ahead of schedule for developing colorectal cancer, Alexandrov says. Rather than being diagnosed in their 60s or 70s, they faced the disease in their 30s or 40s. Cynthia Sears, an infectious disease expert and professor of oncology at the Johns Hopkins University School of Medicine, who was not involved in the study, believes the study was done 'carefully and thoroughly,' but also leaves questions unanswered. 'We don't understand the biology of these organisms and the circumstances that allow them to be mutational,' she says. Alexandrov agrees. He says this new study shows a 'strong association' between childhood colibactin exposure and early-onset colorectal cancer. However, proving that colibactin actually causes colorectal cancer would be 'very complicated.' How colibactin could lead to colorectal cancer Colibactin is a genotoxin—think of it as a weapon certain bacteria deploy to protect themselves against other microbes. Experts theorize that, in some people, these bacteria become dominant and then start hurting their hosts, Alexandrov explains. Once they colonize the colon, they can latch onto healthy tissues, attack cells, and generate DNA mutations. Fluorescence micrograph of human colon cancer cells in a three-dimensional extracellular matrix, where the cells organize into cancer organoids as they would in human tissue. Micrograph by Dr Torsten Wittmann, Science Photo Library A colored 3D computed tomography (CT) scan of the colon of a 54-year-old male patient, showing extensive narrowing (stenosis) in the left colon (highlighted, upper right), suggesting the presence of a cancerous lesion. Image by Zephr/Science Photo Library But not everyone with colibactin-producing bacteria winds up with colorectal cancer—estimates show 20 to 30 percent of people harbor these strains. So what's prompting the bugs to go rogue in certain individuals? 'We think something is happening to give them an advantage over the other bacteria,' Alexandrov says. He cites previous studies that suggest people in Westernized countries (particularly urban areas), like the U.S. and parts of Europe, tend to have a higher prevalence of colibactin-producing bacteria in their guts than those in more rural or non-industrialized regions. 'To me, this is a window of opportunity to zero in on environmental influences in different sectors of the world,' Sears says. In particular, evidence suggests that a Western diet—typically higher in red and processed meats, added sugar, and refined grains and lower in fruits and vegetables—is associated with a higher risk of colorectal cancer. As for the reason why colibactin, specifically, could be more 'mutagenic' in the setting this diet creates in the gut? 'We just don't have this information,' Sears says. The new study didn't analyze the participants' individual cancer risk or track changes in their environment or diet, so any combination of these components could be at play. Alexandrov and his team suspect factors that can substantially alter a person's immune system and microbiome in their earliest years, like whether they were born via a C-section or vaginally, took antibiotics, were breastfed or formula-fed, or were fed a lot of processed foods. (How your fiber intake impacts your colon cancer risk) Some colibactin-producing bacteria may also trigger an immune response that further injures the cells. Those are the strains that 'get us into trouble,' Sears says. But it's 'extremely complex' to figure out what makes these bacteria stick in different parts of the gut. 'The rectum is different than the sigmoid colon,' she explains. 'Each of these regions has a somewhat different biology and predilection to tumor formation.' Where the research goes from here Alexandrov and Sears agree that longitudinal data is needed. Ideally, researchers would follow people in early life, give them probiotics designed to target colibactin-producing bacteria, and then track whether participants develop the associated mutations, and thus, early-onset colorectal cancer. 'If we can create the right probiotic that would bump off the bad actors, that might be a prevention strategy that would be easy and not harmful to people,' Sears says. Alexandrov and his team are looking into future studies that explore this possibility. He also believes they could design a stool test that pinpoints colibactin-related mutations. If this DNA damage is detected in the test, then the individual would be encouraged to start colorectal cancer screening earlier—say, in their 20s versus their 40s. (Will a new colon cancer blood test replace your colonoscopy?) All that said, Sears believes focusing on colibactin alone likely isn't the 'holy grail' solution to the rise in early-onset cases. 'We don't want to be too short-sighted about the spectrum of the research that we do,' she says. Until we have more data, focusing on the lifestyle changes you can control is key; Sears points to eating a Mediterranean-style diet, staying active, quitting smoking, and cutting back on alcohol. Awareness is also paramount: Young adults—as well as many medical professionals—are quick to brush off colorectal cancer symptoms like persistent abdominal pain, unexplained weight loss, and rectal bleeding. As Alexandrov stresses, 'they should be aware that it may be something quite serious,' because the sooner the tumors are detected, the easier they will be to treat.
National Geographic
16-05-2025
- Health
- National Geographic
The ability to reverse damage to your lungs and heart is tantalizingly close
After decades of hype and setbacks, scientists have made impressive progress into tricking stem cells into repairing organs. Stem cells (like the ones above, growing in petri dishes) are able to differentiate into any type of cell in the body, including cells that generate and repair tissue that's been damaged by disease. Photograph by Massimo Brega, Science Photo Library In the 1986 movie Star Trek IV: The Voyage Home, Dr. McCoy hands a dialysis patient a single pill and she immediately grows a new kidney. That's the holy grail of regenerative medicine, and it has proven frustratingly elusive. When disease damages crucial organs like the heart or lungs, the best doctors can generally do is stop the harm from worsening. Now, after three decades of trial and error, the prospect of revving up the body's own stem cells to become advanced organ repair shops is tantalizingly close. Stem cells are crucial biological factories that manufacture the cells responsible for tissue growth and repair. A novel approach by Scripps Research, a nonprofit research institute in La Jolla, California, uses medicines to multiply these cells. The technique has brought dead tissue back to life in lab cells, mice, pigs, and a small number of people. Meanwhile, other scientists are finally finding some success with older techniques reprograming stem cells in the lab before implanting them to grow new tissue. If progress continues as expected, these methods could one day dramatically improve survival and quality of life for people with serious diseases, many of which, like osteoarthritis, are linked to aging. (Axolotls stop aging after four years—could studying them help humans live longer?) Most medicines work by slowing down disease progression, but these new drug candidates aim to repair damage. 'We have the potential in the next two to three years to show we can reverse lung damage and heart damage,' says Pete Schultz, CEO and President of Scripps Research, 'and if we do it will fundamentally change the way people think about reversing disease.' All the scientists involved emphasize that testing in people is still needed to confirm that the treatments are safe and effective, and it will likely be a decade before any might be approved for medical care. But after regenerative medicine's many false starts, they are optimistic they've finally turned the corner. Platelet-rich plasma injections are one of the current treatment options for osteoarthritis. While these injections can stimulate healing, the results have been mixed. Photograph by Henadzi Pechan, Getty Images Regenerative medicine has largely focused on extracting stem cells (like this one) from patients, altering them and re-implanting them in patients. Micrograph by Steve Gschmeissner, Science Photo Library At Scripps, the process began by screening millions of potential drug molecules to identify ones that stimulate an organ's naturally occurring, or endogenous, stem cells. Researchers identified compounds that expand the number of the healthy stem cells in the lungs, heart, joints, and eyes. (The concept of using small molecules this way is based on an earlier collaboration between Scripps and the nonprofit Genomics Institute of the Novartis Research Foundation, later integrated into the drug company Novartis.) Such an approach 'is interesting and powerful,' says Chuck Murry, director of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at the University of California's Keck School of Medicine, who is not involved with Scripps' program. Scripps' technique takes a giant step towards the famous scene from Star Trek, Murry says. Scripps' lung medicine activates stem cells in the lower airways, known as type 2 alveolar epithelial (AEC2) cells, responsible for manufacturing crucial cells for exchanging stale oxygen for fresh. In healthy people, new gas-exchange cells continually replace damaged ones, but the process is blunted in medical conditions such as chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, or when lungs are damaged by wildfire smoke or viral infections like COVID-19. Studies in mice show the once-weekly inhaled drug stimulates enough AEC2 stem cells to repair lungs damaged by fibrosis, a severe and often fatal disease where scar tissue makes it hard to breathe. Safety tests in some 70 healthy people are now underway, with plans later add some with fibrosis. Using medicine to stimulate the stem cells in the lungs could be a game changer because it could be widely deployed, says Maurizio Chioccioli, assistant professor of comparative medicine and genetics at the Yale School of Medicine, who is not involved with Scripps. 'You can imagine it easily being used, because someone can inhale the drug that directly targets the cells,' Chioccioli says. His own research using real-time imaging of lung stem cells found they surprisingly move and change shape during repair, processes that must be accounted for when designing treatments. This lab-grown heart was made from pluripotent stem cells. Researchers hope to use drugs to induce heart tissue to regrow in the body rather than in a lab. Photograph by Philip Fong, AFP/Getty Images Slightly behind in the pipeline is another Scripps drug to rebuild cardiac tissue following a heart attack. Today, stents and medicine reopen blood vessels and return flow, a technique that has more than halved heart-attack mortality in recent decades. 'We've dramatically improved survival, but there's still a lot of dead muscle there,' says Richard Stack, a cardiologist at Duke University. 'If we can make that region that was not functioning start beating again, now we've really accomplished something.' Stack is managing partner of the Cardiovascular Masters Consortium, a consulting firm of top-level physicians working with Scripps on the medicine. The drug is a hydrogen gel that is injected into the sac surround the heart muscle days after a heart attack, which activates a protein pathway that otherwise lies dormant once the heart reaches adult size. The newly reactivated stem cells generate healthy cells that fill areas of the heart sustaining damage. The drug works in laboratory mice and a small number of pigs, Scripps says, although results are unpublished and not yet peer-reviewed. Imaging from one pig revealed that its ejection fraction—a crucial gauge of the heart's ability to pump oxygen-rich blood to the body—plunged following the heart attack but returned to normal a month after treatment. Testing in additional pigs is underway, with human trials expected to start in 2027. Stack was 'blown away' by the early animal results. 'I've not seen anything so dramatic in 44 years of practice,' he says. Gaining success with older techniques Meanwhile, Murry and his colleagues at the University of Southern California are reprogramming adult blood stem cells to become heart muscle cells that are then transplanted. After decades of stop-and-go progress, the method finally works. 'We are making new muscles in the heart that is improving heart function; the science is there,' Murry says. The technique has been tested in mice, rats, guinea pigs, nonhuman primates, and pigs, with human trials expected to start in 2027. 'I have a rational basis to say we've hit all the major roadblocks we're going to,' Murry says. The final obstacle was that, in rhesus macaque monkeys, the new cells beat too fast the first few months after transplantation, triggering palpitations. Giving the animals drugs that modulate their heart rhythm or, alternatively, employing gene editing in the cells before implanting solved the problem. In a study published July 2024, two monkeys embraced the new cells without incident when treated after a heart attack, their hearts beating as if they never sustained injury. Past and future speed bumps in regenerative medicine As with older techniques, the approach of using drugs to stimulate the body's natural stem cells isn't without setbacks. Scripps has also been trying to target stem cells to generate new joint cartilage for osteoarthritis, but the drug hit hurdles before its final lap. The medicine proved effective in animal models by inducing stem cells to make new joint tissue. But injecting the drug into the knees of 60 people in an early-stage clinical trial didn't produce sufficient quantities of cartilage to make a meaningful difference, according to unpublished research. Scripps has pulled back further studies until it develops a longer-lasting formulation. Novartis is also testing a drug to stimulate cartilage regrowth, successfully completing a small safety study in some two dozen patients. The company is in the process of testing a larger number of people for safety and effectiveness; company officials are not yet commenting on its progress. While the finish line for regenerative medicine is closer than ever, new challenges may yet emerge. One is ensuring the sweet spot between growing wanted tissue and overstimulating cells, which could lead to cancer. 'The real challenge moving forward is to try to figure out where, when and how much to activate these pathways, to enhance the repair without triggering unintended consequences,' Yale's Chioccioli says. Scientists are so far heartened by the lack of this issue in their smaller safety studies and in Murry's pig research, which found no abnormal cells in the heart or other organs. After decades of experimentation, it may finally soon be possible to repair damaged organs in a way that gives sick people a new shot at a quality life, says Mike Bollong, associate professor of chemistry at Scripps Research. 'That's really what regenerative medicine is about.'
National Geographic
13-05-2025
- Health
- National Geographic
The real science of brain rot
TikTok won't really make your brain rot. That doesn't happen until after death. While most brains rot quickly, researchers have found a surprising number preserved in the archaeological record. Photograph by Zephyr/Science Photo Library In 2024, the Oxford University Press declared 'brain rot' the word of the year. If Ohio is just a midwestern state to you and mewwing is something your cat does, you might not be as familiar with the term as those who have adopted the Gen Z and Alpha lexicons that popularized it. Still, you've probably encountered its effects. 'Brain rot' describes the supposed mental decline resulting from too much time spent in the chasms of the digital world reserved for trivial content. But, while endless hours scrolling on TikTok may prompt a headache, strained eyes, and the latest trending sound to loop in your head, 'your brain doesn't literally rot until after death,' says Andy McKenzie, a neuroscientist who studies functional brain preservation at the nonprofit Apex Neuroscience in Oregon. And the science behind that process is far from dull. While there's actually no one way for a brain to rot, it usually involves dying cells and hungry decomposers, not doomscrolling. Typically, brains decay quickly after death. But researchers are increasingly finding samples of brains that have been preserved for hundreds and even thousands of years. Studying how brains decompose (or don't) is difficult but could reveal clues about the lives of the humans to which they belonged. These brain fragments ocame from an individual buried in a Victorian workhouse cemetery in the United Kingdom, some 200 years ago. No other soft tissue survived amongst the bones, which were dredged from the heavily waterlogged grave. Photograph Courtesy Alexandra L. Morton-Hayward (Here's what happens to your brain when you take a break from social media.) After death, your brain cells eat themselves Eventually, everyone's heart stops beating, their lungs stop respirating, and their brain stops functioning. This begins a process of decomposition. Blood flow stops, and cells stop getting the energy they need to live. 'The cell doesn't really want to die, but it just kind of passively breaks down,' McKenzie says. At the cellular level, this process is called autolysis, and it's responsible for the initial decomposition of the brain. 'The brain is the most metabolically active organ in the body,' says Alexandra Morton-Hayward, a forensic anthropologist at the University of Oxford. 'It's two percent of our body weight that consumes 20 percent of our energy, and cells that have a really high energy demand after death, when there's no more energy input, digest themselves really quickly.' Over a matter of hours and days, as enzymes break down cells and proteins, the brain begins to lose its form. The rippling structures that give a brain its typical look lose their shapes and disintegrate first into a paste and then into an even goopier substance. 'Generally, the brain will liquefy within the first three days,' Morton-Hayward says. If the brain doesn't digest itself quickly enough, there are plenty of organisms willing to help. Coming across a decaying brain is like hitting the buffet jackpot for voracious detritivores—bacteria and other organisms that consume dead tissue. As a forensic archaeologist at the University of Otago in New Zealand, Charlotte King, puts it, 'Everything that's there is this soft, squishy, organic substance that bacteria just love to eat.' The entire decay process from corpse to skeleton can take days, weeks, or even years. 'Just as we're all very different in life, we will decay very differently after death,' says Morton-Hayward, who was an undertaker before she was an anthropologist. Factors from the medications we take in life to the climate we die in can all impact the process drastically. (Alarming levels of microplastics can be found in human brains.) Modern funeral practices, like embalming, can equalize some of these differences, but burial environments vary; a brain of someone who died in Alaska's climate might still look quite different than someone who died in Florida's. In this case, think of Alaska like a refrigerator and Florida like a kitchen table. 'If you leave the milk on the kitchen table, then that's going to unfortunately go bad in a day,' McKenzie says. 'But if you leave it out in the fridge, it's going to be stable for a couple weeks.' There are a few reasons for this, he says. Bacteria tend to thrive a higher temperatures, and autolysis enzymes work best at body temperature. Phoebe Stubblefield, forensic anthropologist and the director of the University of Florida's C.A. Pound Human Identification Lab, sees this happen a lot. 'In warm environments like Florida? Oh yeah, decomp is a daily process, an hourly one,' she says. Some brains resist rotting Regardless of the environment, a brain often decays relatively rapidly compared to other parts of the body. It might last longer than some soft tissues, like the intestines, but it often liquifies faster than many other soft tissues. But there are the outliers, brains that have survived decades, centuries, even millennia, and researchers are finding them more and more often. 'The basic story is that the brain is the first organ to decompose in the human body, and we've just accepted that and run with it,' says Brittany Moller, a Ph.D. student at James Cook University who spearheaded an archaeological project on brains with King. 'And the more you look into that, you realize, well, we don't actually know that. That is an assumption that has been made, and now we're seeing it's not necessarily the case.' In 2024, Morton-Hayward and her colleagues reported that over 4,000 brain specimens from around the globe and across 12,000 years of history exist in the archaeological record. They're shrunken with time, and they're usually orange from residual iron. But all are still clearly human brains. The brains she's studied come from environments as different as they can possibly be, from freezing tundras to warm swamps. Many specimens are well-preserved because they were in environments without water, either dehydrated or frozen. Some were preserved in peat bogs, an environment known to preserve all sorts of soft tissues. And some were even preserved, not despite their moist, swampy environments, but because of them. Medical repositories like the Harvard Brain and Tissue Resource Centre (shown above) store thousands of healthy and diseased brains preserved in formalin and kept in plastic tubs. But in natural environments brains tend to decay very quickly. Photograph by Volker Steger, Science Photo Library 'Conventionally, we think of like a high water content and a high temperature as being absolutely not conducive to preservation,' Morton-Hayward says. A low-oxygen environment can be helpful for preservation because bacteria can't grow, 'but in these waterlogged, oxygen poor environments, we have no other soft tissue remaining. So it suggests that the brain, somehow, in some circumstances behaves differently in a waterlogged environment, which is really weird, and not well understood.' (Did Mount Vesuvius' ash cloud really transform a brain into glass?) What preserved brains can tell us Although researchers don't fully understand long-term brain preservation, preserved brains have already yielded clues about the lives of the people they belonged to. For example, King and Moller found syphilis bacteria in a specimen from a 19th-century gold rush cemetery in New Zealand, though it's unclear if the infection occurred during the individual's life. But for every brain that has survived in these environments, there are many more that haven't. Knowing that certain environments may facilitate preservation doesn't tell us exactly why, when brains typically liquify in a matter of days across a variety of environments, these brains lasted. Still, each new discovery tells us a little more about the people who came before us. 'You are a product of all those people who've come before you, of all their life experiences,' King says. 'If understanding them through their brain tissue is something extra that we can add, then that's great.' While we'll never be able to tell how many TikTok videos someone watched from their preserved brain, perhaps, one day, researchers might be able to detect clues about their mental health. That's something Morton-Hayward hopes to research. 'These things have affected us in our human history for a really long time, but they don't leave any marks on the bones. Depression, schizophrenia…these are kind of silent in history,' she says. 'We have no good way of studying things like mental health or psychiatric disease in the past, and it would be so fascinating to be able to study those with the actual tissue that it affected. But we can't do that in a meaningful way without understanding first, how on earth these things have preserved for thousands of years when they really shouldn't.' But until then, with each brain she studies, Morton-Hayward hopes to raise awareness among archaeologists that not only is brain preservation possible in archaeological settings, it's more common than we might think. Before, archaeologists might have assumed these squiggly structures decayed far earlier or mistaken them for something else entirely. Now, they know what to look for. 'I do think many have been destroyed in the past by accident,' she says, 'But hopefully that's something of the past, no pun intended.'
