By Paula Span For years, the two patients had come to the Penn Memory Center at the University of Pennsylvania, where doctors and researchers follow people with cognitive impairment as they age, as well as a group with normal cognition. Both patients, a man and a woman, had agreed to donate their brains after they died for further research. “An amazing gift,” said Dr. Edward Lee, the neuropathologist who directs the brain bank at the university’s Perelman School of Medicine. “They were both very dedicated to helping us understand Alzheimer’s disease.” The man, who died at 83 with dementia, had lived in the Center City neighborhood of Philadelphia with hired caregivers. The autopsy showed large amounts of amyloid plaques and tau tangles, the proteins associated with Alzheimer’s disease, spreading through his brain. Researchers also found infarcts, small spots of damaged tissue, indicating that he had suffered several strokes. By contrast, the woman, who was 84 when she died of brain cancer, “had barely any Alzheimer’s pathology,” Dr. Lee said. “We had tested her year after year, and she had no cognitive issues at all.” The man had lived a few blocks from Interstate 676, which slices through downtown Philadelphia. The woman had lived a few miles away in the suburb of Gladwyne, Pa., surrounded by woods and a country club. The amount of air pollution she was exposed to — specifically, the level of fine particulate matter called PM2.5 — was less than half that of his exposure. Was it a coincidence that he had developed severe Alzheimer’s while she had remained cognitively normal? With increasing evidence that chronic exposure to PM2.5, a neurotoxin, not only damages lungs and hearts but is also associated with dementia, probably not. © 2025 The New York Times Company

Keyword: Alzheimers; Neurotoxins
Link ID: 30000 - Posted: 11.05.2025

By Ramin Skibba In August, two parents in California filed a lawsuit against OpenAI, claiming that the company was responsible for their teenage son’s suicide. The previous fall, according to Maria and Matthew Raine, their 16-year-old, Adam, had started using the company’s popular AI chatbot ChatGPT as a homework helper. Over the course of several months, the Raines alleged, it shifted to a digital companion and then to a “suicide coach,” advising the teen how to quietly steal vodka from his parent’s liquor cabinet, urging him to keep his suicidal ideations a secret, and then guiding him about the feasibility and load-bearing capacity of a noose. By the time of Adam’s death in April, according to the Raines’ complaint, the chatbot had used the word “suicide” 1,275 times, six times more often than Adam himself. The case of Adam Raines was not an isolated incident, though publicly available data remains limited. And experts worry that more mental health crises, including suicides — the second leading cause of death among people between ages 10 and 24 years — could arise as users increasingly turn to generative AI chatbots for emotional support. Although it is difficult to pinpoint just how many people are relying on chatbots in this way, according to a recent Harvard Business Review survey based primarily on data collected from Reddit forum posts, the practice is common for therapy, companionship, and finding purpose. Researchers have scrambled to understand the trend, including both the potential risks and benefits of the chatbots, most of which were not designed to be used for mental health support. Some users claim that the bots help them, citing their perception that the tools won’t judge or stigmatize them, while others are seeking a substitute for therapy when they can’t access or afford it, experts say. Some users also don’t think of the chatbots as a form of therapy, but rather a kind of mindful journaling as they work through their emotions and problems. According to one example in the Harvard Business Review report, a Reddit user said, “I found a thread where people talked about using AI to analyze their moods, essentially having low-barrier ‘therapy’ sessions.

Keyword: Depression
Link ID: 29999 - Posted: 11.05.2025

Ian Sample Science editor Even modest amounts of daily exercise may slow the progression of Alzheimer’s disease in older people who are at risk of developing the condition, researchers have said. People are often encouraged to clock up 10,000 steps a day as part of a healthy routine, but scientists found 3,000 steps or more appeared to delay the brain changes and cognitive decline that Alzheimer’s patients experience. Results from the 14-year-long study showed cognitive decline was delayed by an average of three years in people who walked 3,000 to 5,000 steps a day, and by seven years in those who managed 5,000 to 7,000 steps daily. “We’re encouraging older people who are at risk of Alzheimer’s to consider making small changes to their activity levels, to build sustained habits that protect or benefit their brain and cognitive health,” said Dr Wai-Ying Yau, the first author on the study at Mass General Brigham hospital in Boston. Dementia affects an estimated 50 million people worldwide, with Alzheimer’s disease the most common cause. In the UK, more than 500,000 people have Alzheimer’s. The condition is linked to the buildup of two toxic forms of proteins in the brain, namely amyloid-beta plaques and tau tangles. Yau and her colleagues analysed data from 296 people aged 50 to 90 who were cognitively unimpaired at the beginning of the study. The data included annual cognitive assessments, step counts measured by pedometers, and PET imaging to detect levels of amyloid and tau in the volunteers’ brains. People with little brain amyloid at the start showed very little cognitive decline or buildup of tau protein over the course of the study. The risk of Alzheimer’s was greater for those with elevated amyloid at baseline, and among them, higher step counts were linked to slower rates of cognitive decline and a delayed buildup of tau proteins. In sedentary individuals, the buildup of tau and cognitive decline was substantially faster, the researchers report in the journal Nature Medicine. © 2025 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29998 - Posted: 11.05.2025

By Denise Grady Dr. Marthe Gautier, a physician and researcher who had a major role in identifying the cause of Down syndrome but whose achievement was undermined when a male colleague took credit for her work, died on April 30, 2022. She was 96. Her death, in a retirement home in Meaux, France, though not widely reported at the time, was confirmed by her great-niece Tatiana Giraud. The New York Times, which had prepared an obituary about Dr. Gautier in advance, in 2018, learned of her death only recently. The disputed research in which Dr. Gautier was involved produced a historic breakthrough: It revealed that people with Down syndrome have an extra chromosome, one of the microscopic strands of DNA and protein that carry a person’s genetic blueprint. Most humans have 46 chromosomes. Down syndrome is also called trisomy 21, meaning that three copies of the 21st chromosome are present instead of two, for a total of 47 chromosomes. The discovery, at the Armand-Trousseau Hospital in Paris in 1958, was the first to link an abnormal number of chromosomes to a disorder that causes intellectual disability. More connections between such conditions and aberrant chromosomes were soon found. Those advances led to the development of tests to diagnose the disorders before birth, making it possible to terminate affected pregnancies in many cases. Dr. Gautier’s story “starts like a fairy tale and ends like villainy,” said Dr. Jean Kachaner, a former student of hers who is a pediatric cardiologist at the Necker Hospital for children in Paris. © 2025 The New York Times Company

Keyword: Development of the Brain; Genes & Behavior
Link ID: 29997 - Posted: 11.05.2025

By Kaia Glickman Anyone with a computer has been asked to “select every image containing a traffic light” or “type the letters shown below” to prove that they are human. While these log-in hurdles — called reCAPTCHA tests — may prompt some head-scratching (does the corner of that red light count?), they reflect that vision is considered a clear metric for differentiating computers from humans. But computers are catching up. The quest to create computers that can “see” has made huge progress in recent years. Fifteen years ago, computers could correctly identify what an image contains about 60 percent of the time. Now, it’s common to see success rates near 90 percent. But many computer systems still fail some of the simplest vision tests — thus reCAPTCHA’s continued usefulness. Digital artwork, one in a series displayed at CERN in Geneva. The foreground shows a particle collision event which is a possible candidate for a decay of the Higgs-like particle to a final state. The background depicts selected pages from articles published by the CMS collaboration at the LHC. Newer approaches aim to more closely resemble the human visual system by training computers to see images as they are — made up of actual objects — rather than as just a collection of pixels. These efforts are already yielding success, for example in helping develop robots that can “see” and grab objects. Computer vision models employ what are called visual neural networks. These networks use interconnected units called artificial neurons that, akin to in the brain, forge connections with each other as the system learns. Typically, these networks are trained on a set of images with descriptions, and eventually they can correctly guess what is in a new image they haven’t encountered before.

Keyword: Vision; Robotics
Link ID: 29996 - Posted: 11.01.2025

By Ellen Barry One of the most popular mental health innovations of the past decade is therapy via text message, which allows you to dip in and out of treatment in the course of a day. Say you wake up anxious before a presentation: You might text your therapist first thing in the morning to say that you can’t stop visualizing a humiliating failure. Three hours later, her response pops up on your phone. She suggests that you label the thought — “I’m feeling nervous about my presentation” — and then try to reframe it. She tells you to take a deep breath before deciding what is true in the moment. You read her answer between meetings. “I’m pretty sure my boss thinks I’m an idiot,” you type. The therapist responds the next morning. “What evidence do you have that she thinks that?” she asks. She tells you to write a list of the available evidence, pros and cons. Text-based therapy has expanded swiftly over the past decade through digital mental health platforms like BetterHelp and Talkspace, which pair users with licensed therapists and offer both live chat and as-needed texting sessions. A new study published on Thursday in the journal JAMA Network Open provides early evidence that the practice is effective in treating mild to moderate depression, finding outcomes similar to those of video-based therapy. In a clinical trial, 850 adults with mild to moderate depression were randomly assigned to two groups: One group received psychotherapy via a weekly video session; the other received unlimited, as-needed messaging or emailing with a therapist. After 12 weeks, participants in both groups reported similar improvement in depression symptoms. © 2025 The New York Times Company

Keyword: Depression
Link ID: 29995 - Posted: 11.01.2025

By Sarah DeWeerdt A temporary increase in neuronal activity in the cortex of newborn mice leads to social deficits in adulthood, according to a new preprint. Those adult rodents also show changes in brain electrical activity, gene expression and connectivity that are reminiscent of autism. The analysis lends support to a prominent hypothesis of autism’s origins, which holds that the condition can arise from an excess of excitatory signaling or insufficient inhibitory signaling in the brain, the study investigators write in their paper. Over the years, support for this signaling imbalance hypothesis has come from other studies in mice and observations that some people with autism have seizures or display excess neuronal activity in electroencephalography (EEG) recordings relative to people without the condition. Postmortem analysis suggests autistic people have more excitatory synapses in the prefrontal cortex than non-autistic people. But determining causality and the role of inhibitory signaling has been difficult. In contrast with most earlier work, the new study “really underscore[s] a different way of looking at excitation-inhibition imbalance, which is looking at it during development as a cause of subsequent changes in brain function that could be associated with autism,” says Vikaas Sohal, professor of psychiatry and behavioral science at the University of California, San Francisco, who was not involved in the work. The study was posted on bioRxiv last month. © 2025 Simons Foundation

Keyword: Development of the Brain; Autism
Link ID: 29994 - Posted: 11.01.2025

Ian Sample Science editor It’s never a great look. The morning meeting is in full swing but thanks to a late night out your brain switches off at the precise moment a question comes your way. Such momentary lapses in attention are a common problem for the sleep deprived, but what happens in the brain in these spells of mental shutdown has proved hard to pin down. Now scientists have shed light on the process and found there is more to zoning out than meets the eye. The brief loss of focus coincides with a wave of fluid flowing out of the brain, which returns once attention recovers. “The moment somebody’s attention fails is the moment this wave of fluid starts to pulse,” said Dr Laura Lewis, a senior author on the study at MIT in Boston. “It’s not just that your neurons aren’t paying attention to the world, there’s this big change in fluid in the brain at the same time.” Lewis and her colleague Dr Zinong Yang investigated the sleep-deprived brain to understand the kinds of attention failures that lead drowsy drivers to crash and tired animals to become a predator’s lunch. In the study, 26 volunteers took turns to wear an EEG cap while lying in an fMRI scanner. This enabled the scientists to monitor the brain’s electrical activity and physiological changes during tests in which people had to respond as quickly as possible to hearing a tone or seeing crosshairs on a screen turn into a square. Each volunteer was scanned after a restful night’s sleep at home and after a night of total sleep deprivation supervised by scientists at the laboratory. Unsurprisingly, people performed far worse when sleep deprived, responding more slowly or not at all. © 2025 Guardian News & Media Limited

Keyword: Sleep; Attention
Link ID: 29993 - Posted: 11.01.2025

Imma Perfetto Anyone who has ever struggled through the day following a poor night’s sleep has had to wrench their attention back to the task at hand after their mind drifted off unexpectedly. Now, researchers have pinpointed exactly what causes these momentary failures of attention. The new study in Nature Neuroscience found that the brains of sleep-deprived people initiate waves of cerebrospinal fluid (CSF), the liquid which cushions the brain, which dramatically impaired attention. This process usually happens during sleep. The rhythmic flow of CSF into and out of the brain carries away protein waste which has built up over the course of the day. When this is maintenance interrupted due to lack of sleep, it seems the brain attempts to play catch up during its waking hours. “If you don’t sleep, the CSF waves start to intrude into wakefulness where normally you wouldn’t see them,” says study senior author Laura Lewis of Massachusetts Institute of Technology’s (MIT) Institute for Medical Engineering and Science. “However, they come with an attentional trade off, where attention fails during the moments that you have this wave of fluid flow. “The results are suggesting that at the moment that attention fails, this fluid is actually being expelled outward away from the brain. And when attention recovers, it’s drawn back in.” © Copyright CSIRO

Keyword: Sleep; Attention
Link ID: 29992 - Posted: 11.01.2025

By Nima Sadrian In the popular narrative, cannabidiol, or CBD, is portrayed as a natural, non-intoxicating cure for a host of ailments — and sometimes that extends to the anxieties of modern adolescence. CBD is everywhere, infused in products such as gummy candies, vapes, skincare serums, and even fizzy seltzers. Usually derived from the hemp plant, CBD is pitched as a calming remedy with none of the stigma of marijuana. Even a 2018 World Health Organization report noted that CBD shows no signs of abuse or dependence potential. But as a physician and neuroscientist who studies how CBD affects the developing brain, I have to offer a different, more troubling answer: We simply don’t know if it’s safe for teens. And early evidence suggests potential for real, lasting harm. The comforting story our culture tells itself about CBD — that it offers harmless, botanical relief for stress and sleep problems — is dangerously out of step with the science. While we have been sold a simple wellness narrative, my own work and that of other scientists reveal a far more complex and cautionary tale — one that challenges the very foundation of the multibillion-dollar CBD industry. How did a compound that the Food and Drug Administration has only approved as a potent prescription drug for severe childhood epilepsy become a common additive? The answer lies in a catastrophic regulatory failure. The 2018 farm bill legalized hemp, but the legislation and its extensions created no framework to ensure that the products made from it were safe, effective, or accurately labeled, nor did the bill set an age limit for it. The result is a market that operates like the Wild West, a gold rush where consumer safety is an afterthought. The FDA-approved CBD medicine, Epidiolex, comes with a long list of documented risks, including liver damage and suicidal ideation, and requires careful medical supervision. Yet numerous consumer products containing CBD are sold without such warnings, mandatory testing, or oversight.

Keyword: Drug Abuse; Development of the Brain
Link ID: 29991 - Posted: 11.01.2025

Joel Snape All vertebrates yawn, or indulge in a behaviour that’s at least recognisable as yawn-adjacent. Sociable baboons yawn, but so do semi-solitary orangutans. Parakeets, penguins and crocodiles yawn – and so, probably, did the first ever jawed fish. Until relatively recently, the purpose of yawning wasn’t clear, and it’s still contested by researchers and scientists. But this commonality provides a clue to what it’s really all about – and it’s probably not what you’re expecting. “When I poll audiences and ask: ‘Why do you think we yawn?’, most people suggest that it has to do with breathing or respiration and might somehow increase oxygen in the blood,” says Andrew Gallup, a professor in behavioural biology at Johns Hopkins University. “And that’s intuitive because most yawns do have this clear respiratory component, this deep inhalation of air. However, what most people don’t realise is that that hypothesis has been explicitly tested and shown to be false.” To test the idea that we yawn to bring in more oxygen or expel excess carbon dioxide, studies published in the 1980s manipulated the levels of both gases in air inhaled by volunteers – and they found that while changes did significantly affect other respiratory processes, they didn’t influence the regularity of yawns. There also doesn’t seem to be any systematically measurable difference in the yawning behaviour of people suffering from illnesses associated with breathing and lung function – which is what you would expect if yawns were respiration-related. This, more or less, was where Gallup came to the subject. “When I was pursuing my honours thesis, my adviser at the time said, well, why not study yawning, because nobody knows why we do it?” he says. “That was intriguing – we knew it had to serve some underlying physiological function. So I started to examine the motor action pattern it involves – this extended gaping of the jaw that’s accompanied by this deep inhalation of air, followed by a rapid closure of the jaw and a quicker exhalation. And it occurred to me that this likely has important circulatory consequences that are localised to the skull.” © 2025 Guardian News & Media Limited

Keyword: Emotions; Sleep
Link ID: 29990 - Posted: 10.29.2025

By Katarina Zimmer The 10 snakes faced a tough predicament. Collected from the Colombian Amazon, they had been without food for several days in captivity and then were presented with extremely unappetizing prey: three-striped poison dart frogs, Ameerega trivittata. The skin of those frogs contains deadly toxins — such as histrionicotoxins, pumiliotoxins and decahydroquinolines — that interfere with essential cell proteins. Six of the royal ground snakes (Erythrolamprus reginae) preferred to go hungry. The other four intrepidly slithered in for the kill. But before swallowing their meals, they dragged the frogs across the ground — akin to the way some birds rub toxins off their prey, noted biologist Valeria Ramírez Castañeda of the University of California, Berkeley, and her colleagues, who conducted the experiment. In a recent study, some royal ground snakes dragged poison frogs along the ground before eating them, probably in an effort to rub off some of the frogs’ deadly toxins. Three of the four snakes survived the meal — suggesting that their bodies were capable of handling the toxins that remained. Living beings have been wielding deadly molecules to kill each other for hundreds of millions of years. First came microbes that used the chemicals to weed out competitors or attack host cells they were invading; then animals, to kill prey or ward off predators, and plants, to defend against herbivores. In response, many animals have evolved ways to survive these toxins. They sometimes even store them to use against opponents.

Keyword: Neurotoxins; Evolution
Link ID: 29989 - Posted: 10.29.2025

By Sara Talpos As a new Ph.D. student in 2011, Steve Ramirez and his mentor performed a groundbreaking experiment in the field of memory manipulation. They placed a mouse in a small distinctive box and administered a mild electrical shock to its feet. When the rodent was placed in the box a second time, it froze up — anticipating another shock. From there, the young neuroscientists placed the mouse in a different box, one where nothing bad had happened. They then directed pulses of light to a very specific region in the mouse’s brain that had been genetically modified to respond to the light. This caused the mouse to immediately freeze. Ramirez and his mentor, it turned out, had found a way to artificially activate a fear-inducing memory. “How to Change a Memory: One Neuroscientist’s Quest to Alter the Past,” by Steve Ramirez will be available on November 4, 2025 (Princeton University Press, 256 pages). What was the point? A central goal of such science is to learn how memories form and function in the brain and to then apply this knowledge to treat brain disorders, writes Ramirez in his forthcoming book, “How to Change a Memory: One Neuroscientist’s Quest to Alter the Past.” Perhaps one day, he suggests, it will be possible to activate positive memories to curb depression or to retrieve memories that have seemingly been lost to Alzheimer’s disease. In the book, Ramirez explores the fascinating science of memory while tracing his own journey to becoming a successful professor at Boston University. His path was not without challenges, including the sudden death of his mentor and a decade-long struggle with alcohol addiction. “This book,” he writes, “is my attempt to make sense of the enigma of memory — the snippets of remembrances, the brief moments in time, the decisions we make, the blackouts, the imagined, and the dreamt of — all the things the brain does to breathe life into the past so that we can heal and become whole again.”

Keyword: Depression; Learning & Memory
Link ID: 29988 - Posted: 10.29.2025

Jon Hamilton In April, the future was looking bleak for an experimental Alzheimer's drug called valiltramiprosate, or ALZ-801. Researchers had just released topline results of a study of more than 300 people age 50 or older, who were genetically predisposed to Alzheimer's. Overall, those who got the drug did no better than those given a placebo. But in September, a closer look at the results revealed benefits for a subgroup of 125 people who had only mild memory problems when they started taking the drug. Those participants, initially diagnosed with mild cognitive impairment rather than mild dementia, "showed very meaningful responses," says Dr. Susan Abushakra, chief medical officer of Alzheon, the drug's maker. By one measure, the drug slowed cognitive decline by 52% in people with mild cognitive impairment. That result appears comparable with benefits from the two Alzheimer's drugs now on the market: lecanemab and donabemab. But the true effect of ALZ-801 is hard to quantify because of the relatively small number of participants in the group with mild cognitive impairment. Three scientists learned they carry genes that significantly increase their risk for Alzheimer’s. Here's how they're grapping with the news, and working to keep their brains healthy. More robust results came from measures of brain atrophy — the shrinkage that tends to come with Alzheimer's. © 2025 npr

Keyword: Alzheimers
Link ID: 29987 - Posted: 10.29.2025

By Roberta McLain Two small genetic changes reshaped the human pelvis, setting our early ancestors on the path to upright walking, scientists say. One genetic change flipped the ilium — the bone your hands rest on when you put them on your hips — 90 degrees. The rotation reoriented the muscles that attach to the pelvis, turning a system for climbing and running on all four legs into one for standing and walking on two legs. The other change delayed how long it takes for the ilium to harden from soft cartilage into bone, evolutionary biologist Gayani Senevirathne of Harvard University and colleagues report in the Sept. 25 Nature. The result: a distinctive bowl-shaped pelvis that supports an upright body. While nonhuman primates can walk upright to some extent, they typically move on all fours. The newly identified changes to human pelvic development were “essential for creating and shifting muscles that are usually on the back of the animal, pushing the animal forward, to now being on the sides, helping us stay upright as we walk,” says coauthor Terence Capellini, a Harvard evolutionary biologist. The researchers examined tiny slices of developing pelvic tissue from humans, chimpanzees and mice under a microscope, and paired those findings with CT imaging. Human ilium cartilage grows sideways, not vertically as it does in other primates, the team found. What’s more, the cartilage transitions to bone more slowly than in nonhuman primates and in other human body parts. Together, these shifts allow the pelvis to expand sideways and maintain its wide, bowl-like shape as it grows. © Society for Science & the Public 2000–2025.

Keyword: Evolution
Link ID: 29986 - Posted: 10.29.2025

By Rachel Nuwer No one knows why magic mushrooms evolved to produce psilocybin, a powerful psychedelic molecule. But this trait was apparently so beneficial for fungi that it independently evolved in two distantly related types of mushrooms. An even greater surprise to biologists was that rather than arriving at the same solution for producing psilocybin, the two groups pursued completely different biochemical pathways, according to a study published last month in the journal Angewandte Chemie International Edition. “This finding reminds us that nature finds more than one way to make important molecules,” said Dirk Hoffmeister, a pharmaceutical microbiologist at Friedrich Schiller University Jena in Germany and an author of the study. He added that it was also evidence that mushrooms were “brilliant chemists.” Practically speaking, Dr. Hoffmeister said, the research also suggested a possible new path for synthesizing psilocybin for use in scientific research and therapies. “We can expand our toolbox,” he said. Psilocybe and Inocybe mushrooms occur in some of the same habitats, but they follow different lifestyles. Psilocybe, the group that includes what are traditionally called magic mushrooms, thrives on decaying material such as decomposing organic matter or cow dung. Inocybe, commonly known as fiber caps, are symbiotic organisms that form intimate, mutually beneficial relationships with trees. In 1958, Albert Hofmann, the Swiss chemist who discovered LSD, became the first researcher to isolate psilocybin from Psilocybe mushrooms. Some scientists later suspected that a few Inocybe mushrooms also produced the compound. Since then, psilocybin has been identified in around half a dozen Inocybe species. (The other species tend to produce a potent neurotoxin.) © 2025 The New York Times Company

Keyword: Drug Abuse; Evolution
Link ID: 29985 - Posted: 10.25.2025

By Holly Barker At first glance, the mice in Pierre Vanderhaeghen’s lab in Leuven, Belgium, seem unremarkable. But inside their tiny heads, their cerebral cortex contains a mix of mouse and human neurons at two stages of development: Their native synapses are fully mature, but the connections formed from human cells are delayed and comparable to those of a newborn human baby. Vanderhaeghen and his colleagues are studying the chimeric mice to explore this drawn-out process of synaptic development, a feature that distinguishes human brains from those of other mammals. Many aspects of human brain development proceed slowly—neurogenesis, myelination, gliogenesis—but synaptic maturation is particularly protracted. In the prefrontal cortex, for instance, some synapses don’t fully develop until a person reaches their mid-20s. Deviations from this maturation rate could mean that “milestones won’t be reached at the same time” and might underlie some forms of autism or intellectual disability, says Vanderhaeghen, professor of neurosciences and group leader at the VIB-KU Leuven Center for Brain and Disease Research. An evolutionarily conserved protein called SRGAP2 controls this timing in most mammals. Humans, however, have partially duplicated copies—SRGAP2B and SRGAP2C—that inhibit the ancestral protein, two teams reported in 2012. Like other duplicated genes found only in humans, SRGAP2 resides in a repetitive—and therefore unstable—part of the genome, says Evan Eichler, professor of genome sciences at the University of Washington, and an investigator on one of the 2012 studies. “These regions create liability by predisposing us to genomic rearrangement, [but] to persist in the population, they must have an advantage. It’s part of the cost of what it is to be human.” © 2025 Simons Foundation

Keyword: Development of the Brain
Link ID: 29984 - Posted: 10.25.2025

Will Stone Doctors have long known that antidepressants come with side effects for cardiovascular and metabolic health. But a major analysis from a team of researchers in the U.K. has, for the first time, pulled together data from more than 150 clinical trials to compare the physical side effects of dozens of antidepressants. The study, published in the Lancet this week, details how each medication can affect weight, blood pressure, heart rate, cholesterol and other areas of health. The end result is something akin to a "sports league table" for 30 different antidepressants based on their side effect profile, says lead author Dr. Toby Pillinger, a psychiatrist at King's College London. "It's never been done at this scale before and no one's ever put specific numbers to the amount of weight you'll put on, or to the amount that your cholesterol goes up," he says. The findings are based on existing data, mostly from 8-week drug studies, that altogether represent more than 58,000 patients. The most frequently prescribed antidepressants in the U.S. — selective serotonin reuptake inhibitors, or SSRIs, like Zoloft and Prozac — tended to have fewer physical side effects, according to the analysis. Other medications, particularly some of the older drugs, were shown to have more significant impacts. © 2025 npr

Keyword: Depression
Link ID: 29983 - Posted: 10.25.2025

By Meghan Rosen It sounds like something from a horror movie: A disease that eats through bone, dissolving the fused plates of the skull like bubbling acid. But a type of brain cancer called glioblastoma actually does something similar, triggering the erosion of living skull tissue, researchers report October 3 in Nature Neuroscience. The work shows in gory detail that brain cancer can erode bone, a harmful effect that wasn’t previously known, says Jinan Behnan, a brain tumor immunologist at Albert Einstein College of Medicine in Bronx, New York. Behnan’s findings uncover a creepy new facet of glioblastoma, an enigmatic cancer still cloaked in scientific questions. “We really still don’t understand exactly what this disease is,” she says. Glioblastoma is an aggressive form of brain cancer that’s particularly lethal and nearly impossible to cure. In the United States, doctors diagnose more than 12,000 new cases every year. Five years after diagnosis, only about five percent of patients over 40 years old survive. © Society for Science & the Public 2000–2025

Keyword: Miscellaneous
Link ID: 29982 - Posted: 10.25.2025

By Gina Kolata For the first time, researchers restored some vision to people with a common type of eye disease by using a prosthetic retinal implant. If approved for broader use in the future, the treatment could improve the lives of an estimated one million, mostly older, people in the United States who lose their vision to the condition. The patients’ blindness occurs when cells in the center of the retina start to die, what is known as geographic atrophy resulting from age-related macular degeneration. Without these cells, patients see a big black spot in the center of their vision, with a thin border of sight around it. Although their peripheral vision is preserved, people with this form of advanced macular degeneration cannot read, have difficulty recognizing faces or forms and may have trouble navigating their surroundings. In a study published Monday in The New England Journal of Medicine, vision in 27 out of 32 participants improved so much that they could read with their artificial retinas. The vision that is restored is not normal: It’s black and white, blurry, and the field of view is small. But after getting the retinal implant, patients who could barely see gained on average five lines on a standard eye chart. The implant gets signals from glasses and a camera that projects infrared images to the artificial retina. The camera has a zoom feature that can magnify images like letters, allowing people to read, albeit slowly because with the zoom they don’t see many letters at a time. “This is at the forefront of science,” said Dr. Demetrios Vavvas, director of the retina service at Massachusetts Eye and Ear, a specialty hospital in Boston. He was not involved in the study and emphasized that the implant was not a cure for macular degeneration. But he called it the dawn of a new technology that he predicted will significantly advance. The treatment is only for people with a loss of retinal photoreceptors, so it would not work for other forms of blindness. The study participants had an average age of 79 and had been told that once vision was lost, it was gone forever. © 2025 The New York Times Company

Keyword: Vision; Robotics
Link ID: 29981 - Posted: 10.22.2025