Helen Pearson On 16 April, Robert F. Kennedy Jr held a press conference about rising diagnoses of autism. The US Health and Human Services (HHS) secretary pointed to new data showing that autism prevalence in the United States had risen steeply from one in 150 eight-year-olds in 2000 to one in 31 in 2022. He called it an “epidemic” caused by “an environmental toxin” — and said he would soon be announcing a study to find the responsible agent. The next month, the US National Institutes of Health (NIH), part of the department that Kennedy leads, announced the Autism Data Science Initiative (ADSI). The initiative offered up to US$50 million to fund studies on the causes of autism. The winning applications are expected to be announced in September. Usually, big investments in research are welcomed by scientists — but not this time. Many were dismayed that these developments seemed to ignore decades of work on the well-documented rise in autism diagnoses and on causes of the developmental condition. Although Kennedy said that environmental factors are the main cause of autism, research has shown that genetics plays a bigger part. Population studies1 have linked a handful of environmental factors — mostly encountered during pregnancy — to increased chances of autism, but their precise role has been hard to pin down. More than anything, research has shown that the drivers of autism are fiendishly complicated. “There will never be a sound-bite answer to what causes autism,” says Helen Tager-Flusberg, a psychologist who studies neurodevelopmental conditions at Boston University, Massachusetts. The rise in prevalence, many researchers say, is predominantly caused by an increase in diagnoses rather than a true rise in the underlying symptoms and traits. “We don’t see an epidemic of autism, but we see an ‘epidemic’ of diagnoses,” says Sven Bölte, a specialist in child and adolescent psychiatric science at the Karolinska Institute in Stockholm. Researchers are concerned that Kennedy, an anti-vaccine advocate, will use the ADSI to promote the disproven idea that vaccines are linked to autism. © 2025 Springer Nature Limited

Keyword: Autism
Link ID: 29905 - Posted: 08.27.2025

Welcome to Entanglements. In this episode, hosts Brooke Borel and Anna Rothschild ask: Should we try to prevent autism? It’s a question that has divided the autistic community, and the answer has significant implications on how to focus scientific research and funding. Their guests this week are Jill Escher, a philanthropist, president of the National Council on Severe Autism, and parent of two young adults with severe nonverbal autism, and Eric García, the Washington bureau chief at The Independent and the author of “We’re Not Broken: Changing the Autism Conversation,” who is himself autistic. Robert F. Kennedy Jr: These are kids who will never pay taxes, they’ll never hold a job, they’ll never play baseball, they’ll never write a poem, they’ll never go out on a date. Many of them will never use a toilet unassisted. And we have to recognize we are doing this to our children. Anna Rothschild: That was Health and Human Services Secretary Robert F. Kennedy Jr., talking about autism back in April of 2025. And he promised to find some answers about the cause of the condition, which he called an epidemic. Robert F. Kennedy Jr: This is a preventable disease. We know it’s an environmental exposure. It has to be. Genes do not cause epidemics. Anna Rothschild: On that note, welcome to Entanglements, the show where we wade into the murkiest scientific controversies and search for common ground. I’m science journalist Anna Rothschild. Brooke Borel: And I’m Brooke Borel, articles editor at Undark Magazine. And that was a dramatic cold open. Anna, what’s happening here? Are you about to do an episode on whether vaccines cause autism? Anna Rothschild: No, that is not a murky controversy. That has been rigorously disproven. Brooke Borel: Yeah. Anna Rothschild: No, today we are asking the question: Should we try to prevent autism?

Keyword: Autism
Link ID: 29904 - Posted: 08.27.2025

By Claudia López Lloreda fMRI researchers have long faced a conundrum: Given finite resources and time to spend on scanning, is it better to scan lots of participants for a short time each, or a smaller number of people for a longer time? A new study quantifies this tradeoff for brain-wide association studies (BWAS), which aim to link brain differences to physical and cognitive traits. Using large-scale public fMRI datasets, the team found that their ability to accurately predict cognitive features from functional connectivity data increased with sample size and with scan length, up to 20 minutes. But accuracy began to plateau for longer scans, and beyond 30 minutes, the added length (and cost) provided diminishing returns. A half-hour seems to be the optimal scanning time, says Thomas Yeo, associate professor of electrical and computer engineering at the National University of Singapore and principal investigator of the study. Scan duration is “essentially providing a different knob for people to tune” to meet power requirements in their fMRI experiments, he says. Although the neuroimaging community already knew that scan time is important and five minutes is insufficient, “this is one of the first major studies in the past few years to really quantitatively map that out” for BWAS studies, says Brenden Tervo-Clemmens, assistant professor of psychiatry and behavioral sciences at the University of Minnesota, who was not involved with the study. Tervo-Clemmens and his colleagues had previously shown in a 2022 study the importance of sample size in BWAS, calculating that these analyses need thousands of participants to get meaningful associations. This new study adds another part of the equation, he says. Yeo’s team developed the Optimal Scan Time Calculator to help other neuroscientists design their own studies. “Democratizing these complex methodological issues into a usable package is really, really useful,” Tervo-Clemmens says. © 2025 Simons Foundation

Keyword: Brain imaging
Link ID: 29903 - Posted: 08.27.2025

Nicola Davis Science correspondent Big hands might mean big feet, but it seems long thumbs are linked to large brains – at least in primates. Researchers say the results suggest the brain co-evolved with manual dexterity in such mammals. “We imagine an evolutionary scenario in which a primate or human has become more intelligent, and with that comes the ability to think about action planning, think about what you are doing with your hands, and realise that actually you are more efficient at doing it one way or another,” said Dr Joanna Baker, lead author of the research from the University of Reading. “And those that have longer thumbs or more ability to manipulate the objects in the way that the mind can see were likely to be more successful.” Large brains and manual dexterity are both thought to have played an important role in human evolution, with opposable thumbs a key feature that enabled a greater ability to grip and manipulate items – including tools. However, with some other primates having partly opposable thumbs, questions have remained over whether other changes in the hand – such as thumb length – could also be important in the evolution of tool use. “In general terms, you can say that the longer the thumb you have, the more motion you have to pick up and control small objects,” said Baker. To explore the issue Baker and colleagues studied the estimated brain mass and thumb length of 94 primate species, from five of our ancient hominin relatives to lemurs. The results, published in the journal Communications Biology, reveal humans and most other hominins have thumbs that are significantly longer than would be predicted based on the hand proportions of primates as a while. However, further analysis revealed an intriguing pattern. “When you have longer thumbs relative to your overall hand, that tends to come in conjunction with overall increased brain size,” said Baker. © 2025 Guardian News & Media Limited

Keyword: Evolution
Link ID: 29902 - Posted: 08.27.2025

By Claudia López Lloreda As cats age, they may yowl more than usual at night, have trouble sleeping or sleep too much, and act generally confused or disoriented. Now a new study shows that, just like in humans with Alzheimer’s disease, amyloid-beta plaques build up in the brains of aging felines and may contribute to dementia-like behaviors. In cats, that buildup could be causing a cascade of problems within the brain, such as hyperactivation of immune and other supporting brain cells that attack the synapses that connect nerve cells, researchers report August 11 in European Journal of Neuroscience. Aged cats with and without dementia had similar features and only a small number of cats were studied. But these findings could start helping researchers better understand how cats age and potentially develop treatments for feline dementia, as well as provide new insights into how the disease progresses in humans. Earlier studies had found amyloid beta in the brains of cats, but scientists didn’t know to what extent it was disrupting brain function. Robert McGeachan, a veterinarian at the University of Edinburgh, knew that the number of synapses decreased early in Alzheimer’s disease in humans. And so he and his team decided to focus on these connections in their cat study. They looked at the postmortem brains of seven young cats and 18 older ones, including eight with behavioral signs of dementia. Using fluorescent markers that find and cling to amyloid beta, the team found that the brains of aged cats, with or without dementia, had more of the protein than the younger brain samples. The amyloid beta plaques in the older cats also tended to accumulate right around synapses. © Society for Science & the Public 2000–2025.

Keyword: Alzheimers
Link ID: 29901 - Posted: 08.27.2025

By Angie Voyles Askham The adult cortex can rewire itself after injury, according to a series of classic experiments. When a monkey loses sensory input from a finger, for example, the region of the somatosensory cortex dedicated to that finger becomes overrun by inputs from the animal’s nearby fingers or face; the cortical map for the unused finger fades, and nearby maps of other body parts expand. “This is what I read in my textbook. This is what the lecturers told me in my lectures in university,” says Tamar Makin, professor of cognitive neuroscience at the University of Cambridge. But—contrary to those classic findings—such large-scale cortical reorganization did not happen in three people who lost an arm, according to a new functional imaging study Makin and her colleagues published today in Nature Neuroscience. Instead, the somatosensory map of each person’s hands, feet and lips, generated when they moved or attempted to move that body part, remained stable in the years before and after their hand was removed. “The representation of the hand persists,” says Makin, who led the study. The work is the first longitudinal look at whether amputation changes that cortical mapping. The results confirm what previous cross-sectional studies have hinted at, and they should put an end to the debate about how readily the adult cortex can shift its function, Makin says. But not everyone agrees. The study is an important contribution to the field, and it shows that maps of somatosensation driven by motor input remain stable after amputation, says Ben Godde, professor of neuroscience at Constructor University, who was not involved in the new work or the classic experiments. But that does not mean that other cortical maps are not shifting as a result of changing inputs, he says. “It’s not evidence that there’s no plasticity.” © 2025 Simons Foundation

Keyword: Pain & Touch; Development of the Brain
Link ID: 29900 - Posted: 08.23.2025

By Nora Bradford During her training in anthropology, Dorsa Amir, now at Duke University, became fascinated with the Müller-Lyer illusion. The illusion is simple: one long horizontal line is flanked by arrowheads on either side. Whether the arrowheads are pointing inward or outward dramatically changes the perceived length of the line—people tend to see it as longer when the arrowheads point in and as shorter when they point out. Graphic shows how the Müller-Lyer illusion makes two equal-length lines seem to have different lengths because of arrowlike tips pointing inward or outward. Most intriguingly, psychologists in the 1960s had apparently discovered something remarkable about the illusion: only European and American urbanites fell for the trick. The illusion worked less well, or didn’t work at all, on groups surveyed across Africa and the Philippines. The idea that this simple illusion supposedly only worked in some cultures but not others compelled Amir, who now studies how culture shapes the mind. “I always thought it was so cool, right, that this basic thing that you think is just so obvious is the type of thing that might vary across cultures,” Amir says. But this foundational research—and the hypothesis that arose to explain it, called the “carpentered-world” hypothesis—is now widely disputed, including by Amir herself. This has left researchers like her questioning what we can truly know about how culture shapes how we see the world. When researcher Marshall Segall and his colleagues conducted the cross-cultural experiment on the Müller-Lyer illusion in the 1960s, they came up with a hypothesis to explain the strange results: difference in building styles. The researchers theorized that the prevalence of carpentry features, such as rectangular spaces and right angles, trained the visual systems of people in more wealthy, industrialized cultures to perceive these angles in a way that make them more prone to the Müller-Lyer illusion. © 2025 SCIENTIFIC AMERICAN

Keyword: Vision; Attention
Link ID: 29899 - Posted: 08.23.2025

Ian Sample Science editor Women should ensure they are getting enough omega fatty acids in their diets according to researchers, who found unusually low levels of the compounds in female patients with Alzheimer’s disease. The advice follows an analysis of blood samples from Alzheimer’s patients and healthy individuals, which revealed levels of unsaturated fats, such as those containing omega fatty acids, were up to 20% lower in women with the disease. The low levels were not seen in men with Alzheimer’s, suggesting there may be sex differences in how the disease takes hold and affects a person’s physiology. “The difference between the sexes was the most shocking and unexpected finding,” said Dr Cristina Legido-Quigley, a senior author on the study at King’s College London published in the Alzheimer’s & Dementia journal. “There’s an indication that having less of these compounds could be causal in Alzheimer’s, but we need a clinical trial to confirm that.” Alzheimer’s disease is twice as common in women as in men. Factors including women’s longer average lifespan, differences in hormones, immune responses and educational opportunities can all play a role in the development of the disease. In the latest study, researchers analysed the levels of lipids, which are fatty compounds, in the blood of 306 people with Alzheimer’s, 165 people with mild cognitive impairment and 370 people who were cognitively healthy controls. Lipids can be saturated or unsaturated, with the former generally considered unhealthy and the latter broadly healthy. © 2025 Guardian News & Media Limited

Keyword: Alzheimers; Sexual Behavior
Link ID: 29898 - Posted: 08.23.2025

By Eric Reinhart A recent study in the journal JAMA Psychiatry claims to offer reassuring news to hundreds of millions of people who are taking, or considering taking, antidepressants: Withdrawal from the medications, it said, is usually mild and below the threshold for clinical significance. The analysis, which drew on data from more than 17,000 patients, was quickly picked up by international news outlets. Critics responded just as quickly, calling it misleading and dismissive of real-world suffering. As both a practicing psychiatrist and critic of the harms inadvertently inflicted by my own field, I fear we’re having the wrong debate — again. Conceptual image of an orange seesaw with a pink brain and an oversized pill balancing on it, could illustrate ideas around ssri, anti-depressants, headache pills and other medication for mental and brain health Every few years, another study or media exposé reignites controversy over these drugs: How effective are they really? Are withdrawal symptoms real or imagined? Are antidepressants harming people more than they help? These questions, while important, are stuck inside the narrow terms set by a medication-centric psychiatric industry, even when criticizing it. They flatten the experience of patients and ignore the intersecting role of clinicians, families, institutions, media, culture, and public policy in shaping both suffering and relief, trapping us in circular debates and deflecting attention from other ways of understanding and addressing what ails us. Yes, antidepressant withdrawal is real. Yes, some people suffer greatly while trying to come off these drugs, with withdrawal risk varying among different kinds of antidepressants. I have also seen many patients appear to benefit greatly from such medications. But when we focus only on the biology of response and withdrawal, or treat psychiatric medications as purely pharmacologic agents whose harms and benefits can be definitively measured and settled by clinical trials, we obscure the more complex — and far more consequential — dynamics by which these medications affect self-perception, social relationships, and political life.

Keyword: Depression
Link ID: 29897 - Posted: 08.23.2025

Nell Greenfieldboyce The early bird gets the worm, as the old saying goes. And now a lot of birds around the globe are starting their days earlier than ever, because of unnaturally bright skies caused by light pollution. "For these birds, effectively their day is almost an hour longer. They start vocalizing about 20 minutes earlier in the morning and they stop vocalizing about 30 minutes later in the evening," says Neil Gilbert, a wildlife ecologist with Oklahoma State University. That's the conclusion of a sweeping study that analyzed bird calls from over 500 bird species in multiple continents, giving researchers an unprecedented look at how human-created lights are affecting the daily lives of birds worldwide. Scientists already knew that light pollution affects birds. It can send migrating birds off course, and some observations have linked artificial lighting to unusual bird activity, including one recent report of American Robins feeding their babies in their nest at night. But Gilbert and Brent Pease, with Southern Illinois University, took a more comprehensive view, by analyzing millions of recordings of birdsong. The audio was collected by thousands of devices installed in backyards and other locations, mostly by birdwatchers and other wildlife enthusiasts, as part of a program called BirdWeather. The BirdWeather devices automatically register bird calls and use them to identify the species, mostly to let bird fans know what's flitting through their yards. © 2025 npr

Keyword: Biological Rhythms
Link ID: 29896 - Posted: 08.23.2025

By Lydia Denworth A remarkably bright pulsing dot has appeared on the monitor in front of us. We are watching, in real time, the brain activity of a graduate student named Nick, who is having an afternoon nap inside an imaging machine at the Massachusetts Institute of Technology, where Lewis has her laboratory. The bright spot first appears toward the bottom of the screen, about where Nick’s throat meets his jaw. It moves slowly upward, fades and then is followed by another bright dot. “It really comes and goes,” says Lewis, who is also affiliated with Massachusetts General Hospital. “It’s in waves.” This moving dot depicts something few people have ever seen: fresh cerebrospinal fluid flowing from the spinal cord into the brain, part of a process that researchers are now learning is vital for keeping us healthy. For decades biologists have pondered a basic problem. As human brains whir and wonder throughout the day, they generate waste—excess proteins and other molecules that can be toxic if not removed. Among those proteins are amyloid beta and tau, key drivers of Alzheimer’s disease. Until recently, it was entirely unclear how the brain takes out this potentially neurotoxic trash. In the rest of the body, garbage removal is handled initially by the lymphatic system. Excess fluid and the waste it carries move from tissue into the spleen, lymph nodes and other parts of the system, where certain particles are removed and put into the bloodstream to be excreted. It was long thought that the brain can’t use the same trick, because the so-called blood-brain barrier, a protective border that keeps infections from reaching critical neural circuitry, stops the transport of most everything in and out. © 2025 SCIENTIFIC AMERICAN,

Keyword: Sleep; Neuroimmunology
Link ID: 29895 - Posted: 08.20.2025

Simon Makin Andrew Moseson experienced severe depression for many years. “Some days I wasn’t able to get out bed. I had long periods of unemployment and was living in my car for a time.” He struggled to find relief, nothing worked. “I tried medications, exercise, volunteering, psychedelics. I read books about happiness, about depression,” he says. “Everything helped a little, but it was still there.” Then, in the spring of 2023, he found a clinical trial that would change his life. The trial was for people with clinical depression who, like Moseson, had not found success with existing medication. It involved faecal microbiota transplantation (FMT), in which stool from a healthy donor is transferred into a recipient’s gastrointestinal tract to restore a healthy balance of gut bacteria. The procedure did not work as well for everyone who took part in the trial, but for Moseson the results were transformative — and they came fast. “Within about a week, I started feeling better,” he says. “I felt like my brain was refreshed.” Two years later, Moseson is still taking his previously prescribed medication. “My doctor doesn’t want me to quit my antidepressants,” he says. “There’s a thought that this transplant could make antidepressants work better.” Whatever the mechanism, the change seems stark. “I feel like I’ve been cured,” Moseson says. Numerous psychiatric and neurological conditions have been linked to disturbances in people’s gut microbiota — the community of trillions of microorganisms that live symbiotically in the gastrointestinal tract. These are just correlations, but studies in rodents show compelling evidence of causality, and other animal research points to multiple pathways through which the microbiota communicates with the brain. © 2025 Springer Nature Limited

Keyword: Depression; Obesity
Link ID: 29894 - Posted: 08.20.2025

By Marta Hill Most people flinch when a rat scurries into their path, but not one New York City-based research team: These researchers actively seek out urban rats to study their day-to-day behaviors and interactions. The work is part of a growing trend of neuroscientists studying animals in their natural environments rather than in the lab. “It’s a classic neuroscience model organism, but we don’t really know that much about their natural ecology,” says team member Emily Mackevicius, senior research scientist at Basis Research Institute. The fact that urban rats are ubiquitous presents a convenient opportunity for naturalistic study, adds Ralph Peterson, a postdoctoral fellow at the institute, who is also part of the team. Last year, Peterson, Mackevicius and their colleagues held a series of rat behavior stakeouts around New York City—in the Union Square subway station, in a wooded area of Central Park and on a street corner in Harlem. The team used thermal cameras to track the animals as they foraged in the dark and ultrasonic audio recorders to eavesdrop on rat vocalizations. Rats in the wild vocalize differently than laboratory rats, the team found. For example, lab rats typically emit calls at 22 kilohertz in negative contexts, such as when they sense danger, according to a 2021 review article. By contrast, the city rats used that frequency across more varied scenarios, including while they were foraging. The team posted their results on bioRxiv last month. “This creature that we see out at night all the time, running around, is actually vocalizing all the while, and we can’t hear it,” Peterson says. © 2025 Simons Foundation

Keyword: Animal Communication; Evolution
Link ID: 29893 - Posted: 08.20.2025

By Carl Zimmer For decades, neuroengineers have dreamed of helping people who have been cut off from the world of language. A disease like amyotrophic lateral sclerosis, or A.L.S., weakens the muscles in the airway. A stroke can kill neurons that normally relay commands for speaking. Perhaps, by implanting electrodes, scientists could instead record the brain’s electric activity and translate that into spoken words. Now a team of researchers has made an important advance toward that goal. Previously they succeeded in decoding the signals produced when people tried to speak. In the new study, published on Thursday in the journal Cell, their computer often made correct guesses when the subjects simply imagined saying words. Christian Herff, a neuroscientist at Maastricht University in the Netherlands who was not involved in the research, said the result went beyond the merely technological and shed light on the mystery of language. “It’s a fantastic advance,” Dr. Herff said. The new study is the latest result in a long-running clinical trial, called BrainGate2, that has already seen some remarkable successes. One participant, Casey Harrell, now uses his brain-machine interface to hold conversations with his family and friends. In 2023, after A.L.S. had made his voice unintelligible, Mr. Harrell agreed to have electrodes implanted in his brain. Surgeons placed four arrays of tiny needles on the left side, in a patch of tissue called the motor cortex. The region becomes active when the brain creates commands for muscles to produce speech. A computer recorded the electrical activity from the implants as Mr. Harrell attempted to say different words. Over time, with the help of artificial intelligence, the computer accurately predicted almost 6,000 words, with an accuracy of 97.5 percent. It could then synthesize those words using Mr. Harrell’s voice, based on recordings made before he developed A.L.S. © 2025 The New York Times Company

Keyword: Language; Robotics
Link ID: 29892 - Posted: 08.16.2025

Heidi Ledford Scientists are closing in on the ability to apply genome editing to a formidable new target: the human brain. In the past two years, a spate of technological advances and promising results in mice have been laying the groundwork for treating devastating brain disorders using techniques derived from CRISPR–Cas9 gene editing. Researchers hope that human trials are just a few years away. “The data have never looked so good,” says Monica Coenraads, founder and chief executive of the Rett Syndrome Research Trust in Trumbull, Connecticut. “This is less and less science fiction, and closer to reality.” Daunting challenge Researchers have already developed gene-editing therapies to treat diseases of the blood, liver and eyes. In May, researchers reported1 a stunning success using a bespoke gene-editing therapy to treat a baby boy named KJ with a deadly liver disease. But the brain poses special challenges. The molecular components needed to treat KJ were inserted into fatty particles that naturally accumulate in the liver. Researchers are searching for similar particles that can selectively target the brain, which is surrounded by a defensive barrier that can prevent many substances from entering. Although KJ’s story was exciting, it was also frustrating for those whose family members have neurological diseases, says Coenraads, whose organization focuses on Rett syndrome, a rare disorder that affects brain development. “The question that I hear from our families is, ‘It was done so quickly for him. What’s taking us so long?’” she says. That pool of concerned families is growing as physicians and families increasingly turn to genome sequencing to find the causes of once-mysterious brain disorders, says Cathleen Lutz, a geneticist at The Jackson Laboratory in Bar Harbor, Maine. “People are starting to now find out that their child’s seizures, for example, are related to particular genetic mutations,” she says. © 2025 Springer Nature Limited

Keyword: Genes & Behavior
Link ID: 29891 - Posted: 08.16.2025

By Sofia Caetano Avritzer Vomiting up a droplet of sugar might not seem like the most romantic gesture from a potential suitor. But for one fly species, males that spill their guts are quite a catch. Drosophila subobscura flies’ peculiar “romantic” barfing might have evolved by repurposing brain cells that usually control digestion for more romantic pursuits, researchers report August 14 in Science. Most male fruit flies court by following the females around and vibrating their wings to serenade them with a species-specific love song, says Adriane Otopalik. But some fly species, like D. subobscura, spice things up a little. The males will vomit a bit of their last meal and offer it to females they are interested in, says Otopalik, a neuroscientist at Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Va. Nuptial gifts like these are common in some animals, like male spiders attempting to win over their mates without getting their heads bitten off. Scientists think female flies, which can be “very choosy,” might use this romantic barf to pick suitable suitors, says Otopalik, who was not involved in the study. The thousands of neurons that control most of male fruit flies’ courtship produce a male-specific version of a protein called fruitless. Artificially activating these neurons can make D. subobscura males go through the motions of their seduction dance — even when there aren’t any females around, says Daisuke Yamamoto, an evolutionary biologist at National Institute of Information and Communications Technology in Kobe, Japan. Yamamoto and his collaborators wondered if somewhere in these courtship brain cells was the key to understanding how nuptial gift giving evolved. © Society for Science & the Public 2000–2025

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 29890 - Posted: 08.16.2025

By Pam Belluck Sometimes the pain felt like lightning bolts. Or snakes biting. Or needles. “Just imagine the worst burn you’ve ever had, all over your body, never going away,” said Ed Mowery, 55, describing his life with chronic pain. “I would wake up in the middle of night, screaming at the top of my lungs.” Beginning with a severe knee injury he got playing soccer at 15, he underwent about 30 major surgeries for various injuries over the decades, including procedures on his knees, spine and ankles. Doctors put in a spinal cord stimulator, which delivers electrical pulses to relieve pain, and prescribed morphine, oxycodone and other medications, 17 a day at one point. Nothing helped. Unable to walk or sit for more than 10 minutes, Mr. Mowery, of Rio Rancho, N.M., had to stop working at his job selling electronics to engineering companies and stop playing guitar with his death metal band. Out of options four years ago, Mr. Mowery signed up for a cutting-edge experiment: a clinical trial involving personalized deep brain stimulation to try to ease chronic pain. The study, published on Wednesday, outlines a new approach for the most devastating cases of chronic pain, and could also provide insights to help drive invention of less invasive therapies, pain experts said. “It’s highly innovative work, using the experience and technology they have developed and applying it to an underserved area of medicine,” said Dr. Andre Machado, chief of the Neurological Institute at Cleveland Clinic, who was not involved in the study. Chronic pain, defined as lasting at least three months, afflicts about 20 percent of adults in the United States, an estimated 50 million people, according to the Centers for Disease Control and Prevention. In about a third of cases, the pain substantially limits daily activities, the C.D.C. reported. © 2025 The New York Times Company

Keyword: Pain & Touch
Link ID: 29889 - Posted: 08.16.2025

Hannah Devlin Science correspondent Attention deficit hyperactivity disorder medication is linked to significantly lower risk of suicidal behaviours, substance misuse, transport accidents and criminality, according to a study of the wider outcomes of treatment. The research, based on the medical records of nearly 150,000 people in Sweden, suggested that the drugs could have meaningful benefits beyond helping with the core symptoms of ADHD. Although the study was not a randomised trial – and so cannot definitively prove that medication caused improved outcomes – it adds to evidence of the substantial value of treatment. “We found that ADHD medication was associated with significantly reduced rates of first occurrences of suicidal behaviours, substance misuse, transport accidents and criminality,” said Prof Samuele Cortese, a child and adolescent psychiatrist and researcher at the University of Southampton. “Our results should inform the debate on the effects and safety of ADHD medications.” After accounting for factors including age, sex, education level, psychiatric diagnoses and medical history, ADHD medication was associated with reduced rates of a first occurrence of four of the five outcomes investigated: a 17% reduction for suicidal behaviour, 15% for substance misuse, 12% for transport accidents and 13% for criminality. It is well established that ADHD, thought to affect about 5% of children and 2.5% of adults worldwide, is linked to higher rates of mental health problems including suicide, substance misuse and accidental injuries. People with ADHD are also disproportionately represented within the criminal justice system. © 2025 Guardian News & Media Limited

Keyword: ADHD; Depression
Link ID: 29888 - Posted: 08.16.2025

By Dan Samorodnitsky Water is the most fundamental need for all life on Earth. Not every organism needs oxygen, and many make their own food. But for all creatures, from deep-sea microbes and slime molds to trees and humans, water is nonnegotiable. “The first act of life was the capture of water within a cell membrane,” a pair of neurobiologists wrote in a recent review. Ever since, cells have had to stay wet enough to stay alive. Water is the medium in which all chemical reactions in an organism take place, and those reactions are finely tuned to a narrow range of ratios between water and salt, another essential ingredient in life’s chemistry. The cells in your body are permeable to water, so if the water-salt balance of the surrounding fluid — blood, lymph or cerebrospinal fluid, for example — is outside its healthy range, cells can swell or shrink, shrivel or potentially burst. An imbalance can cause brain cells to malfunction, losing their ability to manage ion concentrations across their membranes and propagate action potentials. Although these effects of insufficient water are felt by every cell in the body, cells themselves do not cry out in thirst. Instead, it’s the brain that monitors the body’s water levels and manifests the experience of thirst — a dry tongue, hot throat and rapid onset of malaise — which compels a behavior: acquire water. “These neural circuits that control hunger and thirst are located deep in primitive brain structures like the hypothalamus and brainstem,” said Zachary Knight (opens a new tab), a neuroscientist at the University of California, San Francisco, who recently co-authored a review paper in Neuron (opens a new tab) on the neurobiology of thirst. Because these brain areas are difficult to study — due not only to their location, but also to their composition, with many different cell types and crisscrossed circuitry — it’s only in the last decade or so that neuroscientists have begun to understand how thirst fundamentally works. The body, researchers have found, is filled with sensors that feed clues to the brain about how much water or salt an organism needs to consume. How those sensors work, or what they even are, continues to elude scientists. Their existence offers a tantalizing insight: Water may be fundamental to life, but thirst is an educated guess. © 2025 Simons Foundation

Keyword: Obesity
Link ID: 29887 - Posted: 08.13.2025

By Phie Jacobs When it comes to telling males and females apart, many bird species reject subtlety altogether. Roosters stand out thanks to their big, bright comb and ear-splitting “cock-a-doodle-doo.” Bachelor birds-of-paradise flaunt their vibrant plumage to attract more subdued females. And the male peacock’s feathered train is so ostentatious it famously threw even Charles Darwin for a loop. But that’s not the case for all bird species. When males and females look pretty much the same, scientists must try harder—often using DNA testing—to separate the sexes. According to a new study of wild Australian birds, these methods may be leading to misidentification in cases where an individual’s gonads and outward appearance don’t align with the genetic sex determined by its chromosomes. As scientists report today in Biology Letters, this phenomenon—known as sex reversal—may be more common than anyone expected. The discovery is likely to “raise some eyebrows” (or is it ruffle some feathers?), says Blanche Capel, a biologist at Duke University who wasn’t involved in the new work. Although sex determination is often viewed as a straightforward process, she explains, the reality is much more complicated. In humans, individuals with XX chromosomes typically develop as female, whereas those with XY chromosomes are usually male. But Judith Mank, a zoologist at the University of British Columbia, notes it’s the genes carried on those chromosomes—not the chromosomes—that are the main players. The SRY gene on the Y chromosome, for example, kick-starts male development in mammals. Anyone missing this key gene will end up developing as female, even if they have XY chromosomes. “We think of sex chromosomes as being sex determining,” says Mank, who also wasn’t involved in the new research. “That’s not true.” What’s more, it can matter how these genes are expressed on a cell-by-cell basis. In some species such as fruit flies, zebrafish, and chickens, individual cells have their own sexual identity based on the genes they happen to contain or express, rather than being influenced by the body’s overall hormone levels. When different cells contain different sets of chromosomes, this process can give rise to individuals called gynandromorphs, which exhibit both male and female characteristics. © 2025 American Association for the Advancement of Science.

Keyword: Sexual Behavior; Evolution
Link ID: 29886 - Posted: 08.13.2025