Most Recent Links
Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.
Ian Sample Science editor A three-minute brainwave test can detect memory problems linked to Alzheimer’s disease long before people are typically diagnosed, raising hopes that the approach could help identify those most likely to benefit from new drugs for the condition. In a small trial, the test flagged specific memory issues in people with mild cognitive impairment, highlighting who was at greater risk of developing Alzheimer’s. Trials in larger groups are under way. The Fastball test is a form of electroencephalogram (EEG) that uses small sensors on the scalp to record the brain’s electrical activity while people watch a stream of images on a screen. The test detects memory problems by analysing the brain’s automatic responses to images the person sees before the test. “This shows us that our new passive measure of memory, which we’ve built specifically for Alzheimer’s disease diagnosis, can be sensitive to those individuals at very high risk but who are not yet diagnosed,” said Dr George Stothart, a cognitive neuroscientist at the University of Bath, where the test was developed. The trial, run with the University of Bristol, involved 54 healthy adults and 52 patients with mild cognitive impairment (MCI). People with MCI have problems with memory, thinking or language, but these are not usually severe enough to prevent them doing their daily activities. Before the test, volunteers were shown eight images and told to name them, but not specifically to remember them or look out for them in the test. The researchers then recorded the participants’ brain activity as they watched hundreds of images flash up on a screen. Each image appeared for a third of a second and every fifth picture was one of the eight they had seen before. © 2025 Guardian News & Media Limited
Keyword: Alzheimers; Attention
Link ID: 29914 - Posted: 09.03.2025
Jon Hamilton People who inherit two copies of a gene variant called APOE4 have a 60% chance of developing Alzheimer's by age 85. Only about 2% to 3% of people in the U.S. have this genetic profile, and most of them don't know it because they've never sought genetic testing. But three scientists are among those who did get tested, and learned that they are in the high-risk group. Now, each is making an effort to protect not only their own brain, but the brains of others with the genotype known as APOE4-4. "I just felt like the end of the world," says June, who asked to use only her first name out of fear that making her genetic status public could affect her job or health insurance. June was 57 when she found out. As someone with a doctorate in biochemistry, she quickly understood what the results meant. New tests of blood and spinal fluid could help doctors quickly identify patients who would most benefit from treatment. "People with our genotype are almost destined to get the disease," she says. "We tend to get symptoms 7 to 10 years earlier than the general population, which means that I had about seven years left before I may get the disease." At first, June spent sleepless nights online, reading academic papers about Alzheimer's and genetics. She even looked into physician-assisted suicide in an effort to make sure she would not become a burden to her adult son. © 2025 npr
Keyword: Alzheimers; Genes & Behavior
Link ID: 29913 - Posted: 09.03.2025
Rachel Fieldhouse A man with partial paralysis was able to operate a robotic arm when he used a non-invasive brain device partially controlled by artificial intelligence (AI), a study reports1. The AI-enabled device also allowed the man to perform screen-based tasks four times better than when he used the device on its own. Brain–computer interfaces (BCIs) capture electrical signals from the brain, then analyse them to determine what the person wants to do and translate the signals into commands. Some BCIs are surgically implanted and record signals directly from the brain, which typically makes them more accurate than non-invasive devices that are attached to the scalp. Jonathan Kao, who studies AI and BCIs at the University of California, Los Angeles, and his colleagues wanted to improve the performance of non-invasive BCIs. The results of their work are published in Nature Machine Intelligence this week. First, the team tested its BCI by tasking four people — one with paralysis and three without — with moving a computer cursor to a particular spot on a screen. All four were able to complete the task the majority of the time. When the authors added an AI co-pilot to the device, the participants completed the task more quickly and had a higher success rate. The device with the co-pilot doesn’t need to decode as much brain activity because the AI can infer what the user wants to do, says Kao. “These co-pilots are essentially collaborating with the BCI user and trying to infer the goals that the BCI user is wishing to achieve, and then helps to complete those actions,” he adds. The researchers also trained an AI co-pilot to control a robotic arm. The participants were required to use the robotic arm to pick up coloured blocks and move them to marked spots on a table. The person with paralysis could not complete the task using the conventional, non-invasive BCI, but was successful 93% of the time using the BCI with an AI co-pilot. Those without paralysis also completed the task more quickly when using the co-pilot. © 2025 Springer Nature Limited
Keyword: Robotics
Link ID: 29912 - Posted: 09.03.2025
By Lauren Schenkman Microglia safeguard the proliferation and survival of young GABAergic interneurons by secreting insulin-like growth factor 1 (IGF-1), according to a new study of human brain tissue and organoids. The finding points to the potential origin of the brain signaling imbalance implicated in autism and other conditions. Microglia contribute to brain development, past findings show, but their exact function has been unclear. Some experiments showed that these cells prune neural circuits, but later work called that idea into question. The new research “identifies microglia as really an important source of IGF, and one that sets the supply of GABAergic interneurons in the developing brain,” says Damon Page, principal investigator at Seattle Children’s Research Institute. Page was not involved in this work but led an earlier investigation that showed IGF-1 prevents microcephaly in a mouse model of autism when administered during a critical window soon after birth. This new study “extends back that window into the embryonic period,” he says, with implications for understanding both typical development and conditions such as autism. The study was published 6 August in Nature. The investigators used staining techniques to pinpoint microglia in the medial ganglionic eminence, where interneurons form, in human brain tissue samples at various developmental stages. At early developmental stages, microglia were sprinkled throughout brain matter, but later on these cells arranged themselves around clusters of GABAergic neuroblasts, with their processes extending into the clusters. Microglia also aligned themselves with radial glia, the precursors to many brain cells. Based on existing data, IGF-1 emerged as the chemical most likely to mediate microglia’s effects on developing cell types, and in organoid models of the developing human brain, the cells secreted IGF-1, they found. © 2025 Simons Foundation
Keyword: Glia; Learning & Memory
Link ID: 29911 - Posted: 09.03.2025
By Joshua Cohen Roughly 40 percent of adult Americans are considered obese, and weight-loss drugs have come to play a central role in medical treatment over the past few years. As of the spring of 2024, one in eight U.S. adults had taken drugs including Wegovy, Zepbound, or Ozempic, among others, for weight loss. These products belong to a class of drugs known as glucagon-like peptide-1 agonists, or GLP-1s, which can be remarkably effective, but when patients go off GLP-1s, weight rebound occurs. And as it turns out, a relatively large portion of patients discontinue these medications within one year. Prime Therapeutics, a company that manages prescription drug coverage benefits for insurers, employers, and government programs, has been documenting this phenomenon. In 2023, the company published research indicating that merely 32 percent of patients remained on their GLP-1 at the end of one year. A follow-up analysis found that by year two, only 15 percent remained on the drug. And in a new review, the company found that only 8 percent of patients remained on the drugs after three years. The main reason for discontinuation — cited by almost half of patients in a large-scale survey — is concern about the medications’ side effects. People may quit their medication after experiencing common side effects, such as uncomfortable gastrointestinal issues. They may also quit out of fear of more serious ones, like certain cancers — although research suggests GLP-1s are associated with a lower risk for many types of cancer. Additionally, some GLP-1 users may also be at risk of nutrient deficiency and muscle or bone loss without a proper diet and exercise regimen. Health and nutrition experts suggest that optimizing the benefits conferred by GLP-1s requires lifestyle interventions aimed at modifying patient behavior. GLP-1 medicines work for weight loss by curbing hunger and slowing digestion, but they don’t replace the need for improved diet and increased physical activity. Rather, these prescription pharmaceuticals and other non-GLP-1 obesity drugs work together with nutrition and exercise to promote optimal health. In an email to Undark, Jody Dushay, an assistant professor at Harvard Medical School, wrote that “nutrition and exercise hugely benefit overall health” and increase the positive effects of the medications.
Keyword: Obesity
Link ID: 29910 - Posted: 09.03.2025
By R. Douglas Fields It is late at night. You are alone and wandering empty streets in search of your parked car when you hear footsteps creeping up from behind. Your heart pounds, your blood pressure skyrockets. Goose bumps appear on your arms, sweat on your palms. Your stomach knots and your muscles coil, ready to sprint or fight. Now imagine the same scene, but without any of the body’s innate responses to an external threat. Would you still feel afraid? Experiences like this reveal the tight integration between brain and body in the creation of mind — the collage of thoughts, perceptions, feelings and personality unique to each of us. The capabilities of the brain alone are astonishing. The supreme organ gives most people a vivid sensory perception of the world. It can preserve memories, enable us to learn and speak, generate emotions and consciousness. But those who might attempt to preserve their mind by uploading its data into a computer miss a critical point: The body is essential to the mind. How is this crucial brain-body connection orchestrated? The answer involves the very unusual vagus nerve. The longest nerve in the body, it wends its way from the brain throughout the head and trunk, issuing commands to our organs and receiving sensations from them. Much of the bewildering range of functions it regulates, such as mood, learning, sexual arousal and fear, are automatic and operate without conscious control. These complex responses engage a constellation of cerebral circuits that link brain and body. The vagus nerve is, in one way of thinking, the conduit of the mind. How could stimulating a single nerve potentially have such wide-ranging psychological and cognitive benefits? Nerves are typically named for the specific functions they perform. Optic nerves carry signals from the eyes to the brain for vision. Auditory nerves conduct acoustic information for hearing. The best that early anatomists could do with this nerve, however, was to call it the “vagus,” from the Latin for “wandering.” The wandering nerve was apparent to the first anatomists, notably Galen, the Greek polymath who lived until around the year 216. But centuries of study were required to grasp its complex anatomy and function. This effort is ongoing: Research on the vagus nerve is at the forefront of neuroscience today. © 2025Simons Foundation
Keyword: Emotions
Link ID: 29909 - Posted: 08.30.2025
Mohana Basu People with a psychiatric disorder are more likely to marry someone who has the same condition than to partner with someone who doesn’t, according to a massive study1 suggesting that the pattern persists across cultures and generations. Researchers had previously noted this trend in Nordic countries, but the phenomenon has seldom been investigated outside Europe until now. The latest study, published in Nature Human Behaviour today, used data from more than 14.8 million people in Taiwan, Denmark and Sweden. It examined the proportion of people in those couples who had one of nine psychiatric disorders: schizophrenia, bipolar disorder, depression, anxiety, attention-deficit hyperactivity disorder, autism, obsessive–compulsive disorder (OCD), substance-use disorder and anorexia nervosa. Scientists lack a definitive understanding of what causes people to develop psychiatric disorders — but genetics and environmental factors are both thought to play a part. The team found that when one partner was diagnosed with one of the nine conditions, the other was significantly more likely to be diagnosed with the same or another psychiatric condition. Spouses were more likely to have the same conditions than to have different ones, says co-author Chun Chieh Fan, a population and genetics researcher at the Laureate Institute for Brain Research in Tulsa, Oklahoma. “The main result is that the pattern holds across countries, across cultures, and, of course, generations,” Fan says. Even changes in psychiatric care over the past 50 years have not shifted the trend, he notes. Only OCD, bipolar disorder and anorexia nervosa showed different patterns across countries. For instance, in Taiwan, married couples were more likely to share OCD than were couples in Nordic countries. © 2025 Springer Nature Limited
Keyword: Depression; Schizophrenia
Link ID: 29908 - Posted: 08.30.2025
By Holly Barker When scientists produced the first map of all synaptic connections in the roundworm Caenorhabditis elegans in 1986, many hailed it as a blueprint for the flow of brain signals. As it turned out, though, models of neuronal activity based on this wiring diagram bore little resemblance to the functional maps of brain activity measured in living worms. This disconnect isn’t limited to worms. Mice, for instance, appear to have widespread silent synapses—wired connections that don’t send signals—and the actual responses of some cells in the fruit fly’s visual system do not match the responses the connectome predicts. A new preprint helps to explain why: Most network features, in C. elegans at least, are not conserved between the anatomical and functional connectomes. Yet the anatomical connectome can still forecast—albeit in a complex way—observed neuronal activity in the worms, according to a second preprint by the same team, because “most signaling is happening along the wires,” says Andrew Leifer, associate professor of physics and neuroscience at Princeton University and principal investigator on both preprints. The findings begin to address the long-standing challenge of reconciling structure and function, and show that “we weren’t entirely wrong” about the importance of synaptic connectivity, says Jihong Bai, professor of basic sciences at the Fred Hutchinson Cancer Center, who was not involved in the work. The debut of a color-coded map of cell types in the worm brain in 2021 split the neuroscience community. It made it possible to identify individual neurons in whole-brain recordings and compare annotated recordings with the connectome—an exercise that revealed no correlation between the two. © 2025 Simons Foundation
Keyword: Brain imaging
Link ID: 29907 - Posted: 08.30.2025
By Carl Zimmer Charles Darwin unveiled his theory of evolution in 1859, in “On the Origin of Species.” But it took him another 12 years to work up the courage to declare that humans evolved, too. In “The Descent of Man,” published in 1871, Darwin argued that humans arose from apes. And one of the most profound changes they underwent was turning into upright walkers. “Man alone has become a biped,” Darwin wrote. Bipedalism, he declared, was one of humanity’s “most conspicuous characters.” Scientists have now discovered some of the crucial molecular steps that led to that conspicuous character millions of years ago. A study published in the journal Nature on Wednesday suggests that our early ancestors became bipeds, as old genes started doing new things. Some genes became active in novel places in the human embryo, while others turned on and off at different times. Scientists have long recognized that a key feature for walking upright is a bone called the ilium. It’s the biggest bone in the pelvis; when you put your hand on your hip, that’s the ilium you feel. The left and right ilium are both fused to the base of the spine. Each ilium sweeps around the waist to the front of the belly, creating a bowllike shape. Many of the leg muscles we use in walking are anchored to the ilium. The bone also supports the pelvic floor, a network of muscles that acts like a basket for our inner organs when we stand up. As vital as the ilium is to everyday life, the bone can also be a source of suffering. The ilium can flare up with arthritis, grow brittle in old age, especially in women, and fracture from a fall. Genetic disorders can deform it, making walking difficult. The ilium also forms much of the birth canal — where babies can sometimes get stuck, endangering the mother’s life. © 2025 The New York Times Company
Keyword: Evolution
Link ID: 29906 - Posted: 08.30.2025
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