By Diana Kwon Charlene Sunkel was 19 when she started hearing voices and strange thoughts began filling her head. People wanted to infiltrate her mind, to poison her, to rat her out to the police. She stopped making eye contact, convinced that it would enable others to steal her thoughts. Once sociable and outgoing, Sunkel withdrew from friends and family, worried that they were conspiring against her. On her way to work, she had visions of men in hoods from the corner of her eye. As the illness progressed, she lost the ability to understand what people were saying, and when she spoke, the words would not come out right. About a year after her symptoms started, Sunkel was diagnosed with schizophrenia. Delusions, hallucinations and disordered thinking are collectively known as psychosis. These “positive” symptoms are among the most widely recognized aspects of schizophrenia. For about two thirds of patients with schizophrenia—which affects approximately 23 million people around the world—traditional antipsychotic drugs are often highly effective at treating psychosis. But these drugs frequently come with problematic side effects. And they do little to help with the so-called negative symptoms of schizophrenia, such as emotional flatness and social withdrawal, or with other issues involving thinking and memory referred to as cognitive problems. Until quite recently, all antipsychotics worked in essentially the same way. They blocked the activity of dopamine, a chemical messenger in the brain involved in motivation, learning, habit formation, and other processes. The successful treatment of psychosis with dopamine blockers led many clinicians to believe that they understood schizophrenia and that its underlying cause was an imbalance in dopamine. When a particular antipsychotic did not work in a patient, all doctors needed to do, they thought, was up the dosage or try another dopamine-targeting drug. But the arrival last September of a new drug, KarXT, supports an emerging awareness among clinicians that schizophrenia is more complex than most of them had realized. KarXT is the first antipsychotic to target a molecule other than dopamine. © 2024 SCIENTIFIC AMERICAN,

Keyword: Schizophrenia
Link ID: 29711 - Posted: 03.19.2025

By Ellen Barry On a recent Friday morning, Daniel, a lawyer in his early 40s, was in a Zoom counseling session describing tapering off lithium. Earlier that week he had awakened with racing thoughts, so anxious that he could not read, and he counted the hours before sunrise. At those moments, Daniel doubted his decision to wean off the cocktail of psychiatric medications which had been part of his life since his senior year in high school, when he was diagnosed with bipolar disorder. Was this his body adjusting to the lower dosage? Was it a reaction to the taco seasoning he had eaten the night before? Or was it what his psychiatrist would have called it: a relapse? “It still does go to the place of — what if the doctors are right?” said Daniel. On his screen, Laura Delano nodded sympathetically. Ms. Delano is not a doctor; her main qualification, she likes to say, is having been “a professional psychiatric patient between the ages of 13 and 27.” During those years, when she attended Harvard and was a nationally ranked squash player, she was prescribed 19 psychiatric medications, often in combinations of three or four at a time. Then Ms. Delano decided to walk away from psychiatric care altogether, a journey she detailed in a new memoir, “Unshrunk: A Story of Psychiatric Treatment Resistance.” Fourteen years after taking her last psychotropic drug, Ms. Delano projects a radiant good health that also serves as her argument — living proof that, all along, her psychiatrists were wrong. Since then, to the alarm of some physicians, an online DIY subculture focused on quitting psychiatric medications has expanded and begun to mature into a service industry. © 2025 The New York Times Company

Keyword: Schizophrenia
Link ID: 29710 - Posted: 03.19.2025

By Claudia López Lloreda For a neuroscientist, the opportunity to record single neurons in people doesn’t knock every day. It is so rare, in fact, that after 14 years of waiting by the door, Florian Mormann says he has recruited just 110 participants—all with intractable epilepsy. All participants had electrodes temporarily implanted in their brains to monitor their seizures. But the slow work to build this cohort is starting to pay off for Mormann, a group leader at the University of Bonn, and for other researchers taking a similar approach, according to a flurry of studies published in the past year. For instance, certain neurons selectively respond not only to particular scents but also to the words and images associated with them, Mormann and his colleagues reported in October. Other neurons help to encode stimuli, form memories and construct representations of the world, recent work from other teams reveals. Cortical neurons encode specific information about the phonetics of speech, two independent teams reported last year. Hippocampal cells contribute to working memory and map out time in novel ways, two other teams discovered last year, and some cells in the region encode information related to a person’s changing knowledge about the world, a study published in August found. These studies offer the chance to answer questions about human brain function that remain challenging to answer using animal models, says Ziv Williams, associate professor of neurosurgery at Harvard Medical School, who led one of the teams that worked on speech phonetics. “Concept cells,” he notes by way of example, such as those Mormann identified, or the “Jennifer Aniston” neurons famously described in a 2005 study, have proved elusive in the monkey brain. © 2025 Simons Foundation

Keyword: Attention; Learning & Memory
Link ID: 29709 - Posted: 03.19.2025

Nicola Davis Science correspondent Cat owners are being asked share their pet’s quirky traits and even post researchers their fur in an effort to shed light on how cats’ health and behaviour are influenced by their genetics. The scientists behind the project, Darwin’s Cats, are hoping to enrol 100,000 felines, from pedigrees to moggies, with the DNA of 5,000 cats expected to be sequenced in the next year. The team say the goal is to produce the world’s largest feline genetic database. “Unlike most existing databases, which tend to focus on specific breeds or veterinary applications, Darwin’s Cats is building a diverse, large-scale dataset that includes pet cats, strays and mixed breeds from all walks of life,” said Dr Elinor Karlsson, the chief scientist at the US nonprofit organisation Darwin’s Ark, director of the vertebrate genomics group at the Broad Institute of MIT and Harvard and associate professor at the UMass Chan medical school. “It’s important to note, this is an open data project, so we will share the data with other scientists as the dataset grows,” she added. The project follows on the heels of Darwin’s Dogs, a similar endeavour that has shed light on aspects of canine behaviour, disease and the genetic origins of modern breeds. Darwin’s Cats was launched in mid-2024 and already has more than 3,000 cats enrolled, although not all have submitted fur samples. Participants from all parts of the world are asked to complete a number of free surveys about their pet’s physical traits, behaviour, environment, and health. © 2025 Guardian News & Media Limited

Keyword: Genes & Behavior; Development of the Brain
Link ID: 29708 - Posted: 03.19.2025

By Evan Bush, Aria Bendix and Denise Chow “This is simply the end.” That was the five-word message that Rick Huganir, a neuroscientist at Johns Hopkins University in Baltimore, received from a colleague just before 6 p.m. two Fridays ago, with news that would send a wave of panic through the scientific community. When Huganir clicked on the link in the email, from fellow JHU neuroscientist Alex Kolodkin, he saw a new National Institutes of Health policy designed to slash federal spending on the indirect costs that keep universities and research institutes operating, including for new equipment, maintenance, utilities and support staff. “Am I reading this right 15%??” Huganir wrote back in disbelief, suddenly worried the cut could stall 25 years of work. In 1998, Huganir discovered a gene called SYNGAP1. About 1% of all children with intellectual disabilities have a mutation of the gene. He’s working to develop drugs to treat these children, who often have learning differences, seizures and sleep problems. He said his research is almost entirely reliant on NIH grants. The search for a cure for these rare disorders is a race against time, because researchers think treatment will be most effective if administered when patients are children. “We’re developing therapeutics for the kids and may have a therapeutic that could be curing these kids in the next several years, but that research is going to be compromised,” Huganir said in an interview, estimating that scientists in his field could start a Phase 1 clinical trial within the next five years. “Any delay or anything that inhibits our research is devastating to the parents.”

Keyword: Miscellaneous
Link ID: 29707 - Posted: 03.15.2025

By Emily Kwong You probably know the feeling of having a hearty meal at a restaurant, and feeling full and satisfied … only to take a peek at the dessert menu and decide the cheesecake looks just irresistible. So why is it that you just absolutely couldn't have another bite, but you somehow make an exception for a sweet treat? Or as Jerry Sienfeld might put it back in the day "Whhaaaat's the deal with dessert?!" Scientists now have a better understanding of the neural origins of this urge thanks to a recent study published in the journal Science. Sponsor Message Working with mice, researchers tried to set up a scenario similar to the human experience described above. They started by offering a standard chow diet to mice who hadn't eaten since the previous day. That "meal" period lasted for 90 minutes, and the mice ate until they couldn't eat any more. Then it was time for a 30-minute "dessert" period. The first round of the experiment, researchers offered mice more chow for dessert, and the mice ate just a little bit more. The second time around, during the "dessert" period, they offered a high sugar feed to the mice for 30 minutes. The mice really went for the sugary feed, consuming six times more calories than when they had regular chow for dessert. In the mice, researchers monitored the activity of neurons that are associated with feelings of fullness, called POMC neurons. They're located in a part of the brain called the hypothalamus, which is "very important for promoting satiety," says Henning Fenselau, one of the study authors and a researcher at the Max Planck Institute for Metabolism Research in Cologne, Germany. © 2025 npr

Keyword: Obesity
Link ID: 29706 - Posted: 03.15.2025

By Christina Caron Victoria Ratliff, the wealthy financier’s wife on season 3 of HBO’s “The White Lotus,” has a problem: She keeps popping pills. And her drug of choice, the anti-anxiety medication lorazepam, has left her a little loopy. In the show, which follows guests vacationing at a fictional resort, Victoria pairs her medication with wine, which leads her to nod off at the dinner table. Sometimes she slurs her words. When she notices that her pill supply is mysteriously dwindling, she asks her children if they’re stealing them. “You don’t have enough lorazepam to get through one week at a wellness spa?” her daughter, Piper, asks “The White Lotus” is not the only show to recently feature these drugs. The new Max series “The Pitt,” which takes place in an emergency department, includes a story line about a benzodiazepine called Librium. This isn’t a case of Hollywood taking dramatic liberties. Benzodiazepines such as lorazepam and chlordiazepoxide are notorious for having the potential to be highly addictive. They may also come with difficult — sometimes fatal — withdrawal symptoms. The characters’ misuse of benzodiazepine drugs is not uncommon, said Dr. Ian C. Neel, a geriatrician at UC San Diego Health. “We definitely see that a lot in real life as well.” And in recent years, he added, studies have shown that it’s a bigger problem than doctors initially realized. The drugs, which are often called benzos or downers, are commonly used to treat anxiety, panic attacks and sleep disorders like restless leg syndrome. But they can also be used for other reasons, such as to help people manage alcohol withdrawal. © 2025 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 29705 - Posted: 03.15.2025

By Gina Kolata Women’s brains are superior to men’s in at least in one respect — they age more slowly. And now, a group of researchers reports that they have found a gene in mice that rejuvenates female brains. Humans have the same gene. The discovery suggests a possible way to help both women and men avoid cognitive declines in advanced age. The study was published Wednesday in the journal Science Advances. The journal also published two other studies on women’s brains, one on the effect of hormone therapy on the brain and another on how age at the onset of menopause shapes the risk of getting Alzheimer’s disease. The evidence that women’s brains age more slowly than men’s seemed compelling. Researchers, looking at the way the brain uses blood sugar, had already found that the brains of aging women are years younger, in metabolic terms, than the brains of aging men. Other scientists, examining markings on DNA, found that female brains are a year or so younger than male brains. And careful cognitive studies of healthy older people found that women had better memories and cognitive function than men of the same age. Dr. Dena Dubal, a professor of neurology at the University of California, San Francisco, set out to understand why. “We really wanted to know what could underlie this female resilience,” Dr. Dubal said. So she and her colleagues focused on the one factor that differentiates females and males: the X chromosome. Females have two X chromosomes; males have one X and one Y chromosome. Early in pregnancy, one of the X chromosomes in females shuts down and its genes go nearly silent. But that silencing changes in aging, Dr. Dubal found. © 2025 The New York Times Company

Keyword: Alzheimers; Sexual Behavior
Link ID: 29704 - Posted: 03.12.2025

By Kelly Servick New York City—A recent meeting here on consciousness started from a relatively uncontroversial premise: A newly fertilized human egg isn’t conscious, and a preschooler is, so consciousness must emerge somewhere in between. But the gathering, sponsored by New York University (NYU), quickly veered into more unsettled territory. At the Infant Consciousness Conference from 28 February to 1 March, researchers explored when and how consciousness might arise, and how to find out. They also considered hints from recent brain imaging studies that the capacity for consciousness could emerge before birth, toward the end of gestation. “Fetal consciousness would have been a less central topic at a meeting like this a few years ago,” says Claudia Passos-Ferreira, a bioethicist at NYU who co-organized the gathering. The conversation has implications for how best to care for premature infants, she says, and intersects with thorny issues such as abortion. “Whatever you claim about this, there are some moral implications.” How to define consciousness is itself the subject of debate. “Each of us might have a slightly different definition,” neuroscientist Lorina Naci of Trinity College Dublin acknowledged at the meeting before describing how she views consciousness—as the capacity to have an experience or a subjective point of view. There’s also vigorous debate about where consciousness arises in the brain and what types of neural activity define it. That makes it hard to agree on specific markers of consciousness in beings—such as babies—that can’t talk about their experience. Further complicating the picture, the nature of consciousness could be different for infants than adults, researchers noted at the meeting. And it may emerge gradually versus all at once, on different timescales for different individuals.

Keyword: Consciousness; Development of the Brain
Link ID: 29703 - Posted: 03.12.2025

By Mark Humphries There are many ways neuroscience could end. Prosaically, society may just lose interest. Of all the ways we can use our finite resources, studying the brain has only recently become one; it may one day return to dust. Other things may take precedence, like feeding the planet or preventing an asteroid strike. Or neuroscience may end as an incidental byproduct, one of the consequences of war or of thoughtlessly disassembling a government or of being sideswiped by a chunk of space rock. We would prefer it to end on our own terms. We would like neuroscience to end when we understand the brain. Which raises the obvious question: Is this possible? For the answer to be yes, three things need to be true: that there is a finite amount of stuff to know, that stuff is physically accessible and that we understand all the stuff we obtain. But each of these we can reasonably doubt. The existence of a finite amount of knowledge is not a given. Some arguments suggest that an infinite amount of knowledge is not only possible but inevitable. Physicist David Deutsch proposes the seemingly innocuous idea that knowledge grows when we find a good explanation for a phenomenon, an explanation whose details are hard to vary without changing its predictions and hence breaking it as an explanation. Bad explanations are those whose details can be varied without consequence. Ancient peoples attributing the changing seasons to the gods is a bad explanation, for those gods and their actions can be endlessly varied without altering the existence of four seasons occurring in strict order. Our attributing the changing seasons to the Earth’s tilt in its orbit of the sun is a good explanation, for if we omit the tilt, we lose the four seasons and the opposite patterns of seasons in the Northern and Southern hemispheres. A good explanation means we have nailed down some property of the universe sufficiently well that something can be built upon it. © 2025 Simons Foundation

Keyword: Consciousness
Link ID: 29702 - Posted: 03.12.2025

By Meghan Rosen and Laura Sanders Millions of Americans take antidepressants to help manage everything from depression and anxiety to post-traumatic stress disorder. Now, the Trump administration has announced that these drugs, which have been in use for decades and gone through rigorous testing, will be subject to new scrutiny. Invoking a burden of chronic disease, including in children, the administration has pledged to, in its words, “assess the prevalence of and threat posed by” certain commonly prescribed medications. In the coming months, its “Make America Healthy Again” commission plans to review a slew of existing medications, including SSRIs, or selective serotonin reuptake inhibitors. More than 10 percent of U.S. adults took antidepressants over the previous 30 days, data from 2015 to 2018 show. And SSRIs are among the most widely prescribed of those drugs. U.S. Health and Human Services Secretary Robert F. Kennedy Jr. has long questioned the safety of antidepressants and other psychiatric medicines, making misleading and unsubstantiated claims about the drugs. For instance, as recently as his January confirmation hearings, he likened taking SSRIs to having a heroin addiction. He also has suggested — without evidence — that SSRIs play a role in school shootings. With the executive order and statements like these, “it’s implied there is something nefarious or harmful” about antidepressants and related medications, says Lisa Fortuna, chair of the American Psychiatric Association’s Council on Children, Adolescents and Their Families. “People may think that they’re dangerous drugs.” © Society for Science & the Public 2000–2025

Keyword: Depression; Sexual Behavior
Link ID: 29701 - Posted: 03.12.2025

By Angie Voyles Askham Synaptic plasticity in the hippocampus involves both strengthening relevant connections and weakening irrelevant ones. That sapping of synaptic links, called long-term depression (LTD), can occur through two distinct routes: the activity of either NMDA receptors or metabotropic glutamate receptors (mGluRs). The mGluR-dependent form of LTD, required for immediate translation of mRNAs at the synapse, appears to go awry in fragile X syndrome, a genetic condition that stems from loss of the protein FMRP and is characterized by intellectual disability and often autism. Possibly as a result, mice that model fragile X exhibit altered protein synthesis regulation in the hippocampus, an increase in dendritic spines and overactive neurons. Treatments for fragile X that focus on dialing down the mGluR pathway and tamping down protein synthesis at the synapse have shown success in quelling those traits in mice, but they have repeatedly failed in human clinical trials. But the alternative pathway—via the NMDA receptor—may provide better results, according to a new study. Signaling through the NMDA receptor subunit GluN2B can also decrease spine density and alleviate fragile-X-linked traits in mice, the work shows. “You don’t have to modulate the protein synthesis directly,” says Lynn Raymond, professor of psychiatry and chair in neuroscience at the University of British Columbia, who was not involved in the work. Instead, activation of part of the GluN2B subunit can indirectly shift the balance of mRNAs that are translated at the synapse. “It’s just another piece of the puzzle, but I think it’s a very important piece,” she says. Whether this insight will advance fragile X treatments remains to be seen, says Wayne Sossin, professor of neurology and neurosurgery at Montreal Neurological Institute-Hospital, who was not involved in the study. Multiple groups have cured fragile-X-like traits in mice by altering what happens at the synapse, he says. “Altering translation in a number of ways seems to change the balance that is off when you lose FMRP. And it’s not really clear how specific that is for FMRP.” © 2025 Simons Foundation

Keyword: Development of the Brain; Learning & Memory
Link ID: 29700 - Posted: 03.12.2025

By Pam Belluck Postpartum depression affects about one in every seven women who give birth, but little is known about what happens in the brains of pregnant women who experience it. A new study begins to shed some light. Researchers scanned the brains of dozens of women in the weeks before and after childbirth and found that two brain areas involved in the processing and control of emotions increased in size in women who developed symptoms of postpartum depression. The results, published Wednesday in the journal Science Advances, constitute some of the first evidence that postpartum depression is associated with changes in the brain during pregnancy. Researchers found that women with symptoms of depression in the first month after giving birth also had increases in the volume of their amygdala, a brain area that plays a key role in emotional processing. Women who rated their childbirth experience as difficult or stressful — a perception that is often associated with postpartum depression — also showed increases in the volume of the hippocampus, a brain area that helps regulate emotions. “This is really the first step in trying to understand how does the brain change in people who have a normal course of pregnancy and then those who experience perinatal depression, and what can we do about it,” said Dr. Sheila Shanmugan, an assistant professor of psychiatry, obstetrics-gynecology and radiology at the University of Pennsylvania who was not involved in the study. “The big takeaways are about how there are these really profound brain changes during pregnancy and how now we’re seeing it in depression circuitry specifically,” she said. The study was conducted in Madrid by a team that has led efforts to document the effects of pregnancy on the brain. It is part of a growing body of research that has found that certain brain networks, especially those involved in social and emotional processing, shrink during pregnancy, possibly undergoing a fine-tuning process in preparation for parenting. Such changes correspond with surges in pregnancy hormones, especially estrogen, and some last at least two years after childbirth, researchers have found. © 2025 The New York Times Company

Keyword: Hormones & Behavior; Depression
Link ID: 29699 - Posted: 03.08.2025

By Katherine Bourzac Women tend to live longer than men and are often more resilient to cognitive decline as they age. Now researchers might have uncovered a source for this resilience: the second X chromosome in female cells that was previously considered ‘silent’. In work published today in the journal Science Advances1, a team reports that, at least in female mice, ageing activates expression of genes on what is usually the ‘silent’, or inactivated, X chromosome in cells in the hippocampus, a brain region crucial to learning and memory. And when the researchers gave mature mice of both sexes a type of gene therapy to boost expression of one of those genes, it improved their cognition, as measured by how well they explored a maze. Assuming these results can be confirmed in humans, the team suggests it could mean that women’s brains are being protected by their second X chromosome as they age — and that the finding could translate into future therapies boosting cognition for everyone. “The X chromosome is powerful,” says Rachel Buckley, a neurologist who studies sex differences in Alzheimer’s disease at Massachusetts General Hospital in Charlestown, and who was not involved in the research. This kind of work, she says, is helping researchers to understand “where female resilience lies and how to harness it”. (This article uses ‘women’ and ‘female’ to describe people with two X chromosomes and no Y chromosome, reflecting the language of the study. Nature recognizes that not all people who identify as women have this chromosomal make-up.) Double dose Female cells typically have two X chromosomes, one from each parent; male cells usually have one X and one Y. Early in development, one of the two X chromosomes in female cells is inactivated — coated in various proteins and RNA molecules that prevent its genes from being expressed. Which one is ‘silenced’ — meaning which parent it comes from — is random, and the tissues in the body are a mosaic of both types. © 2025 Springer Nature Limited

Keyword: Sexual Behavior; Stress
Link ID: 29698 - Posted: 03.08.2025

Andrew Gregory Health editor Doctors in London have successfully restored a sense of smell and taste in patients who lost it due to long Covid with pioneering surgery that expands their nasal airways to kickstart their recovery. Most patients diagnosed with Covid-19 recover fully. But the infectious disease can lead to serious long-term effects. About six in every 100 people who get Covid develop long Covid, with millions of people affected globally, according to the World Health Organization. Losing a sense of smell and taste are among more than 200 different symptoms reported by people with long Covid. Now surgeons at University College London Hospitals NHS Foundation Trust (UCLH) have cured a dozen patients, each of whom had suffered a profound loss of smell after a Covid infection. All had experienced the problem for more than two years and other treatments, such as smell training and corticosteroids, had failed. In a study aiming to find new ways to resolve the issue, surgeons tried a technique called functional septorhinoplasty (fSRP), which is typically used to correct any deviation of the nasal septum, increasing the size of nasal passageways. This boosts airflow into the olfactory region, at the roof of the nasal cavity, which controls smell. Doctors said the surgery enabled an increased amount of odorants – chemical compounds that have a smell – to reach the roof of the nose, where sense of smell is located. They believe that increasing the delivery of odorants to this area “kickstarts” smell recovery in patients who have lost their sense of smell to long Covid. © 2025 Guardian News & Media Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29697 - Posted: 03.08.2025

By Felicity Nelson A region in the brainstem, called the median raphe nucleus, contains neurons that control perseverance and exploration.Credit: K H Fung/Science Photo Library Whether mice persist with a task, explore new options or give up comes down to the activity of three types of neuron in the brain. In experiments, researchers at University College London (UCL) were able to control the three behaviours by switching the neurons on and off in a part of the animals’ brainstem called the median raphe nucleus. The findings are reported in Nature today1. “It’s quite remarkable that manipulation of specific neural subtypes in the median raphe nucleus mediates certain strategic behaviours,” says neuroscientist Roger Marek at the Queensland Brain Institute in Brisbane, Australia, who was not involved in the work. Whether these behaviours are controlled in the same way in humans needs to be confirmed, but if they are, this could be relevant to certain neuropsychiatric conditions that are associated with imbalances in the three behavioural strategies, says Sonja Hofer, a co-author of the paper and a systems neuroscientist at UCL. For instance, an overly high drive to persist with familiar actions and repetitive behaviours can be observed in people with obsessive–compulsive disorder and autism, she says. Conversely, pathological disengagement and lack of motivation are symptoms of major depressive disorder, and an excessive drive to explore and inability to persevere with a task is seen in attention deficit hyperactivity disorder. “It could be that changes in the firing rate of specific median raphe cell types could contribute to certain aspects of these conditions,” says Hofer. © 2025 Springer Nature Limited

Keyword: Attention
Link ID: 29696 - Posted: 03.08.2025

Nicola Davis Science correspondent Which songs birds sing can – as with human music – be influenced by age, social interactions and migration, researchers have found. Not all birds learn songs, but among those that do, individuals, neighbourhoods and populations can produce different collections of tunes, akin to different music albums. Now researchers have found that changes in the makeup of a group of birds can influence factors including which songs they learn, how similar those songs are to each other and how quickly songs are replaced. Dr Nilo Merino Recalde, the first author of the study, from the University of Oxford, said: “This is very interesting, I think, partly because it shows that there are all these kind of common elements at play when it comes to shaping learned traits, [similar to] what happens with human languages and human music.” But he said the parallels had their limits. “The function and the role of human music and language is very, very different to the function of birdsong,” he said. “Birdsong is used to repel rivals, to protect territories, to entice mates, this kind of thing. And that also shapes songs.” Writing in the journal Current Biology, Recalde and colleagues describe how they used physical tracking as well as artificial intelligence to match recorded songs to individual male great tits living in Wytham Woods in Oxford. In total, the study encompassed 20,000 hours of sound recordings and more than 100,000 songs, captured over three years. The researchers used their AI models to analyse the repertoires of individual birds, those within neighbourhoods and across the entire population to explore how similar the various songs were. As a result, the team were able to unpick how population turnover, immigration and age structure influenced the songs. © 2025 Guardian News & Media Limited

Keyword: Animal Communication; Language
Link ID: 29695 - Posted: 03.08.2025

By Tim Vernimmen On a rainy day in July 2024, Tim Bliss and Terje Lømo are in the best of moods, chuckling and joking over brunch, occasionally pounding the table to make a point. They’re at Lømo’s house near Oslo, Norway, where they’ve met to write about the late neuroscientist Per Andersen, in whose lab they conducted groundbreaking experiments more than 50 years ago. The duo only ever wrote one research paper together, in 1973, but that work is now considered a turning point in the study of learning and memory. Published in the Journal of Physiology, it was the first demonstration that when a neuron — a cell that receives and sends signals throughout the nervous system — signals to another neuron frequently enough, the second neuron will later respond more strongly to new signals, not for just seconds or minutes, but for hours. It would take decades to fully understand the implications of their research, but Bliss and Lømo had discovered something momentous: a phenomenon called long-term potentiation, or LTP, which researchers now know is fundamental to the brain’s ability to learn and remember. Today, scientists agree that LTP plays a major role in the strengthening of neuronal connections, or synapses, that allow the brain to adjust in response to experience. And growing evidence suggests that LTP may also be crucially involved in a variety of problems, including memory deficits and pain disorders. Bliss and Lømo never wrote another research article together. In fact, they would soon stop working on LTP — Bliss for about a decade, Lømo for the rest of his life. Although the researchers knew they had discovered something important, at first the paper “didn’t make a big splash,” Bliss says. By the early 1970s, neuroscientist Eric Kandel had demonstrated that some simple forms of learning can be explained by chemical changes in synapses — at least in a species of sea slug. But scientists didn’t yet know if such findings applied to mammals, or if they could explain more complex and enduring types of learning, such as the formation of memories that may last for years.

Keyword: Learning & Memory
Link ID: 29694 - Posted: 03.05.2025

By Sydney Wyatt Numerous actions by the Trump administration over the past month have caused confusion and fear throughout the U.S. scientific community. In response, a group called Stand Up for Science, which says it opposes attacks on science and on efforts to improve diversity, equity and inclusion (DEI) in research, has planned rallies on 7 March in Washington, D.C., and across the United States. “The biggest thing for us is that science is for everyone, in that it benefits every person,” says rally co-organizer Colette Delawalla, a graduate student in clinical psychology at Emory University. “It doesn’t matter who you voted for. It doesn’t even matter if you voted or not.” The event is reminiscent of the 2017 March for Science, which drew more than 1 million attendees in 600 cites around the world to show support for scientific research and protest proposed budget cuts to the U.S. National Institutes of Health and other federal agencies during Donald Trump’s first term as president. Scientists were divided in their views about that march, with some criticizing it for a lack of concrete goals and others saying it engaged more people with science and policy than ever before. This year is no different. Some scientists say protests do little to change minds, whereas others say it can raise awareness. The effectiveness of a protest depends on several factors, including the clarity of its goals, the scope of the target audience, the tactics used and whether the movement continues after the initial event, says Susan Olzak, professor emerita of sociology at Stanford University. “Temporary, fleeting protests are not likely to have much of an effect on anything, but if you have a sustained campaign, then you’re more likely to have some kind of impact, even if it’s just on public opinion,” Olzak says. © 2025 Simons Foundation

Keyword: Miscellaneous
Link ID: 29693 - Posted: 03.05.2025

By Jyoti Madhusoodanan In June 2021, 63-year-old Lisa Daurio was making the two-hour drive from her hometown of Pueblo, Colorado, to a doctor’s appointment in Denver when she settled on a life-changing decision: She would tell her doctor she was ready to stop taking her weekly injections to treat her multiple sclerosis. Daurio was not cured, but her condition had remained stable for more than a decade. As she got older, her doctor had periodically asked if she wanted to consider halting her medication. It’s an unusual question in modern medicine: Clinicians don’t typically ask people with arthritis, high cholesterol, diabetes, or other chronic conditions whether they’d like to stop taking their medication as they get older. But MS is an unusual disease, the result of immune cells attacking a person’s brain, optic nerves and spinal cord. The subsequent nerve injuries trigger burning pain, numbness, loss of balance, and a range of other symptoms. These hallmark immune assaults and symptoms flare up sporadically in younger adults and, for some people, seem to quiet down as they age into their 50s and beyond. Still, Daurio’s decision to stop wasn’t straightforward. Her MS symptoms began when she was in her late 30s, with a sense of overwhelming fatigue, a numbness in her legs, and a “feeling of fire ants” that ran “from the back of my neck around the front of my face,” she said. She was diagnosed with MS in 2003, when her entire left side went numb, and she thought she was having a stroke. The weekly injections had kept all of those symptoms at bay for more than a decade. When her doctor broached the idea of stopping them, Daurio’s reaction was “it’s working, let’s not mess with what’s not broken,” she said. Staying on her medication wasn’t always easy. For about 10 years, every dose made her feel like she had the flu. After each shot, she spent two days on Tylenol and a steroid named prednisone to cope with the side effects. But Daurio stuck with the regimen because the injection seemed to help; she had not had a single relapse since 2009, and periodic MRI scans showed no new signs of immune attacks on her brain.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 29692 - Posted: 03.05.2025