By Simon Makin Positive thinking may boost the body’s defenses against disease. Increasing activity in a brain region that controls motivation and expectation, specifically the brain’s reward system, is linked with making more antibodies after receiving a vaccine. The finding suggests these boosts were related to the placebo effect, researchers report January 19 in Nature Medicine. “Placebo is a self-help mechanism, and here we actually harness it,” says Talma Hendler, a neuroscientist at Tel Aviv University. “This suggests we could use the brain to help the body fight illness.” The work is important because it “is first-in-human evidence of a relationship between brain reward systems and immune function,” says Tor Wager, a neuroscientist at Dartmouth College in Hanover, N.H., who was not involved in the study. The study was not designed to test vaccine effectiveness. Larger studies, including more complete immune assessments, will be required to test this association as a medical intervention. Scientists have found many links between the brain and bodily health. Both negative and positive mental states can affect the immune system, and studies in rodents have suggested that the brain’s reward network is involved in these effects. To find out if the same circuitry was at play in humans, Hendler and colleagues trained healthy volunteers to regulate their brain activity using neurofeedback, a technique that uses brain imaging to show users the activity of the area they are trying to boost. The team randomly assigned 85 participants to receive training aimed at increasing activity in either their reward network or a different network, or to receive no training. © Society for Science & the Public 2000–2026.

Keyword: Neuroimmunology
Link ID: 30099 - Posted: 01.31.2026

By Alessio Cozzolino After a heart attack, the heart “talks” to the brain. And that conversation may make recovery worse. Shutting down nerve cells that send messages from injured heart cells to the brain boosted the heart’s ability to pump and decreased scarring, experiments in mice show. Targeting inflammation in a part of the nervous system where those “damage” messages wind up also improved heart function and tissue repair, scientists report January 27 in Cell. “This research is another great example highlighting that we cannot look at one organ and its disease in isolation,” says Wolfram Poller, an interventional cardiologist at Massachusetts General Hospital and Harvard Medical School who was not involved in the study. “And it opens the door to new therapeutic strategies and targets that go beyond the heart.” Someone in the United States has a heart attack about every 40 seconds, according to the U.S. Centers for Disease Control and Prevention. That adds up to about 805,000 people each year. A heart attack is a mechanical problem caused by the obstruction of a coronary artery, usually by a blood clot. If the blockage lasts long enough, the affected cells may start to die. Heart attacks can have long-term effects such as a weakened heart, a reduced ability to pump blood, irregular heart rhythms, and a higher risk of heart failure or another heart attack. Although experts knew from previous research that the nervous and immune systems could amplify inflammation and slow healing, the key players and pathways involved were unknown, says Vineet Augustine, a neurobiologist at the University of California, San Diego. © Society for Science & the Public 2000–2026

Keyword: Neuroimmunology
Link ID: 30098 - Posted: 01.28.2026

By Joshua P. Johansen Growing up in the 1980s in Santa Cruz, California, where redwood-covered mountains descend to the rocky edge of the Pacific, might sound idyllic. But in the dark wake of the drug-fueled ’70s, the beach town could also be frightening. There was a bully at my high school who once chased me down the street threatening to hurt me. Unsurprisingly, catching sight of him in the hallways or at the skate park filled me with dread. Just walking past his house would trigger a wave of anxiety. Yet if I saw him in class, with teachers present, I felt more at ease. How did my brain know to fear him only in specific circumstances? More broadly, how did I infer emotional significance from the world around me? The fact that I or anyone can make these judgments suggests that emotion arises from an internal model in the brain that supports inference, abstraction and flexible, context-dependent evaluations of threat or safety. These model-based emotion systems helped me infer danger from otherwise innocuous features of the environment, such as the bully’s house, or to downgrade my alarm, as I did when an adult was present. Understanding the neural basis of emotion is a central question in neuroscience, with profound implications for the treatment of anxiety, trauma and mood disorders. Yet the field remains divided over what emotions are and how they should be defined, limiting progress. On one side are neurobiologists focused on the neural underpinnings of simple learned and innate defensive behaviors. On the other are psychological theorists who view emotions as subjective experiences arising from complex conceptual brain models of the world that are unique to humans. This divide fuels persistent arguments over whether emotion should be defined primarily as a conscious state or not. Though subjective feelings are undeniably important, limiting our definitions to conscious phenomena prevents us from studying the underlying mechanisms in nonhuman species. To move forward, we need to identify the conserved neural processes that support higher-order, internal-model-based emotional experiences across species, regardless of whether they rise to consciousness. © 2026 Simons Foundation

Keyword: Emotions; Consciousness
Link ID: 30096 - Posted: 01.28.2026

Heidi Ledford For decades, researchers have noted that cancer and Alzheimer’s disease are rarely found in the same person, fuelling speculation that one condition might offer some degree of protection from the other. Now, a study in mice provides a possible molecular solution to the medical mystery: a protein produced by cancer cells seems to infiltrate the brain, where it helps to break apart clumps of misfolded proteins that are often associated with Alzheimer’s disease. The study, which was 15 years in the making, was published on 22 January in Cell1 and could help researchers to design drugs to treat Alzheimer’s disease. “They have a piece of the puzzle,” says Donald Weaver, a neurologist and chemist at the Krembil Research Institute at the University of Toronto in Canada, who was not involved in the study. “It’s not the full picture by any stretch of the imagination. But it’s an interesting piece.” Alzheimer’s mystery Weaver has been interested in that puzzle ever since he began his medical training, when a senior pathologist made an offhand comment: “If you see someone with Alzheimer’s disease, they’ve never had cancer.” The remark stuck with Weaver over the years as he diagnosed thousands of people with Alzheimer’s disease. “I can’t remember a single one that has had cancer,” he says. Epidemiological data do not draw such a clear divide, but a 2020 meta-analysis of data from more than 9.6 million people found that cancer diagnosis was associated with an 11% decreased incidence of Alzheimer’s disease2. It has been a difficult relationship to unpick: researchers must control for a variety of external factors. For example, people might die of cancer before they are old enough to develop symptoms of Alzheimer’s disease, and some cancer treatments can cause cognitive difficulties, which could obscure an Alzheimer’s diagnosis. © 2026 Springer Nature Limited

Keyword: Alzheimers; Stress
Link ID: 30092 - Posted: 01.24.2026

By Darren Incorvaia Much like his ninja namesake, Naruto the white-lipped peccary was a bit of a loner. Named after the titular character from a popular manga and anime, Naruto was the youngest male and one of the least social in his group of 17 peccaries, all of whom were born and raised in captivity at the Laboratory of Applied Ethology at the State University of Santa Cruz in Ilhéus, Brazil. Destined for reintroduction into Brazil’s Estação Veracel Private Natural Heritage Reserve and the Pau-Brasil Ecological Station, the peccaries were each given a personality test of sorts by lab researchers. The piglike mammals were video recorded as they went about their daily lives, resulting in 17 hours’ worth of behavioral data. Their aggressive actions, friendly touches and moments of exploration were tallied so that the peccaries could be ranked in traits such as boldness and sociability. The goal was to determine whether an individual peccary’s behavioral traits influenced its survival when released into the wild. White-lipped peccaries (Tayassu pecari) are listed as vulnerable by the International Union for Conservation of Nature, or IUCN. In Brazil, the size of the species’ historical range had plunged by 60 percent by 2020, and past efforts to reintroduce them had met limited success. Around the globe, scientists are increasingly recognizing how a reintroduced animal’s personality can impact how both individuals and groups fare in the wild. Such work is part of a growing trend to infuse the study of personality, and how it affects behavior, into conservation. When working with wild animals and tight budgets, personality tests may not always be possible. But understanding animal personality could help conservationists choose which individuals stand the best chance of surviving — helping to restore populations threatened with extinction. © Society for Science & the Public 2000–2026.

Keyword: Emotions; Evolution
Link ID: 30083 - Posted: 01.17.2026

Lynne Peeples Sometimes the hardest part of doing an unpleasant task is simply getting started — typing the first word of a long report, lifting a dirty dish on the top of an overfilled sink or removing clothes from an unused exercise machine. The obstacle isn’t necessarily a lack of interest in completing a task, but the brain’s resistance to taking the first step. Now, scientists might have identified the neural circuit behind this resistance, and a way to ease it. In a study1 published today in Current Biology, researchers describe a pathway in the brain that seems to act as a ‘motivation brake’, dampening the drive to begin a task. When the team selectively suppressed this circuit in macaque monkeys, goal-directed behaviour rebounded. “The change after this modulation was dramatic,” says study co-author Ken-ichi Amemori, a neuroscientist at Kyoto University in Japan. The motivation brake, which can be particularly stubborn for people with certain psychiatric conditions, such as schizophrenia and major depressive disorder, is distinct from the avoidance of tasks driven by risk aversion in anxiety disorders. Pearl Chiu, a computational psychiatrist at Virginia Tech in Roanoke, who was not involved in the study, says that understanding this difference is essential for developing new treatments and refining current ones. “Being able to restore motivation, that’s especially exciting,” she says. Motivated macaques Previous work on task initiation has implicated a neural circuit connecting two parts of the brain known as the ventral striatum and ventral pallidum, both of which are involved in processing motivation and reward2,3,4. But attempts to isolate the circuit’s role have fallen short. Electrical stimulation, for example, inadvertently activates downstream regions, affecting motivation, but also anxiety. © 2026 Springer Nature Limited

Keyword: Learning & Memory; Emotions
Link ID: 30079 - Posted: 01.14.2026

By Natalia Mesa Nestled in the ventromedial nucleus of the hypothalamus lies a cluster of neurons that can make otherwise mild-mannered mice fly into a rage. Stimulating these neurons, as if flipping a switch, prompts male mice to attack their cagemates. The optogenetic manipulation of these and other specialized hypothalamic neurons, starting in the early 2010s, supported the long-standing idea that distinct cell types act as an “on” switch for different innate behaviors. But it has proved challenging to disentangle the neural signals that underlie those innate behaviors from ones that drive an animal’s internal state—such as anger, hunger or sexual arousal. Mounting evidence suggests that the hypothalamus also gives rise to these internal states, which can shape innate perceptions and behaviors. Rather than triggering an innate behavior, a specific pattern of population activity encodes the intensity and duration of anger and sexual arousal, according to four studies published within the past three years. This work is “revolutionary for the hypothalamus community,” says Tatiana Engel, associate professor of computational neuroscience at the Princeton Neuroscience Institute, who was not involved in the studies. It upends the notion that the neurons in the hypothalamus merely act as a simple switchboard, Engel says. Instead, local computations in the hypothalamus keep track of the animal’s internal state and influence its behavior, the studies suggest. The hypothalamic signals that encode the intensity and duration of aggression and sexual arousal can be represented by a mathematical model called a line attractor, the four studies show. © 2026 Simons Foundation

Keyword: Emotions; Evolution
Link ID: 30073 - Posted: 01.10.2026

By Sachin Rawat One can spend hours looking at a calm sunset or a clear night sky. These scenes are not only effortless on the eyes — they may also be easy on the brain. People tend to like visual stimuli that require little cognitive effort to process, researchers report in the December PNAS Nexus. The brain is the most energy-guzzling organ in the body, and visual processing alone accounts for nearly half of its energy use. Researchers have long studied how the visual system conserves energy. But the new study addresses the question from a different perspective. “Not only is the visual system optimized for efficiency, but we might have aesthetic preferences for stimuli that are efficient to process,” says Mick Bonner, a neuroscientist at Johns Hopkins University who was not involved in the study. Neuroscientist Dirk Bernhardt-Walther of the University of Toronto and his colleagues suspected that such preferences could have evolved as cognitive shortcuts, helping organisms avoid excessive effort as they navigate their environment. To probe the energy consumed in visual processing, the researchers turned to an existing functional MRI dataset, in which four individuals viewed 5,000 images while their brain activity was monitored. Measurements of oxygen consumption in different parts of the brain provided an indicator of metabolic activity. The team also ran these images through an artificial neural network trained on object and scene recognition, using the proportion of activated “neurons” as a proxy for metabolic expense. The researchers then compared these metabolic cost estimates — both human and artificial — to the images’ aesthetic ratings, gathered from more than 1,000 online survey respondents who scored each picture on a five-point scale. In both cases, the metabolic effort required to process the images was inversely proportional to their aesthetic ratings. © Society for Science & the Public 2000–2026.

Keyword: Vision; Emotions
Link ID: 30072 - Posted: 01.10.2026

By Carl Zimmer If you live in the United States, chances are you’re familiar with the game rock-paper-scissors. You put out your hand in one of three gestures: clenching it in a fist (rock), holding it out flat (paper) or holding up two fingers in a “V” (scissors). Rock beats scissors, scissors beat paper and paper beats rock. Americans by no means have a monopoly on the game. People play it around the world in many variations, and under many names. In Japan, where the game has existed for thousands of years, it’s known as janken. In Indonesia, it’s known as earwig-man-elephant: The elephant kills the man, the man kills the earwig and the earwig crawls up through the elephant’s trunk and eats its brain. The game is so common that it exists beyond our own species. Over millions of years, animals have evolved their own version of rock-paper-scissors. For them, winning the game means passing down their genes to future generations. A study published on Thursday in the journal Science reveals the hidden biology that makes the game possible — and shows how it may be an important source of nature’s diversity. The first clues that nature also played rock-paper-scissors emerged three decades ago in the dry hills outside Merced, Calif. Barry Sinervo, a biologist then at Indiana University, studied the common side-blotched lizard there. He would mark the lizards — named for the dark blue or black spot on their side, just behind the front leg — release them into the tall grass and catch the survivors to check up on them in later years. Dr. Sinervo, who later joined the faculty at the University of California, Santa Cruz, and who died in 2021, grew fascinated by the strange mating habits of the lizards. At the start of every breeding season, the males developed one of three colors on their throats: blue, orange or yellow. And depending on their color, the males behaved differently. © 2026 The New York Times Company

Keyword: Aggression; Animal Communication
Link ID: 30071 - Posted: 01.07.2026

Andrew Gregory Health editor Scientists have discovered two new subtypes of multiple sclerosis with the aid of artificial intelligence, paving the way for personalised treatments and better outcomes for patients. Millions of people have the disease globally – but treatments are mostly selected on the basis of symptoms, and may not be effective because they don’t target the underlying biology of the patient. Now, scientists have detected two new biological strands of MS using AI, a simple blood test and MRI scans. Experts said the “exciting” breakthrough could revolutionise treatment of the disease worldwide. In research involving 600 patients, led by University College London (UCL) and Queen Square Analytics, researchers looked at blood levels of a special protein called serum neurofilament light chain (sNfL). The protein can help indicate levels of nerve cell damage and signal how active the disease is. The sNfL results and scans of the patients’ brains were interpreted by a machine learning model, called SuStaIn. The results, published in medical journal Brain, revealed two distinct types of MS: early sNfL and late sNfL. In the first subtype, patients had high levels of sNfL early on in the disease, with visible damage in a part of the brain called the corpus callosum. They also developed brain lesions quickly. This type appears to be more aggressive and active, scientists said. In the second subtype, patients showed brain shrinkage in areas like the limbic cortex and deep grey matter before sNfL levels went up. This type seems to be slower, with overt damage occurring later. Researchers say the breakthrough will enable doctors to more precisely understand which patients are at higher risk of different complications, paving the way for more personalised care. © 2025 Guardian News & Media Limited

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 30058 - Posted: 12.31.2025

By Calli McMurray For the past two and a half years, a team of five labs in the San Francisco Bay Area have endeavored to nail down how psilocybin affects the way mice behave. Psilocybin and other psychedelic drugs have been shown to improve anxiety and depression symptoms in people, but results in mouse studies are less consistent. Those inconsistencies spell trouble for researchers trying to unpack the drug’s mechanism, because if behavioral changes in mice don’t mirror those in humans, the underlying biological changes might be irrelevant, says team member Boris Heifets, associate professor of anesthesiology, perioperative and pain medicine at Stanford University. So, to establish a behavioral ground truth, the five labs gave about 200 mice the same dose of psilocybin and measured how the drug affected the animals’ performance on a range of simple behavioral assays, including the elevated plus maze and open field, tail suspension and forced swim tests, while taking the drug as well as 24 hours later. While on psilocybin, the mice showed a temporary increase in anxiety-like behaviors, including spending less time than usual exploring new objects and open areas, the team reported in April. But, unlike in people, the drug had no lasting effects once it wore off. The issue, some behavioral neuroscientists argue, is not replication between labs—it’s the assays themselves. “I love the idea of these multisite experiments in animal models, but the models—the behavioral models—still have to be the right ones,” says Jennifer Mitchell, professor of neurology and psychiatry and behavioral sciences at the University of California, San Francisco. “The tests themselves—I’m not sure how much they tell us about what a psychedelic is actually doing.” © 2025 Simons Foundation

Keyword: Depression; Drug Abuse
Link ID: 30055 - Posted: 12.20.2025

Lynne Peeples Near the end of his first series of chess matches against IBM’s Deep Blue computer in 1996, the Russian grandmaster Garry Kasparov lamented what he saw as an unfair disadvantage: “I’m really tired. These games took a lot of energy. But if I play a normal human match, my opponent would also be exhausted.” Why thinking hard makes us feel tired Whereas machine intelligence can keep running as long as it has a power supply, a human brain will become fatigued — and you don’t have to be a chess grandmaster to understand the feeling. Anyone can end up drained after a long day of work, at school or juggling the countless decisions of daily life. This mental exhaustion can sap motivation, dull focus and erode judgement. It can raise the odds of careless mistakes. Especially when combined with sleep loss or circadian disruption, cognitive fatigue can also contribute to deadly medical errors and road traffic accidents. It was partly Kasparov’s weary comments that inspired Mathias Pessiglione, a cognitive neuroscientist and research director at the Paris Brain Institute, to study the tired brain. He wanted to know: “Why is this cognitive system prone to fatigue?” Researchers and clinicians have long struggled to define, measure and treat cognitive fatigue — relying mostly on self-reports of how tired someone says they feel. Now, however, scientists from across disciplines are enlisting innovative experimental approaches and biological markers to probe the metabolic roots and consequences of cognitive fatigue. The efforts are getting a boost in attention and funding in large part because of long COVID, which afflicts roughly 6 in every 100 people after infection with the coronavirus SARS-CoV-2, says Vikram Chib, a biomedical engineer at Johns Hopkins University in Baltimore, Maryland. “The primary symptom of long COVID is fatigue,” says Chib. “I think that has opened a lot of people’s eyes.” © 2025 Springer Nature Limited

Keyword: Neuroimmunology; Attention
Link ID: 30049 - Posted: 12.13.2025

Jonathan Lambert For centuries, the nature of a fever — and whether it's good or bad — has been hotly contested. In ancient Greece, the physician Hippocrates thought that fever had useful qualities, and could cook an illness out of a patient. Later on, around the 18th century, many physicians regarded fever as a distinct illness, one that could actually cook the patient, and so should be treated. These days, researchers understand that fever is part of the immune system's response to a pathogen, one that's shared by many animal species. And while there's accumulating evidence that fevers can help kick an infection, precisely how they can help remains mysterious. Sponsor Message "There's a cultural knowledge that there's this relationship between temperature and viruses, but at a molecular level, we're quite unsure how temperature might be impacting viruses," says Sam Wilson, a microbiologist at the University of Cambridge. There are two main ideas, he says. The heat of a fever itself could be harming the virus, akin to Hippocrates' hypotheses. Alternatively, the heat is a means to an end, either stoking our immune system to work better, or simply a regrettable, but unavoidable byproduct of fighting off an infection. "The fact that there weren't definitive answers to these questions piqued my interest," says Wilson. That interest led to a study, published Thursday in Science, that suggests — at least in mice — that elevated temperature alone is enough to fight off some viruses. © 2025 npr

Keyword: Neuroimmunology
Link ID: 30035 - Posted: 12.03.2025

By Trip Gabriel Paul Ekman, a psychologist who linked thousands of facial expressions to the emotions they often subconsciously conveyed, and who used his research to advise F.B.I. interrogators and screeners for the Transportation Security Administration as well as Hollywood animators, died on Nov. 17 at his home in San Francisco. He was 91. His daughter, Eve Ekman, confirmed the death. Dr. Ekman sought to add scientific exactitude to the human impulse to interpret how others feel through their facial expressions. He recorded 18 types of smiles, for example, distinguishing between a forced smile and a spontaneous one; a genuine smile, he discovered, crinkles the orbicularis oculi muscle — that is, it creates crow’s feet around the eyes. Sometimes described as the world’s most famous face reader, Dr. Ekman was ranked No. 15 in 2015 by the American Psychological Association in its list of 200 eminent psychologists of the modern era. He was influential in reshaping the way facial expressions were understood — as the product of evolution rather than environment — and his findings crossed over to popular culture. The Fox TV drama “Lie to Me,” which ran for three seasons starting in 2009, featured a psychologist modeled on Dr. Ekman (played by Tim Roth) who assists criminal investigations by decoding the hidden meanings of facial expressions and body language. The show was developed by the producer Brian Grazer, who was inspired by a lengthy profile of Dr. Ekman by Malcolm Gladwell in The New Yorker in 2002. “The idea that you could tell a liar by some scientific test and know what they’re feeling just by looking at them was staggering to me,” the show’s writer, Samuel Baum, told The New York Times in 2009. As a young research psychologist in the late 1960s, Dr. Ekman changed the scientific consensus on facial expressions. In the postwar era, the conventional wisdom of eminent anthropologists like Margaret Mead was that human facial expressions were learned and that they varied across cultures. © 2025 The New York Times Company

Keyword: Emotions; Evolution
Link ID: 30031 - Posted: 11.29.2025

Mark Brown Sophisticated and deadly “brain weapons” that can attack or alter human consciousness, perception, memory or behaviour are no longer the stuff of science fiction, two British academics argue. Michael Crowley and Malcolm Dando, of Bradford University, are about to publish a book that they believe should be a wake-up call to the world. They are this weekend travelling to The Hague for a key meeting of states, arguing that the human mind is a new frontier in warfare and there needs to be urgent global action to prevent the weaponisation of neuroscience. “It does sound like science fiction,” said Crowley. “The danger is that it becomes science fact.” The book, published by the Royal Society of Chemistry, explores how advances in neuroscience, pharmacology and artificial intelligence are coming together to create a new threat. “We are entering an era where the brain itself could become a battlefield,” said Crowley. “The tools to manipulate the central nervous system – to sedate, confuse or even coerce – are becoming more precise, more accessible and more attractive to states.” The book traces the fascinating, if appalling, history of state-sponsored research into central nervous system (CNS)-acting chemicals. During the cold war and after, the US, Soviet Union and China all “actively sought” to develop CNS-acting weapons, said Crowley. Their purpose was to cause prolonged incapacitation to people, including “loss of consciousness or sedation or hallucination or incoherence or paralysis and disorientation”. © 2025 Guardian News & Media Limited

Keyword: Drug Abuse; Aggression
Link ID: 30023 - Posted: 11.22.2025

On 19 November 2025, the U.S. Centers for Disease Control and Prevention changed language on a “vaccine safety” page on its website to assert that the statement “vaccines do not cause autism” is not evidence based. The updated CDC page now incorrectly suggests that a link between infant vaccination and autism exists, and it casts doubt on a wealth of research that has produced evidence to the contrary. The updated language contradicts decades of research findings that show vaccines do not cause autism. The move has also prompted backlash from multiple groups, including the Coalition of Autism Scientists and the Autism Science Foundation. “These sort of claims have been repeatedly debunked by good science and multiple independent replications of negative studies, and for years no scientist has opined that more research is needed,” Eric Fombonne, professor emeritus of psychiatry at Oregon Health & Science University, told The Transmitter. He noted several problems with the arguments presented on the CDC website, including the citation of “fringe studies executed by uncredentialed authors with poor methodologies and published in low-quality journals.” Fombonne described the authors of the page as having “cherry pick[ed data] … in support of their preconceived beliefs” and mischaracterizing well-conducted and replicated research. Experts The Transmitter spoke with raised many concerns about the agency’s statements, including how those statements could confuse families and whether they indicate shifts in priorities that threaten solid scientific research. “Families deserve honest answers,” says David Mandell, professor of psychiatry at the University of Pennsylvania and director of the Penn Center for Mental Health. © 2025 Simons Foundation

Keyword: Autism; Neuroimmunology
Link ID: 30020 - Posted: 11.22.2025

Steven Morris Some people respond to the unwanted attentions of a gull eyeing up a bag of chips or a Cornish pasty by frantically flapping their hands at the hungry bird while others beat a rapid retreat into the nearest seaside shelter. But researchers have found that a no-nonsense yell – even a relatively quiet one – may be the best way to get rid of a pesky herring gull. Animal behaviourists from the University of Exeter tried to establish the most effective method of countering a feathery threat by placing a portion of chips in a place where gulls were bound to find them. Once a gull approached, they played three recordings. First, a male voice shouting: “No, stay away, that’s my food, that’s my pasty!” Then, the same voice speaking the same words was played, followed by the “neutral” birdsong of a robin. Study finds shouting is best way to get rid of pesky seagulls – video They tested 61 gulls across nine seaside towns in Cornwall and found nearly half of the birds exposed to the shouting voice flapped away within a minute. Only 15% of the gulls exposed to the speaking male voice flew off, though the rest walked away from the food, still apparently sensing danger. In contrast, 70% of gulls exposed to the robin song stayed put. The volume of the “shouting” and “speaking” voices was the same, meaning the gulls seemed to be responding to the acoustic properties of the message rather than the loudness. © 2025 Guardian News & Media Limited

Keyword: Aggression
Link ID: 30008 - Posted: 11.12.2025

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

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

Katie Kavanagh Why are we able to remember emotional events so well? According to a study published today in Nature1, a type of cell in the brain called an astrocyte is a key player in stabilizing memories for long-term recall. Astrocytes were thought to simply support neurons in creating the physical traces of memories in the brain, but the study found that they have a much more active role — and can even be directly triggered by repeated emotional experiences. The researchers behind the finding suggest that the cells could be a fresh target for treating memory conditions such as those associated with post-traumatic stress disorder and Alzheimer’s disease. “We provide an answer to the question of how a specific memory is stored for the long term,” says study co-author Jun Nagai, a neuroscientist at RIKEN Center for Brain Science in Wako, Japan. By studying astrocytes, Nagai said, the study identifies how the brain selectively filters important memories at the cellular level. Stable memories Nagai and his colleagues focused on the question of memory stabilization: how a short-term memory becomes more permanent in the brain. Previous research had found physical traces of memories in neuronal networks in brain regions such as the hippocampus and amygdala2. But it was unclear how these ‘engrams’ were stored in the brain as lasting memories after repeated exposure to the same stimulus. To dig deeper, the researchers developed a method for measuring activation patterns in astrocytes across a whole brain of a mouse as it completes a memory task. They measured the upregulation of a gene called Fos — an early marker of cell activity that is associated with the physical traces of memories in the brain3. © 2025 Springer Nature Limited

Keyword: Learning & Memory; Emotions
Link ID: 29975 - Posted: 10.18.2025

By Michele Cohen Marill Like many first-time mothers, Lisette Lopez-Rose thought childbirth would usher in a time of joy. Instead, she had panic attacks as she imagined that something bad was going to happen to her baby, and she felt weighed down by a sadness that wouldn’t lift. The San Francisco Bay Area mother knew her extreme emotions weren’t normal, but she was afraid to tell her obstetrician. What if they took her baby away? At about six months postpartum, she discovered an online network of women with similar experiences and ultimately opened up to her primary care doctor. “About two months after I started medication, I started to feel like I was coming out of a deep hole and seeing light again,” she says. Today, Lopez-Rose works at Postpartum Support International, coordinating volunteers to help new mothers form online connections. About one in eight US women go through a period of postpartum depression, making it among the most common complications of childbirth. It typically occurs in the first few weeks after delivery, when there’s a sudden drop in the reproductive hormones estrogen and progesterone. As scientists unravel chemical and genetic changes caused by those shifting hormones, they are discovering new ways to diagnose and treat postpartum depression, and even ways to identify who is at risk for it. Graph showing a steady rise in levels of estradiol and progesterone after conception and then a very steep drop-off right after birth. The hormones estradiol (the main form of estrogen) and progesterone rise during pregnancy. In some women, their sudden drop after childbirth triggers the onset of postpartum depression. The first-ever drug for postpartum depression, containing a derivative of progesterone, received US Food and Drug Administration approval in 2019. That marked a new approach to the disorder. This winter, in another major advance, a San Diego-based startup company will launch a blood test that predicts a pregnant woman’s risk of postpartum depression with more than 80 percent accuracy. © 2025 Annual Reviews

Keyword: Depression; Hormones & Behavior
Link ID: 29972 - Posted: 10.18.2025