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

By Lauren Schneider Bad news for mouse poker players: Their facial movements offer “tells” about decision-making variables that the animals track without always acting on them, according to a study published today in Nature Neuroscience. The findings indicate that “cognition is embodied in some surprising ways,” says study investigator Zachary Mainen, a researcher at the Champalimaud Center for the Unknown. And this motor activity holds promise as a noninvasive bellwether of cognitive patterns. The study builds on mounting evidence that mouse facial expressions are not solely the result of a task’s motor demands and provides a “very clear” illustration of how this movement reflects cognitive processes, says Marieke Schölvinck, a researcher at the Ernst Strüngmann Institute for Neuroscience, who was not involved with the work. For years, mouse facial movements have mostly served as a way for researchers to gauge an animal’s pain levels. Now, however, machine-learning technology has made it possible to analyze this fine motor behavior in greater detail, says Schölvinck, who has investigated how facial expressions reflect inner states in mice and macaques. Evidence that mouse facial expressions correspond to emotional states inspired the new analysis, according to Fanny Cazettes, who conducted the experiments as a postdoctoral researcher in Mainen’s lab. She says she wondered what other ways the “internal, private thoughts of animals” might manifest on their faces. Two variables shape most mouse decisions over different foraging sites, the team found: the number of failures at a site (unrewarded licks from a source of sugar water) and the site’s perceived value (the difference between reward and failure). © 2025 Simons Foundation

Keyword: Emotions; Evolution
Link ID: 29950 - Posted: 10.01.2025

By Bethany Brookshire Even hearing the phrase “Huntington’s disease” will make a room suddenly somber. So the joy that accompanied a recent announcement of results of an experimental gene therapy for the deadly diseases signaled an unfamiliar sense of hope. In a small clinical trial, brain injections of a virus that codes for a tiny segment of RNA may have prevented the formation of the rogue proteins that make Huntington’s so devastating. The early results, announced September 24 in a news release, show that over three years, the treatment slowed Huntington’s progression by up to 75 percent. While not a cure, the treatment could potentially give people living with Huntington’s disease, who might otherwise face early disability and death, the gift of many more years of life. “We’re doing science because it’s interesting and important, but we’re also in this game to save our friends and family from a horrible fate,” says Ed Wild, a neurologist at University College London. “That’s the most meaningful thing, looking my friends in the eye and [saying], ‘We did it.’” Huntington’s disease currently has no effective treatments or cures. It is relatively rare, affecting about 7 out of every 100,000 people, and is the result of mutation in a single gene, appropriately called huntingtin. In the disease, that gene is mutated in only one way, making the front end of the resulting protein grow, says Russell Snell, a geneticist at the University of Auckland in New Zealand who was not involved in the study. This expanded huntingtin is a protein gone toxic. It aggregates in the brain and kills cells largely in brain areas crucial for voluntary movements. Patients end up with increasing involuntary movements, stiffness, difficulties speaking and swallowing and cognitive decline. Huntington’s is genetically dominant — it takes only one copy of the defective gene to cause it — so a patient’s offspring have a 50 percent chance of inheriting the disease. Wild and his colleagues, working with the Dutch pharmaceutical company uniQure, used microRNA — tiny segments of RNA that can trigger machinery to break down huntingtin RNA before it gets made into protein. Some other trials have tried simply injecting some of these RNAs, but have not succeeded, possibly because they were injected into the cerebrospinal fluid and couldn’t infiltrate the right areas of the brain. This time, the scientists injected them directly into the brain, packaged inside a well-studied viral vector. The virus would “infect” neurons in the brain with the RNA, and “it basically reprograms the neuron to become a factory for a molecule that tells it not to make huntingtin protein,” Wild says. © Society for Science & the Public 2000–2025.

Keyword: Huntingtons; Genes & Behavior
Link ID: 29946 - Posted: 09.27.2025

Heidi Ledford After a mouse received treatment to eliminate immune cells called microglia, it was injected with human progenitor cells that developed into human immune cells (green, pink and blue) in the animal’s brain.Credit: M. M.-D. Madler et al./Nature A fresh supply of the immune cells that keep the brain tidy might one day help to treat a host of conditions, from ultra-rare genetic disorders to more familiar scourges, such as Alzheimer’s disease. In the past few months, a spate of new studies have highlighted the potential of a technique called microglia replacement and explored ways to make it safer and more effective. “This approach is very promising,” says Pasqualina Colella, who studies gene and cell therapy at Stanford University School of Medicine in California. “But the caveat is the toxicity of the procedure.” Microglia are immune cells that patrol the brain, gobbling up foreign invaders, damaged cells and harmful substances. They can help to protect neurons — cells that transmit and receive messages to and from other tissues — during seizures and strokes, and they prune unneeded connections between neurons during normal brain development. “Microglia do a lot of important things,” says Chris Bennett, a psychiatrist who studies microglia at the Children’s Hospital of Philadelphia in Pennsylvania. “So, it’s not surprising that they are involved in the pathogenesis of many diseases.” Those diseases include a suite of rare disorders caused by genetic mutations that directly affect microglia. Malfunctioning microglia have also been implicated in more familiar conditions with complex causes, such as Alzheimer’s disease and Parkinson’s disease, as well as ageing, says Bo Peng, a neuroscientist at Fudan University in Shanghai, China. © 2025 Springer Nature Limited

Keyword: Development of the Brain; Glia
Link ID: 29944 - Posted: 09.27.2025

By Brandon Keim Should you meet a turtle basking on a log in the sun, you might reasonably conclude that the turtle is in a good mood. Granted, there has been little scientific evidence that reptiles experience such emotional richness — until now, at least. Researchers in England identified what they describe as “mood states” — emotional experiences that are more than momentary — in red-footed tortoises by administering cleverly designed tests that use responses to ambiguity as windows into the psyche. The results of the study, published in the journal Animal Cognition in June, could apply to many more reptiles and have profound implications for how people treat them. “There was an acceptance that reptiles could do these short-term emotions,” said Oliver Burman, who studies animal behavior at the University of Lincoln in England and is an author of the paper. “They could respond to positive things and unpleasant things. But the long-term mood states are really important.” As for why it took so long to show this in reptiles, Dr. Burman said, “maybe we just haven’t asked them correctly.” Reptiles have a longstanding reputation as being unintelligent. Writing in 1892, Charles Henry Turner, the pioneering comparative psychologist, described reptiles as “intellectual dwarfs.” Eight decades later, in 1973, prominent scientists were referring to them as “reflex machines” and (in a paper titled “The Evolutionary Advantages of Being Stupid”) as possessing “a very small brain which does not function vigorously. Dr. Burman is among the scientists responsible for what some have called a “reptilian renaissance.” An array of findings — tortoises learning from one another, snakes with social networks, crocodiles displaying complex communication — indicate that reptiles are no less brainy than mammals and birds. © 2025 The New York Times Company

Keyword: Emotions; Evolution
Link ID: 29938 - Posted: 09.20.2025

Ian Sample Science editor The cry of a distressed baby triggers a rapid emotional response in both men and women that is enough to make them physically hotter, researchers say. Thermal imaging revealed that people experienced a rush of blood to the face that raised the temperature of their skin when they were played recordings of babies wailing. The effect was stronger and more synchronised when babies were more distressed, leading them to produce more chaotic and disharmonious cries. The work suggests that humans respond automatically to specific features in cries that ramp up when babies are in pain. “The emotional response to cries depends on their ‘acoustic roughness’,” said Prof Nicolas Mathevon at the University of Saint-Etienne in France. “We are emotionally sensitive to the acoustic parameters that encode the level of pain in a baby’s cry.” Evolution equipped baby humans with a hard-to-ignore wail to boost their odds of getting the care they need. But not all infant cries are the same. When a baby is in real distress, they forcefully contract their rib cage, producing higher pressure air that causes chaotic vibrations in the vocal cords. This produces “acoustic roughness”, or more technically, disharmonious sounds called nonlinear phenomena (NLP). To see how men and women responded to infants’ cries, scientists played recordings to volunteers with little or no experience with babies. While listening, the participants were filmed with a thermal camera that captured subtle changes in their facial temperature. © 2025 Guardian News & Media Limited

Keyword: Sexual Behavior; Emotions
Link ID: 29924 - Posted: 09.10.2025