By Carl Zimmer Consciousness may be a mystery, but that doesn’t mean that neuroscientists don’t have any explanations for it. Far from it. “In the field of consciousness, there are already so many theories that we don’t need more theories,” said Oscar Ferrante, a neuroscientist at the University of Birmingham. If you’re looking for a theory to explain how our brains give rise to subjective, inner experiences, you can check out Adaptive Resonance Theory. Or consider Dynamic Core Theory. Don’t forget First Order Representational Theory, not to mention semantic pointer competition theory. The list goes on: A 2021 survey identified 29 different theories of consciousness. Dr. Ferrante belongs to a group of scientists who want to lower that number, perhaps even down to just one. But they face a steep challenge, thanks to how scientists often study consciousness: Devise a theory, run experiments to build evidence for it, and argue that it’s better than the others. “We are not incentivized to kill our own ideas,” said Lucia Melloni, a neuroscientist at the Max Planck Institute for Empirical Aesthetics in Frankfurt, Germany. Seven years ago, Dr. Melloni and 41 other scientists embarked on a major study on consciousness that she hoped would break this pattern. Their plan was to bring together two rival groups to design an experiment to see how well both theories did at predicting what happens in our brains during a conscious experience. The team, called the Cogitate Consortium, published its results on Wednesday in the journal Nature. But along the way, the study became subject to the same sharp-elbowed conflicts they had hoped to avoid. Dr. Melloni and a group of like-minded scientists began drawing up plans for their study in 2018. They wanted to try an approach known as adversarial collaboration, in which scientists with opposing theories join forces with neutral researchers. The team chose two theories to test. © 2025 The New York Times Company

Keyword: Consciousness
Link ID: 29773 - Posted: 05.03.2025

By Anil Seth On stage in New York a couple years ago, noted neuroscientist Christof Koch handed a very nice bottle of Madeira wine to philosopher David Chalmers. Chalmers had won a quarter-century-long bet about consciousness—or at least our understanding of it. Nautilus Members enjoy an ad-free experience. Log in or Join now . The philosopher had challenged the neuroscientist in 1998—with a crate of fine wine on the line—that in 25 years, science would still not have located the seat of consciousness in the brain. The philosopher was right. But not without an extraordinary—and revealing—effort on the part of consciousness researchers and theorists. Backing up that concession were the results of a long and thorough “adversarial collaboration” that compared two leading theories about consciousness, testing each with rigorous experimental data. Now we finally learn more about the details of this work in a new paper in the journal Nature. Nicknamed COGITATE, the collaboration pitted “global neuronal workspace theory” (GNWT)—an idea advocated by cognitive neuroscientist Stanislas Dehaene, which associates consciousness with the broadcast of information throughout large swathes of the brain—against “integrated information theory” (IIT)—the idea from neuroscientist Giulio Tononi, which identifies consciousness with the intrinsic cause-and-effect power of brain networks. The adversarial collaboration involved the architects of both theories sitting down together, along with other researchers who would lead and execute the project (hats off to them), to decide on experiments that could potentially distinguish between the theories—ideally supporting one and challenging the other. Deciding on the theory-based predictions, and on experiments good enough to test them, was never going to be easy. In consciousness research, it is especially hard since—as philosopher Tim Bayne and I noted—theories often make different assumptions, and attempt to explain different things even if, on the face of it, they are all theories of “consciousness.” © 2025 NautilusNext Inc.,

Keyword: Consciousness
Link ID: 29772 - Posted: 05.03.2025

By Allison Parshall ] Where in the brain does consciousness originate? Theories abound, but neuroscientists still haven’t coalesced around one explanation, largely because it’s such a hard question to probe with the scientific method. Unlike other phenomena studied by science, consciousness cannot be observed externally. “I observe your behavior. I observe your brain, if I do an intracranial EEG [electroencephalography] study. But I don’t ever observe your experience,” says Robert Chis-Ciure, a postdoctoral researcher studying consciousness at the University of Sussex in England. Scientists have landed on two leading theories to explain how consciousness emerges: integrated information theory, or IIT, and global neuronal workspace theory, or GNWT. These frameworks couldn’t be more different—they rest on different assumptions, draw from different fields of science and may even define consciousness in different ways, explains Anil K. Seth, a consciousness researcher at the University of Sussex. To compare them directly, researchers organized a group of 12 laboratories called the Cogitate Consortium to test the theories’ predictions against each other in a large brain-imaging study. The result, published in full on Wednesday in Nature, was effectively a draw and raised far more questions than it answered. The preliminary findings were posted to the preprint server bioRxiv in 2023. And only a few months later, a group of scholars publicly called IIT “pseudoscience” and attempted to excise it from the field. As the dust settles, leading consciousness researchers say that the Cogitate results point to a way forward for understanding how consciousness arises—no matter what theory eventually comes out on top. “We all are very good at constructing castles in the sky” with abstract ideas, says Chis-Ciure, who was not involved in the new study. “But with data, you make those more grounded.” © 2025 SCIENTIFIC AMERICAN,

Keyword: Consciousness
Link ID: 29771 - Posted: 05.03.2025

By Yasemin Saplakoglu In 1943, a pair of neuroscientists were trying to describe how the human nervous system works when they accidentally laid the foundation for artificial intelligence. In their mathematical framework (opens a new tab) for how systems of cells can encode and process information, Warren McCulloch and Walter Pitts argued that each brain cell, or neuron, could be thought of as a logic device: It either turns on or it doesn’t. A network of such “all-or-none” neurons, they wrote, can perform simple calculations through true or false statements. “They were actually, in a sense, describing the very first artificial neural network,” said Tomaso Poggio (opens a new tab) of the Massachusetts Institute of Technology, who is one of the founders of computational neuroscience. McCulloch and Pitts’ framework laid the groundwork for many of the neural networks that underlie the most powerful AI systems. These algorithms, built to recognize patterns in data, have become so competent at complex tasks that their products can seem eerily human. ChatGPT’s text is so conversational and personal that some people are falling in love (opens a new tab). Image generators can create pictures so realistic that it can be hard to tell when they’re fake. And deep learning algorithms are solving scientific problems that have stumped humans for decades. These systems’ abilities are part of the reason the AI vocabulary is so rich in language from human thought, such as intelligence, learning and hallucination. But there is a problem: The initial McCulloch and Pitts framework is “complete rubbish,” said the science historian Matthew Cobb (opens a new tab) of the University of Manchester, who wrote the book The Idea of the Brain: The Past and Future of Neuroscience (opens a new tab). “Nervous systems aren’t wired up like that at all.” A promotional card for Quanta's AI series, which reads Science Promise and the Peril of AI, Explore the Series" When you poke at even the most general comparison between biological and artificial intelligence — that both learn by processing information across layers of networked nodes — their similarities quickly crumble. © 2025 Simons Foundation

Keyword: Consciousness; Robotics
Link ID: 29770 - Posted: 05.03.2025

By Laura Dattaro In 2012, neuroscientists Sebastian Seung and J. Anthony Movshon squared off at a Columbia University event over the usefulness of connectomes—maps of every connection between every cell in the brain of a living organism. Such a map, Seung argued, could crack open the brain’s computations and provide insight into processes such as sensory perception and memory. But Movshon, professor of neural science and psychology at New York University, countered that the relationship between structure and function was not so straightforward—that even if you knew how all of a brain’s neurons connect to one another, you still wouldn’t understand how the organ turns electrical signals into cognition and behavior. The debate in the field continues, even though Seung and his colleagues in the FlyWire Consortium completed the first connectome of a female Drosophila melanogaster in 2023, and even though a slew of new computational models built from that and other connectomes hint that structure does, in fact, reveal something about function. “This is just the beginning, and that’s what’s exciting,” says Seung, professor of neuroscience at the Princeton Neuroscience Institute. “These papers are kicking off a beginning to an entirely new field, which is connectome-based brain simulation.” A simulated fruit fly optic lobe, detailed in a September 2024 Nature paper, for example, accurately predicts which neurons in living fruit flies respond to different visual stimuli. “All the work that’s been done in the past year or two feels like the beginning of something new,” says John Tuthill, associate professor of neuroscience at the University of Washington. Tuthill was not involved in the optic lobe study but used a similar approach to identify a circuit that seems to control walking in flies. Most published models so far have made predictions about simple functions that were already understood from recordings of neural activity, Tuthill adds. But “you can see how this will build up to something that is eventually very insightful.” © 2025 Simons Foundation

Keyword: Brain imaging; Development of the Brain
Link ID: 29769 - Posted: 05.03.2025

Logan S. James It is late at night, and we are silently watching a bat in a roost through a night-vision camera. From a nearby speaker comes a long, rattling trill. The bat briefly perks up and wiggles its ears as it listens to the sound before dropping its head back down, uninterested. Next from the speaker comes a higher-pitched “whine” followed by a “chuck.” The bat vigorously shakes its ears and then spreads its wings as it launches from the roost and dives down to attack the speaker. Bats show tremendous variation in the foods they eat to survive. Some species specialize on fruits, others on insects, others on flower nectar. There are even species that catch fish with their feet. At the Smithsonian Tropical Research Institute in Panama, we’ve been studying one species, the fringe-lipped bat (Trachops cirrhosus), for decades. This bat is a carnivore that specializes in feeding on frogs. Male frogs from many species call to attract female frogs. Frog-eating bats eavesdrop on those calls to find their next meal. But how do the bats come to associate sounds and prey? We were interested in understanding how predators that eavesdrop on their prey acquire the ability to discriminate between tasty and dangerous meals. We combined our expertise on animal behavior, bat cognition and frog communication to investigate. © 2010–2025, The Conversation US, Inc.

Keyword: Hearing; Development of the Brain
Link ID: 29768 - Posted: 05.03.2025

Andrew Gregory Health editor Scientists have used living human brain tissue to mimic the early stages of Alzheimer’s disease, the most common form of dementia, in a breakthrough that will accelerate the hunt for a cure. In a world first, a British team successfully exposed healthy brain tissue from living NHS patients to a toxic form of a protein linked to Alzheimer’s – taken from patients who died from the disease – to show how it damages connections between brain cells in real time. The groundbreaking move offered a rare and powerful opportunity to see dementia developing in human brain cells. Experts said the new way of studying the disease could make it easier to test new drugs and boost the chances of finding ones that work. Dementia presents a big threat to health and social care systems across the world. The number of people affected is forecast to triple to nearly 153 million by 2050, which underlines why finding new ways to study the disease and speed up the search for treatments is a health priority. In the study, scientists and neurosurgeons in Edinburgh teamed up to show for the first time how a toxic form of a protein linked to Alzheimer’s, amyloid beta, can stick to and destroy vital connections between brain cells. Tiny fragments of healthy brain tissue were collected from cancer patients while they were undergoing routine surgery to remove tumours at the Royal Infirmary of Edinburgh. Scientists dressed in scrubs were stationed in operating theatres alongside surgical teams, ready to receive the healthy brain tissue, which would otherwise have been discarded. Once the pieces of brain were retrieved, scientists put them in glass bottles filled with oxygenated artificial spinal fluid before jumping into taxis to transport the samples to their lab a few minutes away. © 2025 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29767 - Posted: 04.30.2025

RJ Mackenzie Neuroscientists have identified a brain signal in mice that kick-starts the process of overwriting fearful memories once danger is passed — a process known as fear extinction. The research is at an early stage, but could aid the development of drugs to treat conditions, such as post-traumatic stress disorder (PTSD), that are linked to distressing past experiences. In a study published on 28 April in the Proceedings of the National Academy of Sciences1, the researchers focused on two populations of neurons in a part of the brain called the basolateral amygdala (BLA). These two types of neuron have contrasting effects: one stimulates and the other suppresses fear responses, says co-author Michele Pignatelli, a neuroscientist at Massachusetts Institute of Technology in Cambridge. Until now, scientists didn’t know what activated these neurons during fear extinction, although previous research implicated the neurotransmitter dopamine, released by a specific group of neurons in another part of the brain called the ventral tegmental area (VTA). To investigate this possibility, the authors used fluorescent tracers injected into the brains of mice to show that the VTA sends dopamine signals to the BLA, and that both pro- and anti-fear neurons in the BLA can respond to these signals. They then studied the effects of these circuits on behaviour, using mice that had been genetically modified so that dopamine activity in their brains produced fluorescent light, which allowed the researchers to record the activity of the VTA–BLA connections using fibre optics. They first placed these mice into chambers that delivered mild but unpleasant electrical shocks to their feet, which made them freeze in fear. The next day, they put the mice back in the chambers but did not give them any shocks. Although initially fearful, the mice began to relax after about 15 minutes, and the researchers saw a dopamine current surge through their ‘anti-fear’ BLA neurons. © 2025 Springer Nature Limited

Keyword: Emotions; Stress
Link ID: 29766 - Posted: 04.30.2025

Hannah Thomasy, PhD In recent decades, scientists have demonstrated that prosocial behaviors are not unique to humans, or even to primates. Rats, in particular, have proved surprisingly sensitive to the distress of conspecifics, and will often come to the aid of a fellow rat in trouble. In 2011, researchers showed that when rats were provided with a clear box containing chocolate chips, they usually opened the box and consumed all the chocolate.1 But when one box contained chocolate and another contained a trapped cagemate, the rats were more likely to open both boxes and share the chocolate. But some rats didn’t play as nicely with others. In versions of the test that did not involve chocolate, only a rat and its trapped cagemate, researchers noticed that while some rats consistently freed their compatriots, others did not. In a new Journal of Neuroscience study, neuroscientists Jocelyn Breton at Northeastern University and Inbal Ben-Ami Bartal at Tel-Aviv University explored the behaviors and neural characteristics of helpers and non-helpers.2 They found that helper rats displayed greater social interactions with their cagemates, greater activity in prosocial neural networks, and greater expression of oxytocin receptors in the nucleus accumbens (NAc), providing clues about the mechanisms that govern prosocial behaviour. “We appear to live in an increasingly polarized society where there is a gap in empathy towards others,” said Bartal in a press release. “This work helps us understand prosocial, or helpful, acts better. We see others in distress all the time but tend to help only certain individuals. The similarity between human and rat brains helps us understand the way our brain mediates prosocial decisions.” To undertake these experiments, the researchers first divided the rats into pairs and allowed them to acclimatize to their cagemates for a few weeks. Then they placed the pair in the testing arena, where they allowed one rat to roam free and restrained the other in a clear box that could only be opened from the outside. While they were not trained to open the box, more than half of the rats figured out how to free their trapped companions and did so during multiple days of consecutive testing. © 1986-2025 The Scientist.

Keyword: Emotions; Evolution
Link ID: 29765 - Posted: 04.30.2025

By Lydia Denworth The rattling or whistling noises of regular snorers are famously hard on those who share their beds. Middle-aged men and people who are overweight come frequently to mind as perpetrators because they are the most common sufferers of sleep apnea, often caused by a temporarily collapsing airway that makes the person snore heavily. But recent studies in children and pregnant women have revealed that even mild snoring can negatively affect health, behavior and quality of life. “We know that disordered breathing and disturbed sleep can have myriad physiological effects,” says Susan Redline, a pulmonologist and epidemiologist at Brigham and Women’s Hospital in Boston. “More people have sleep-disordered breathing than have overt apneas. We shouldn’t forget about them.” Almost everyone snores occasionally. Allergies and respiratory infections can trigger it. When the upper airway at the back of the throat narrows, it causes the tissues there to vibrate, creating the familiar rumble. Physicians worry if people habitually snore three or more nights a week, especially if they have other red flags such as unexplained high blood pressure. The category of sleep-disordered breathing includes apnea’s total pause in breathing, shallow breaths called hypopnea, snoring without apneas, and a subtler problem called flow limitation in which the shape of the airway is narrowed but the sleeper makes no noise. The standard measure of severity is the apnea-hypopnea index (AHI), which counts pauses in breathing per hour and associated drops in oxygen levels. The normal level in adults is fewer than five pauses; more than 30 is severe. In children, 10 pauses could be considered moderately severe. © 2025 SCIENTIFIC AMERICAN,

Keyword: Sleep; Development of the Brain
Link ID: 29764 - Posted: 04.30.2025

Robin Berghaus This article is part of an occasional series in which Nature profiles scientists with unusual career histories or outside interests. From the earliest days of her career, physician Sue Sisley has been passionate about caring for US military veterans. Back then, many of the people she treated were self-medicating with black-market cannabis because, unlike prescription drugs, marijuana allayed nightmares and other symptoms of post-traumatic stress disorder (PTSD). A few puffs helped them to fall asleep. “Initially, I discouraged them and rolled my eyes thinking about it,” says Sisley, whose training taught her to view only approved drugs as medicines. “I lacked sympathy for their claims and thought they were drug seekers.” But over time, Sisley saw how the ineffectiveness of mental-health treatments could fuel hopelessness. Currently, 17 US veterans die by suicide daily, on average. The cannabis users among Sisley’s patients were often the ones who maintained a will to live. “It made me realize that I was very misled, by the government and our training programmes, to believe that cannabis was dangerous,” she says. “I didn’t learn about any medical benefits.” The early lessons from her patients influenced Sisley. Over the next two decades, she challenged US federal agencies, navigated a legal and regulatory maze and creatively secured funding to investigate and develop treatments, based on cannabis and psychedelics, that the US government had blocked for decades. A physician-researcher is born After the US Congress passed the Controlled Substances Act of 1970, cannabis was made illegal and classified as a Schedule I drug, defined as having no accepted medical use. That put marijuana in the same category as heroin and most psychedelic drugs: possession or use of the drug, and growing cannabis without a Schedule I research licence, could land someone in prison. © 2025 Springer Nature Limited

Keyword: Drug Abuse; Depression
Link ID: 29763 - Posted: 04.30.2025

By Gina Kolata Do we really have free will when it comes to eating? It’s a vexing question that is at the heart of why so many people find it so difficult to stick to a diet. To get answers, one neuroscientist, Harvey J. Grill of the University of Pennsylvania, turned to rats and asked what would happen if he removed all of their brains except their brainstems. The brainstem controls basic functions like heart rate and breathing. But the animals could not smell, could not see, could not remember. Would they know when they had consumed enough calories? To find out, Dr. Grill dripped liquid food into their mouths. “When they reached a stopping point, they allowed the food to drain out of their mouths,” he said. Those studies, initiated decades ago, were a starting point for a body of research that has continually surprised scientists and driven home that how full animals feel has nothing to do with consciousness. The work has gained more relevance as scientists puzzle out how exactly the new drugs that cause weight loss, commonly called GLP-1s and including Ozempic, affect the brain’s eating-control systems. The story that is emerging does not explain why some people get obese and others do not. Instead, it offers clues about what makes us start eating, and when we stop. While most of the studies were in rodents, it defies belief to think that humans are somehow different, said Dr. Jeffrey Friedman, an obesity researcher at Rockefeller University in New York. Humans, he said, are subject to billions of years of evolution leading to elaborate neural pathways that control when to eat and when to stop eating. © 2025 The New York Times Company

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 29762 - Posted: 04.26.2025

Sammie Seamon Peter was working late, watching two roulette tables in play at a London casino, when he felt something stir behind his right eye. It was just a shadow of sensation, a horribly familiar tickle. But on that summer night in 2018, as chips hit the tables and gamblers’ conversation swelled, panic set in. He knew he only had a few minutes. Peter found his boss, muttered that he had to leave, now, and ran outside. By then, the tickle had escalated; it felt like a red-hot poker was being shoved through his right pupil. Tears flowed from that eye, which was nearly swollen shut, and mucus from his right nostril. Half-blinded, gripping at his face, he stumbled along the street, eventually escaping into a company car that whisked him home, where he blacked out. Every day that followed, Peter, then in his early 40s, would experience the same attack at 10am, 2pm and 6pm, like perfect clockwork. “Oh God, here it comes,” he’d think to himself, before fireworks exploded in his temple and the poker stabbed into the very roots of his teeth, making him scream and sometimes vomit. “It just grows, and it thumps, and it thumps, and it thumps with my heartbeat,” said Peter, recalling the pain. Peter had experienced these inexplicable episodes since he was a kid, always in the summer. An attack left him shaking and exhausted, and waiting on the next bout was a kind of psychological torture – within the short respites, he dreaded the next. Once, when Peter felt one starting, he threw on his shoes and sprinted through the streets of south London. He didn’t care which turns he took. Maybe if he ran fast enough, his lungs full of air, he could outrun the thing. His heart pumped in his chest, more from fear than the exercise itself. When the pain escalated to an unbearable pitch, he slowed to a stop, dry heaving, and sat down to press on his eye. He was three miles away from home. © 2025 Guardian News & Media Limited

Keyword: Pain & Touch
Link ID: 29761 - Posted: 04.26.2025

Humberto Basilio What Rina Green calls her “living hell” began with an innocuous backache. By late 2022, two years later, pain flooded her entire body daily and could be so intense that she couldn’t get out of bed. Painkillers and physical therapy offered little relief. She began using a wheelchair. Green has fibromyalgia, a mysterious condition with symptoms of widespread and chronic muscle pain and fatigue. No one knows why people get fibromyalgia, and it is difficult to treat. But eight months ago, Green received an experimental therapy: pills containing living microorganisms of the kind that populate the healthy human gut. Her pain decreased substantially, and Green, who lives in Haifa, Israel, and is now 38, can go on walks — something she hadn’t done since her fibromyalgia diagnosis. Green was one of 14 participants in a trial of microbial supplements for the condition. All but two reported an improvement in their symptoms. The trial is so small that “we should take the results with a grain of salt”, says co-organizer Amir Minerbi, a pain scientist at the Technion — Israel Institute of Technology in Haifa. “But it is encouraging [enough] to move forward.” The trial results and data from other experiments linking fibromyalgia to gut microbes are published today in Neuron1. Fibromyalgia affects up to 4% of the global population and occurs in the absence of tissue damage. In 2019, Minerbi and his colleagues discovered that the gut microbiomes — the collection of microbes living in the intestines — of women with fibromyalgia differed significantly from those of healthy women2. This led the scientists to wonder whether a dose of microbes from healthy people would ease the pain and fatigue caused by the condition. After all, previous research3 had shown that gut microbes might indirectly influence an array of chemical signals tied to pain perception. The team transplanted minuscule samples of microbe-laden faeces from both women with fibromyalgia and healthy women into mice without any microbes in their bodies. The researchers found that mice that received microbes from women with fibromyalgia showed signs of greater sensitivity to pain in response to pressure, heat and cold than did mice that got microbes from healthy women. The first group also showed more evidence of spontaneous pain. © 2025 Springer Nature Limited

Keyword: Pain & Touch; Obesity
Link ID: 29760 - Posted: 04.26.2025

By Nicole M. Baran One of the biggest misconceptions among students in introductory biology courses is that our characteristics are determined at conception by our genes. They believe—incorrectly—that our traits are “immutable.” The much more beautiful, complicated reality is that we are in fact a product of our genes, our environment and their interaction as we grow and change throughout our lives. Nowhere is this truer than in the developmental process of sexual differentiation. Early in development when we are still in the womb, very little about us is “determined.” Indeed, the structures that become our reproductive system start out as multi-potential, capable of taking on many possible forms. A neutral structure called the germinal ridge, for example, can develop into ovaries or testes—the structures that produce reproductive cells and sex hormones—or sometimes into something in between, depending on the molecular signals it receives. Our genes influence this process, of course. But so do interactions among cells, molecules in our body, including hormones, and influences from the outside world. All of these can nudge development in one direction or another. Understanding the well-studied science underlying this process is especially important now, given widespread misinformation about—and the politicization of—sex and gender. I am a neuroendocrinologist, which means that I study and teach about hormones and the brain. In my neuroendocrinology classroom, students learn about the complex, messy process of sexual differentiation in both humans and in birds. Because sexual differentiation in birds is both similar to and subtly different from that in humans, studying how it unfolds in eggs can encourage students to look deeper at how this process works and to question their assumptions. So how does sexual differentiation work in birds? Like us, our feathered friends have sex chromosomes. But their sex chromosomes evolved independently of the X and Y chromosomes of mammals. In birds, a gene called DMRT1 initiates sexual differentiation. (DMRT1 is also important in sexual differentiation in mammals and many other vertebrate animals.) Males inherit two copies of DMRT1 and females inherit only one copy. Reduced dosage of the gene in females leads to the production of the sex hormone estradiol, a potent estrogen, in the developing embryo. © 2025 Simons Foundation

Keyword: Sexual Behavior; Evolution
Link ID: 29759 - Posted: 04.26.2025

By Sara Talpos It’s been more than 30 years since the award-winning film “Rain Man,” starring Dustin Hoffman and Tom Cruise, put a spotlight on autism — or, more specifically, on a specific type of autism characterized by social awkwardness and isolation and typically affecting males. Yet as far back as the 1980s, at least one prominent autism researcher wondered whether autism’s male skew might simply reflect the fact that autistic females were, for some reason, going undiagnosed. Over the past decade, spurred by the personal testimonies of late-diagnosed women, autism researchers have increasingly examined this question. As it turns out, many autistic women and girls are driven by a powerful desire to avoid social rejection, so powerful, in fact, that they may adopt two broad strategies — camouflaging and masking — to hide their condition in an attempt to better fit in with neurotypical peers and family members. Such behavior is “at odds with the traditional picture of autism,” writes Gina Rippon, an emeritus professor of cognitive neuroimaging at Aston University in Birmingham, England, in her new book “Off the Spectrum: Why the Science of Autism Has Failed Women and Girls.” And while the ability to blend in might seem like a positive, it can ultimately take a heavy toll. Rippon points, for example, to surveys showing that by age 25, about 20 percent of autistic women have been hospitalized for a psychiatric condition, more than twice the rate of autistic men. In the U.S., the rate of autism has been increasing since at least 2000, and many autism researchers, including Rippon, believe more inclusive diagnostic criteria, coupled with increased awareness, have contributed to the rise. Last week, however, Health and Human Services Secretary Robert F. Kennedy Jr. dismissed this idea and insisted that the condition is caused by environmental factors. The National Institutes of Health has begun work on a research initiative that aims to look into this further.

Keyword: Autism; Sexual Behavior
Link ID: 29758 - Posted: 04.26.2025

By Rachel E. Gross Estrogen is the Meryl Streep of hormones, its versatility renowned among scientists. Besides playing a key role in sexual and reproductive health, it strengthens bones, keeps skin supple, regulates sugar levels, increases blood flow, lowers inflammation and supports the central nervous system. “You name the organ, and it promotes the health of that organ,” said Roberta Brinton, a neuroscientist who leads the Center for Innovation in Brain Science at the University of Arizona. But appreciation for estrogen’s more expansive role has been slow in coming. The compound was first identified in 1923 and was henceforth known as the “female sex hormone” — a one-dimensional reputation baked into its very name. “Estrogen” comes from the Greek “oestrus,” a literal gadfly known for whipping cattle into a mad frenzy. Scientifically, estrus has come to mean the period in the reproductive cycles of some mammals when females are fertile and sexually active. Women don’t enter estrus; they menstruate. Nevertheless, when researchers named estrogen, these were the roles it was cast in: inducing a frenzy and supporting female sexual health. Now, estrogen is gaining recognition for what may be its most important role yet: influencing the brain. Neuroscientists have learned that estrogen is vital to healthy brain development but that it also contributes to conditions including multiple sclerosis and Alzheimer’s. Changes in estrogen levels — either from the menstrual cycle or external sources — can exacerbate migraines, seizures and other common neurological symptoms. “There are a huge number of neurological diseases that can be affected by sex hormone fluctuations,” said Dr. Hyman Schipper, a neurologist at McGill University who listed a dozen of them in a recent review in the journal Brain Medicine. “And many of the therapies that are used in reproductive medicine should be repurposed for these neurological diseases.” Today, the insight that sex hormones are also brain hormones is transforming how doctors approach brain health and disease — helping them guide treatment, avoid harmful interactions and develop new hormone-based therapies.. © 2025 The New York Times Company

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 29757 - Posted: 04.23.2025

By Elise Cutts Food poisoning isn’t an experience you’re likely to forget — and now, scientists know why. A study published April 2 in Nature has unraveled neural circuitry in mice that makes food poisoning so memorable. “We’ve all experienced food poisoning at some point … And not only is it terrible in the moment, but it leads us to not eat those foods again,” says Christopher Zimmerman of Princeton University. Luckily, developing a distaste for foul food doesn’t take much practice — one ill-fated encounter with an undercooked enchilada or contaminated hamburger is enough, even if it takes hours or days for symptoms to set in. The same is true for other animals, making food poisoning one of the best ways to study how our brains connect events separated in time, says neuroscientist Richard Palmiter of the University of Washington in Seattle. Mice usually need an immediate reward or punishment to learn something, Palmiter says; even just a minute’s delay between cause (say, pulling a lever) and effect (getting a treat) is enough to prevent mice from learning. Not so for food poisoning. Despite substantial delays, their brains have no trouble associating an unfamiliar food in the past with tummy torment in the present. Researchers knew that a brain region called the amygdala represents flavors and decides whether or not they’re gross. Palmiter’s group had also shown that the gut tells the brain it’s feeling icky by activating specific “alarm” neurons, called CGRP neurons. “They respond to everything that’s bad,” Palmiter says. © Society for Science & the Public 2000–2025.

Keyword: Learning & Memory; Emotions
Link ID: 29756 - Posted: 04.23.2025

By Bruce Rosen The past two decades—and particularly the past 10 years, with the tool-focused efforts of the BRAIN Initiative—have delivered remarkable advances in our ability to study and manipulate the brain, both in exquisite cellular detail and across increasing swaths of brain territory. These advances resulted from improvements in tools such as optical imaging, chemogenetics and multiprobe electrodes, to name a few. Powerful as these technologies are, though, their invasive nature makes them ill-suited for widespread adoption in human brain research. Fortunately, our fundamental understanding of the physics and engineering behind noninvasive modalities—based largely on recording, generating and manipulating electromagnetic and acoustic fields in the human brain—has also progressed over the past decade. These advances are on the threshold of providing much more detailed recordings of electromagnetic activity, not only across the human cortex but at depth. And these same principles can improve our ability to precisely and noninvasively stimulate the human brain. Though these tools have limitations compared with their invasive counterparts, their noninvasive nature make them suitable for wide-scale investigation of the links between human behavior and action, as well as for individually understanding and treating an array of brain disorders. The most common method to assess brain electrophysiology is the electroencephalogram (EEG), first developed in the 1920s and now routinely used for both basic neuroscience and the clinical diagnosis of conditions ranging from epilepsy to sleep disorders to traumatic brain injury. It’s widely used, given its simplicity and low cost, but it has drawbacks. Understanding exactly where the EEG signals arise from in the brain is often difficult, for example; electric current from the brain must pass through multiple tissue layers (including overlying brain itself) before it can be detected with electrodes on the scalp surface, blurring the spatial resolution. Advanced computational methods combined with imaging data from MRI can partially mitigate these issues, but the analysis is complex, and results are imperfect. Still, because EEG can be readily combined with behavioral assessments and other

Keyword: Brain imaging
Link ID: 29755 - Posted: 04.23.2025

William Wright & Takaki Komiyama Every day, people are constantly learning and forming new memories. When you pick up a new hobby, try a recipe a friend recommended or read the latest world news, your brain stores many of these memories for years or decades. But how does your brain achieve this incredible feat? In our newly published research in the journal Science, we have identified some of the “rules” the brain uses to learn. Learning in the brain The human brain is made up of billions of nerve cells. These neurons conduct electrical pulses that carry information, much like how computers use binary code to carry data. These electrical pulses are communicated with other neurons through connections between them called synapses. Individual neurons have branching extensions known as dendrites that can receive thousands of electrical inputs from other cells. Dendrites transmit these inputs to the main body of the neuron, where it then integrates all these signals to generate its own electrical pulses. It is the collective activity of these electrical pulses across specific groups of neurons that form the representations of different information and experiences within the brain. For decades, neuroscientists have thought that the brain learns by changing how neurons are connected to one another. As new information and experiences alter how neurons communicate with each other and change their collective activity patterns, some synaptic connections are made stronger while others are made weaker. This process of synaptic plasticity is what produces representations of new information and experiences within your brain. In order for your brain to produce the correct representations during learning, however, the right synaptic connections must undergo the right changes at the right time. The “rules” that your brain uses to select which synapses to change during learning – what neuroscientists call the credit assignment problem – have remained largely unclear. © 2010–2025, The Conversation US, Inc.

Keyword: Learning & Memory
Link ID: 29754 - Posted: 04.23.2025