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

By R. Douglas Fields It is late at night. You are alone and wandering empty streets in search of your parked car when you hear footsteps creeping up from behind. Your heart pounds, your blood pressure skyrockets. Goose bumps appear on your arms, sweat on your palms. Your stomach knots and your muscles coil, ready to sprint or fight. Now imagine the same scene, but without any of the body’s innate responses to an external threat. Would you still feel afraid? Experiences like this reveal the tight integration between brain and body in the creation of mind — the collage of thoughts, perceptions, feelings and personality unique to each of us. The capabilities of the brain alone are astonishing. The supreme organ gives most people a vivid sensory perception of the world. It can preserve memories, enable us to learn and speak, generate emotions and consciousness. But those who might attempt to preserve their mind by uploading its data into a computer miss a critical point: The body is essential to the mind. How is this crucial brain-body connection orchestrated? The answer involves the very unusual vagus nerve. The longest nerve in the body, it wends its way from the brain throughout the head and trunk, issuing commands to our organs and receiving sensations from them. Much of the bewildering range of functions it regulates, such as mood, learning, sexual arousal and fear, are automatic and operate without conscious control. These complex responses engage a constellation of cerebral circuits that link brain and body. The vagus nerve is, in one way of thinking, the conduit of the mind. How could stimulating a single nerve potentially have such wide-ranging psychological and cognitive benefits? Nerves are typically named for the specific functions they perform. Optic nerves carry signals from the eyes to the brain for vision. Auditory nerves conduct acoustic information for hearing. The best that early anatomists could do with this nerve, however, was to call it the “vagus,” from the Latin for “wandering.” The wandering nerve was apparent to the first anatomists, notably Galen, the Greek polymath who lived until around the year 216. But centuries of study were required to grasp its complex anatomy and function. This effort is ongoing: Research on the vagus nerve is at the forefront of neuroscience today. © 2025Simons Foundation

Keyword: Emotions
Link ID: 29909 - Posted: 08.30.2025

Mohana Basu People with a psychiatric disorder are more likely to marry someone who has the same condition than to partner with someone who doesn’t, according to a massive study1 suggesting that the pattern persists across cultures and generations. Researchers had previously noted this trend in Nordic countries, but the phenomenon has seldom been investigated outside Europe until now. The latest study, published in Nature Human Behaviour today, used data from more than 14.8 million people in Taiwan, Denmark and Sweden. It examined the proportion of people in those couples who had one of nine psychiatric disorders: schizophrenia, bipolar disorder, depression, anxiety, attention-deficit hyperactivity disorder, autism, obsessive–compulsive disorder (OCD), substance-use disorder and anorexia nervosa. Scientists lack a definitive understanding of what causes people to develop psychiatric disorders — but genetics and environmental factors are both thought to play a part. The team found that when one partner was diagnosed with one of the nine conditions, the other was significantly more likely to be diagnosed with the same or another psychiatric condition. Spouses were more likely to have the same conditions than to have different ones, says co-author Chun Chieh Fan, a population and genetics researcher at the Laureate Institute for Brain Research in Tulsa, Oklahoma. “The main result is that the pattern holds across countries, across cultures, and, of course, generations,” Fan says. Even changes in psychiatric care over the past 50 years have not shifted the trend, he notes. Only OCD, bipolar disorder and anorexia nervosa showed different patterns across countries. For instance, in Taiwan, married couples were more likely to share OCD than were couples in Nordic countries. © 2025 Springer Nature Limited

Keyword: Depression; Schizophrenia
Link ID: 29908 - Posted: 08.30.2025

By Roni Caryn Rabin The Food and Drug Administration on Wednesday approved a medical device that offers new hope to patients incapacitated by rheumatoid arthritis, a chronic condition that afflicts 1.5 million Americans and is often resistant to treatment. The condition is usually managed with medications. The device represents a radical departure from standard care, tapping the power of the brain and nervous system to tamp down the uncontrolled inflammation that leads to the debilitating autoimmune disease. The SetPoint System is an inch-long device that is surgically implanted into the neck, where it sits in a pod wrapped around the vagus nerve, which some scientists believe is the longest nerve in the body. The device electrically stimulates the nerve for one minute each day. The stimulation can turn off crippling inflammation and “reset” the immune system, research has shown. Most drugs used to treat rheumatoid arthritis suppress the immune system, leaving patients vulnerable to serious infections. On a recent episode of the American College of Rheumatology podcast, the SetPoint implant was described as representing a “true paradigm shift” in treatment of the disease, which until now has relied almost entirely on an evolving set of pharmaceutical interventions, from gold salts to powerful agents called biologics. The F.D.A. designated the implant as a breakthrough last year in order to expedite its development and approval. It represents an early test of the promise of so-called bioelectronic medicine to modulate inflammation, which plays a key role in diseases including diabetes, heart disease and cancer. Clinical trials are already underway testing vagus nerve stimulation to manage inflammatory bowel disease in children, lupus and other conditions. Trials for patients with multiple sclerosis and Crohn’s disease are also planned. In a yearlong randomized controlled trial of 242 patients that included a sham-treatment arm, over half of the participants using the SetPoint implant alone achieved remission or saw their disease recede. Measures of joint pain and swelling fell by 60 percent and 63 percent, respectively. © 2025 The New York Times Company

Keyword: Pain & Touch; Neuroimmunology
Link ID: 29873 - Posted: 08.02.2025

By Mohana Ravindranath A new analysis of data gathered from a small Indigenous population in the Bolivian Amazon suggests some of our basic assumptions about the biological process of aging might be wrong. Inflammation is a natural immune response that protects the body from injury or infection. Scientists have long believed that long-term, low-grade inflammation — also known as “inflammaging” — is a universal hallmark of getting older. But this new data raises the question of whether inflammation is directly linked to aging at all, or if it’s linked to a person’s lifestyle or environment instead. The study, which was published today, found that people in two nonindustrialized areas experienced a different kind of inflammation throughout their lives than more urban people — likely tied to infections from bacteria, viruses and parasites rather than the precursors of chronic disease. Their inflammation also didn’t appear to increase with age. Scientists compared inflammation signals in existing data sets from four distinct populations in Italy, Singapore, Bolivia and Malaysia; because they didn’t collect the blood samples directly, they couldn’t make exact apples-to-apples comparisons. But if validated in larger studies, the findings could suggest that diet, lifestyle and environment influence inflammation more than aging itself, said Alan Cohen, an author of the paper and an associate professor of environmental health sciences at Columbia University. “Inflammaging may not be a direct product of aging, but rather a response to industrialized conditions,” he said, adding that this was a warning to experts like him that they might be overestimating its pervasiveness globally. “How we understand inflammation and aging health is based almost entirely on research in high-income countries like the U.S.,” said Thomas McDade, a biological anthropologist at Northwestern University. But a broader look shows that there’s much more global variation in aging than scientists previously thought, he added. © 2025 The New York Times Company

Keyword: Development of the Brain; Neuroimmunology
Link ID: 29847 - Posted: 07.02.2025

Katie Kavanagh Scientists have identified a group of neurons that might explain the mechanism behind how stress gives rise to problems with sleep and memory. The study — published last week in The Journal of Neuroscience1 — shows that neurons in a brain area called the hypothalamus mediate the effects of stress on sleep and memory, potentially providing a new target for the treatment of stress-related sleep disorders. Previous work has shown that in the hypothalamus, neurons in a structure called the paraventricular nucleus communicate with other areas important for sleep and memory. The neurons of the paraventricular nucleus release a hormone called corticotropin and have a role in regulating stress. But the neural mechanisms underlying the effect of stress on sleep and memory have remained elusive. For co-author Shinjae Chung, a neuroscientist at the University of Pennsylvania in Philadelphia, the question of exactly how stress affects these processes is personal, because, she says, “I experience a lot of sleep problems when I’m stressed”. She adds that “when I have an exam deadline, I have a tendency to have bad sleep that really affects my score the next day”. To study how neurons in the paraventricular nucleus translate stress into sleep and memory problems, the researchers put laboratory mice through a stressful experience by physically restraining the animals in a plastic tube. The team then tested the creatures’ spatial memory and monitored their brain activity as they slept. © 2025 Springer Nature Limited

Keyword: Sleep; Stress
Link ID: 29837 - Posted: 06.21.2025

By Andrew Jacobs When Gov. Greg Abbott of Texas approved legislation this week to spend $50 million in state money researching ibogaine, a powerful psychedelic, he put the spotlight on a promising, still illegal drug that has shown promise in treating opioid addiction, traumatic brain injury and depression. Interest in ibogaine therapy has surged in recent years, driven in large part by veterans who have had to travel to other countries for the treatment. The measure, which passed the Texas Legislature with bipartisan support, seeks to leverage an additional $50 million in private investment to fund clinical trials that supporters hope will provide a pathway for ibogaine therapy to win approval from the Food and Drug Administration, a process that could take years. The legislation directs the state to work with Texas universities and hospitals and tries to ensure that the state retains a financial stake in any revenue from the drug’s development. “You can’t put a price on a human life, but if this is successful and ibogaine becomes commercialized, it will help people all across the country and provide an incredible return on investment for the people of Texas,” said State Senator Tan Parker, a Republican who sponsored the bill. The initiative, one of the largest government investments in psychedelic medicine to date, is a watershed moment for a field that continues to gain mainstream acceptance. Regulated psilocybin clinics have opened in Oregon and Colorado, and ketamine has become widely available across the country as a treatment for depression and anxiety. There have been speed bumps. Last year, the F.D.A. rejected MDMA-assisted therapy for PTSD, the first psychedelic compound to make it through much of the agency’s rigorous drug review process. © 2025 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 29833 - Posted: 06.18.2025

By Amber Dance The experiment was a striking attempt to investigate weight control. For six weeks, a group of mice gorged on lard-enriched mouse chow, then scientists infected the mice with worms. The worms wriggled beneath the animals’ skin, migrated to blood vessels that surround the intestines, and started laying eggs. Bruno Guigas, a molecular biologist at the Leiden University Center for Infectious Diseases in the Netherlands, led this study some years back and the results, he says, were “quite spectacular.” The mice lost fat and gained less weight overall than mice not exposed to worms. Within a month or so, he recalls, the scientists barely needed their scale to see that the worm-infested mice were leaner than their worm-free counterparts. Infection with worms, it seems, reversed obesity, the researchers reported in 2015. While it’s true that worms gobble up food their hosts might otherwise digest, that doesn’t seem to be the only mechanism at work here. There’s also some intricate biology within the emerging scientific field of immunometabolism. Over the past couple of decades, researchers have recognized that the immune system doesn’t just fight infection. It’s also intertwined with organs like the liver, the pancreas and fat tissue, and implicated in the progression of obesity and type 2 diabetes. These and other metabolic disorders generate a troublesome immune response — inflammation — that worsens metabolism still further. Metabolic disease, in other words, is inflammatory disease. Scientists have also observed a metabolic influence of worms in people who became naturally infected with the parasites or were purposely seeded with worms in clinical trials. While the physiology isn’t fully understood, the worms seem to dampen inflammation, as discussed in the 2024 Annual Review of Nutrition.

Keyword: Obesity; Neuroimmunology
Link ID: 29828 - Posted: 06.14.2025

Jon Hamilton Get cut off in rush-hour traffic and you may feel angry for the whole trip, or even snap at a noisy child in the back seat. Get an unexpected smile from that same kid and you may feel like rush hour — and even those other drivers — aren't so bad. "The thing about emotion is it generalizes. It puts the brain into a broader state," says Dr. Karl Deisseroth, a psychiatrist and professor at Stanford University. Deisseroth and a team of researchers have come up with an explanation for how that happens. The process involves a signal that, after a positive or negative experience, lingers in the brain, the team reports in the journal Science. Experiences themselves act a bit like piano notes in the brain. Some are staccato, producing only a brief burst of activity that may result in a reflexive response, like honking at another driver, or smiling back at a child. But more profound experiences can be more like a musical note that is held with the sustain pedal and still audible when the next note is played, or the one after that. "You just need it to be sustained long enough to merge with and interact with other notes," Deisseroth says. "And from our perspective, this is exactly what emotion needs." If the team is right, it could help explain the emotional differences seen in some neuropsychiatric conditions. People on the autism spectrum, for example, often have trouble recognizing emotions in others, and regulating their own emotions. Schizophrenia can cause mood swings and reduced emotional expression. © 2025 npr

Keyword: Emotions; Autism
Link ID: 29819 - Posted: 06.04.2025

Nicola Davis Science correspondent Whether it is doing sums or working out what to text your new date, some tasks produce a furrowed brow. Now scientists say they have come up with a device to monitor such effort: an electronic tattoo, stuck to the forehead. The researchers say the device could prove valuable among pilots, healthcare workers and other professions where managing mental workload is crucial to preventing catastrophes. “For this kind of high-demand and high-stake scenario, eventually we hope to have this real-time mental workload decoder that can give people some warning and alert so that they can self-adjust, or they can ask AI or a co-worker to offload some of their work,” said Dr Nanshu Lu, an author of the research from the University of Texas at Austin, adding the device may not only help workers avoid serious mistakes but also protect their health. Writing in the journal Device, Lu and colleagues describe how using questionnaires to investigate mental workload is problematic, not least as people are poor at objectively judging cognitive effort and they are usually conducted after a task. Meanwhile, existing electroencephalography (EEG) and electrooculography (EOG) devices, that can be used to assess mental workload by measuring brain waves and eye movements respectively, are wired, bulky and prone to erroneous measurements arising from movements. By contrast, the “e-tattoo” is a lightweight, flexible, wireless device. © 2025 Guardian News & Media Limited

Keyword: Attention; Stress
Link ID: 29815 - Posted: 05.31.2025

Konstantina Kilteni Gargalesis, or tickle, is one of the most trivial yet enigmatic human behaviors. We do not know how a touch becomes ticklish or why we respond to other people’s tickles but not our own. No theory satisfactorily explains why touch on some body areas feels more ticklish than on others or why some people are highly sensitive while others remain unresponsive. Gargalesis is likely the earliest trigger for laughter in life, but it is unclear whether we laugh because we enjoy it. Socrates, Aristotle, Bacon, Galileo, Descartes, and Darwin theorized about tickling, but after two millennia of intense philosophical interest, experimentation remains scarce. This review argues that gargalesis is an exhilarating scientific puzzle with far-reaching implications for developmental, sensorimotor, social, affective, clinical, and evolutionary neuroscience. We reflect on the challenges in defining and eliciting ticklish sensations in the lab and unraveling their neural mechanism, discuss five classic yet unanswered questions about tickle, and suggest directions for future research. Gargalesis, commonly known as tickle, is a very familiar sensation that most of us have experienced at least once in life. Whether actively tickling our babies, family, friends, partners, or pets, or being on the receiving end of a tickle attack, humans undoubtedly engage in tickling behaviors. However, despite its triviality, the scientific understanding of gargalesis is extremely poor. Today, we do not know why certain areas of the body are more ticklish than others and why some people enjoy being tickled, while others dislike it but still burst into laughter. We have also not fully understood why we cannot tickle ourselves and why some people are very ticklish, while others are not responsive at all. Furthermore, the primary function of tickling in humans, as well as in other species, remains a big enigma. Are these questions new, and is that why we do not have any scientific answers yet? Definitely not! Inquiries about the epistemological role of gargalesis have persisted throughout human history, from Ancient Greece to the Renaissance and beyond (1). Socrates (in Plato’s “Philebus”), Aristotle (in “Parts of Animals”), Desiderius Erasmus (in “Adagia”), Francis Bacon (in “Sylva Sylvarum”), Galileo Galilei (in “Il Saggiatore”), René Descartes (in “Treatise on Man” and “The Passions of the Soul”), and Charles Darwin (in “The Expression of the Emotions in Man and Animals”) all theorized about different aspects of gargalesis including its nature and underlying mechanism.

Keyword: Emotions; Evolution
Link ID: 29805 - Posted: 05.24.2025

By Christina Caron When most people think of obsessive-compulsive disorder, they may picture behaviors they’ve seen on TV — like repetitive hand-washing, flicking light switches on and off and meticulously arranging small items over and over. But the disorder manifests in many other ways. Some patients obsess over thoughts that they might hurt someone, while others fixate on certain aspects of their personal relationships. The comedian Maria Bamford, for example, has called her O.C.D. “unwanted thoughts syndrome.” On “The Late Show With Stephen Colbert,” she shared a story about how she couldn’t stop thinking horrific thoughts about her family members. On social media, people describe many types of obsessions and compulsions: “relationship O.C.D.,” “sexual orientation O.C.D.” or “emotional contamination O.C.D.” These aren’t separate diagnoses, but rather they are different expressions of the same disorder — much like how people with phobias can suffer from different fears, said Dr. Carolyn Rodriguez, an O.C.D. expert and a professor of psychiatry and behavioral sciences at Stanford Medicine. Understanding these distinctions can help clinicians tailor a precise treatment plan, she added. And they’re important for the public to grasp as well. Otherwise, people who experience the disorder might not even recognize they have it, Dr. Rodriguez said. People who are fearful of harming others might think, “Maybe I am a murderer,” she added. “If I tell anybody these things, I’m going to be put in jail.” © 2025 The New York Times Company

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 29793 - Posted: 05.17.2025

By Katharine Gammon Picture this: You’re sitting down, engrossed in a meal, when an unfamiliar person walks by. There’s something about them—Hair? Smile? Vibes?—that instantly draws you in and makes you want to strike up a friendship. A new study suggests that it could be the scent they exude that attracts you to them. Not just the way their skin or hair smells, but the deodorant and shampoo they use, the foods they consume, even their laundry detergent. Our sense of smell tends to operate below the level of conscious awareness, says Jessica Gaby, a psychology researcher at Middle Tennessee State University and an author of the study, so our responses to it are often hidden from us. “But at the same time, it’s inescapable,” she says. “You can’t fake it.” Gaby and her colleagues, who were at Cornell University when the study was conducted, brought 40 women aged 18-30 together in a Cornell dining hall, a large, refurbished barn with café tables that doubles as a beer hall at night. The scent of popcorn, beer, and leftover dinner wafted over the room: The idea was to have a complex olfactory environment. The women all identified as heterosexual, so the researchers could focus on the type of attraction that might lead to friendship. In the first phase of the study, the participants received cotton T-shirts and were instructed to wear them for 12 hours straight without altering their daily routines, and to keep notes about their activities. One participant used spray paint in an art project, another had sex, another said she spilled a small amount of black beans on her shirt. In the second phase of the study, the participants were instructed to view photographs of different individual women, some of whom they would later meet. They then each sniffed the worn T-shirts, then had four-minute meetings, speed-dating style, with the other individual women, then sniffed their T-shirts again. After each step, they judged their friendship potential with the other women on a scale of 1 to 7. © 2025 NautilusNext Inc.,

Keyword: Chemical Senses (Smell & Taste); Emotions
Link ID: 29783 - Posted: 05.11.2025

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

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