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

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

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

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

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

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

By Georgia E. Hodes Psychiatric conditions have long been regarded as issues of “mental health,” a term that inherently ties our understanding of these disorders to the brain. But the brain does not exist in a vacuum. Growing evidence over the past 10 years highlights a link between the body and what we think of as mental health. Many studies, for example, report that the peripheral immune system is altered in people who experience neurological and psychiatric conditions, including mood disorders, anxiety and schizophrenia. Researchers traditionally assumed that peripheral inflammation was a downstream effect of these conditions, but basic research is now revealing that the immune system, the gut microbiome and peripheral inflammation are not just bystanders or results of psychiatric conditions—they are active participants and may hold the key to new treatments. Scientists are beginning to uncover the mechanisms by which the body influences the brain, challenging the notion that mental health is solely a matter of brain chemistry and reshaping ideas on the etiology of psychiatric disorders. Like other neuroscience groups, we started our work in this area with the “brain-first” perspective: the idea that immune changes in the brain trigger stress-induced changes in behavior and peripheral inflammation. Our earliest studies supported this idea, demonstrating that directly infusing an inflammatory molecule, the cytokine interleukin 6 (IL6), into an area of the brain associated with reward behavior made male mice more likely to avoid others. Our later work, however, found that the source of IL6 in the brain is actually peripheral immune cells. Either stopping the immune cells from producing this molecule or just blocking it from entering the brain made the animals resilient to social stress. These studies offered some of the first evidence that treating the body with a compound that does not cross the blood brain-barrier could prevent a brain-mediated behavior. Before this, blood markers were considered only indirect indicators of brain changes—and not direct mediators or potential targets for treatment. © 2025 Simons Foundation

Keyword: Depression; Stress
Link ID: 29670 - Posted: 02.12.2025

By Felicity Nelson Mice immediately bolt for shelter when they see the looming shadow of a bird, just as humans jump when they see a spider. But these instinctive reactions, which are controlled by the brainstem, can be suppressed if animals learn that a scary stimulus is harmless. In Science today, neuroscientists reveal the precise regions of the brain that suppress fear responses in mice1 — a finding that might help scientists to develop strategies for treating post-traumatic stress disorder and anxiety in people. The study showed that two parts of the brain work together to learn to suppress fear. But, surprisingly, only one of these regions is involved in later recalling the learnt behaviour. “This is the first evidence of that mechanism,” says neuroscientist Pascal Carrive at the University of New South Wales in Sydney, Australia. In the study, an expanding dark circle was used to imitate a swooping bird, and caused naive mice to run to a shelter. To teach the mice that this looming stimulus was not dangerous, a barrier was added to prevent the animals from hiding. “I like their behavioural model,” says Christina Perry, a behavioural neuroscientist at Macquarie University in Sydney. “It’s very simple,” she adds. The mice “don’t get eaten, so they learn that this fake predator is not, in fact, a threat”. As the mice were learning to be bolder, the researchers switched specific types of neurons on or off using optogenetics — a well-established technique that allows neurons to be controlled with light. When researchers silenced the parts of the cerebral cortex that analyse visual stimuli (called the posterolateral higher visual areas), the mice did not learn to suppress fear and continued to try to escape from the fake bird — suggesting that this area of the brain is necessary for learning to suppress this fear reaction. © 2025 Springer Nature Limited

Keyword: Emotions; Stress
Link ID: 29664 - Posted: 02.08.2025

By Matt Richtel Cursing is coursing through society. Words once too blue to publicly utter have become increasingly commonplace. “Language is just part of the whole shift to a more casual lifestyle,” said Timothy Jay, a professor emeritus of psychology at the Massachusetts College of Liberal Arts in North Adams, Mass. Dr. Jay has spent a career studying the use of profanity, from what motivates it to the ways in which it satisfies, signals meaning and offends. Although officially retired, he has continued to edit studies on profanity and he recently offered an expert opinion in an ongoing legal dispute in Michigan over whether the phrase “Let’s go Brandon” (a euphemism used to denigrate former President Joseph R. Biden Jr.) should be reasonably interpreted as “profane.” (It should not, Dr. Jay opined.) Dr. Jay posits that the increasingly casual nature of the spoken word derives in part from the way people communicate on social media. One study, published in 2014 by other researchers in the field, found that curse words on Twitter, now known as X, appeared in 7.7 percent of posts, with profanity representing about 1 in every 10 words on the platform. That compared to a swearing rate of 0.5 to 0.7 percent in spoken language, the study found. If that data troubles you, Dr. Jay has some thoughts on how to dial back the profanity. F*@%-free February, anyone? Tis interview has been condensed and edited for clarity, and scrubbed of some of the vernacular that Dr. Jay conceded he regularly uses on the golf course. © 2025 The New York Times Company

Keyword: Emotions; Language
Link ID: 29660 - Posted: 02.08.2025

By Laura Sanders Recovery from PTSD comes with key changes in the brain’s memory system, a new study finds. These differences were found in the brains of 19 people who developed post-traumatic stress disorder after the 2015 terrorist attacks in Paris — and then recovered over the following years. The results, published January 8 in Science Advances, point to the complexity of PTSD, but also to ways that brains can reshape themselves as they recover. With memory tasks and brain scans, the study provides a cohesive look at the recovering brain, says cognitive neuroscientist Vishnu Murty of the University of Oregon in Eugene. “It’s pulled together a lot of pieces that were floating around in the field.” On the night of November 13, 2015, terrorists attacked a crowded stadium, a theater and restaurants in Paris. In the years after, PTSD researchers were able to study some of the people who endured that trauma. Just over half the 100 people who volunteered for the study had PTSD initially. Of those, 34 still had the disorder two to three years later; 19 had recovered by two to three years. People who developed PTSD showed differences in how their brains handled intrusive memories, laboratory-based tests of memory revealed. Participants learned pairs of random words and pictures — a box of tissues with the word “work,” for example. PTSD involves pairs of associated stimuli too, though in much more complicated ways. A certain smell or sound, for instance, can be linked with the memory of trauma. © Society for Science & the Public 2000–2025.

Keyword: Learning & Memory; Stress
Link ID: 29622 - Posted: 01.11.2025

By Ellen Barry Kevin Lopez had just stepped out of his house, on his way to meet his girlfriend for Chinese food, when it happened: He began to hallucinate. It was just a flicker, really. He saw a leaf fall, or the shadow of a leaf, and thought it was the figure of a person running. For a moment, on a clear night last month, this fast-moving darkness seemed to hurtle in his direction and a current of fear ran through him. He climbed into the car, and the door shut and latched behind him with a reassuring thunk. “It’s nothing,” he said. “I don’t know why — I think there’s a person there.” Light had always caused problems for Kevin when symptoms of schizophrenia came on. He thought that the lights were watching him, like an eye or a camera, or that on the other side of the light, something menacing was crouched, ready to attack. But over time, he had found ways to manage these episodes; they passed, like a leg cramp or a migraine. That night, he focused on things that he knew were real, like the vinyl of the car seat and the chill of the winter air. He was dressed for a night out, with fat gemstones in his ears, and had taken a break from his graduate coursework in computer science at Boston University. A “big bearish, handsome nerd” is the way he styled himself at 24. For the past four years, Kevin has been part of a living experiment. Shortly after he began hallucinating, during his junior year at Syracuse University, his doctors recommended him for an intensive, government-funded program called OnTrackNY. It provided him with therapy, family counseling, vocational and educational assistance, medication management and a 24-hour hotline. © 2025 The New York Times Company

Keyword: Schizophrenia; Stress
Link ID: 29614 - Posted: 01.04.2025

By Jason Bittel Have you ever felt like there was a pit in your stomach? What about a flutter in your heart? It turns out that the anatomical connections we make with certain emotions and feelings — what researchers call embodied emotions — may be more universal than you’d think. In fact, people have been making very similar statements about their bodies for about 3,000 years. In a new study published in iScience, researchers catalogued words for body parts and emotions used by people who lived in Mesopotamia between 934 and 612 BCE, in what is now a region that includes Egypt, Iraq, and Türkiye. Then, they compared those ancient ideas etched on clay tablets and other artifacts to commonly used modern-day links between emotions and body parts, using bodily maps to visualize the similarities and differences. “We see certain body areas that are still used in similar contexts in modern times,” says Juha Lahnakoski, lead author of the study and a cognitive neuroscientist at Germany’s LVR Clinic Düsseldorf, in an email. “For example, the heart was often mentioned together with positive emotions such as love, pride, and happiness, as we might still say ‘my heart swelled’ with joy or pride.” © Society for Science & the Public 2000–2024.

Keyword: Emotions
Link ID: 29599 - Posted: 12.14.2024

By Max Kozlov Joylessness triggered by stress creates a distinct brain signature, according to research in mice1. The study also reveals one brain pattern that seems to confer resilience to stress — and another that makes stressed animals less likely to feel pleasure, a core symptom of depression. These findings, published today in Nature, offer clues as to how the brain gives rise to anhedonia, a resistance to enjoyment and pleasure. The results also provide a new avenue for treating the condition — if the findings are validated in humans. “Their approach in this study is spot on,” says Conor Liston, a neuroscientist at Weill Cornell Medicine in New York City, who was not involved in the work. The experiments fill “a big gap”, he says. “Anhedonia is something we don’t understand very well.” More than 70% of people with severe depression experience anhedonia, which is also common in those with schizophrenia, Parkinson’s disease and other neurological and psychiatric conditions. The symptom is notoriously difficult to treat, even in those taking medication, Liston says. “Anhedonia is something that patients care about the most, and feel like it’s least addressed by current treatments,” he says. To understand how the brain gives rise to anhedonia, Mazen Kheirbek, a systems neuroscientist at the University of California, San Francisco, and his colleagues studied mice that had been placed under stress by exposure to larger, more aggressive mice. Typically, mice have a sweet tooth and prefer sugar water over plain water if given the option. But some stressed mice instead preferred plain water — which Kheirbek and his colleagues interpreted as a rodent version of anhedonia. Other mice subjected to the same stress preferred the sugar water. The authors labelled these animals ‘resilient’. © 2024 Springer Nature Limited

Keyword: Stress; Depression
Link ID: 29592 - Posted: 12.07.2024

By Annie Liontas In 2016, Marchell Taylor lay in his windowless, six-by-eight cell in the Denver County Jail. Only 36 days after being released after serving time for drug and robbery convictions, he robbed a Papa John’s and assaulted an employee. Because of his record, Mr. Taylor faced 300 years of imprisonment. He asked himself: Why am I back here? Answering his question may require looking back to 1978, when he was 9 years old and his family’s car slammed into a wall. He woke up to blood on his face. The brain injury he sustained went untreated. Shortly after that, his behavior changed, and he became, in his words, “snappy and violent.” By age 10, he was regularly turning to marijuana and alcohol. At 13, he was breaking into houses. At 14, he robbed a 7-Eleven. In 1993 he was picked up for aggravated robbery and ended up in a maximum security facility. For the next two decades, Mr. Taylor was in and out of institutions like this. That is until the Brain Injury Alliance of Colorado diagnosed him with a brain injury in 2016 while he was awaiting trial. After administering a screening, psychologists at the Men’s Mental Health Transition Unit — a pioneering mental health program in the Denver County Jail — gave Mr. Taylor access to therapies for mental health, including cognitive behavioral therapy and eye movement desensitization and reprocessing therapy, which helps process traumatic memories and experiences. These treatments taught him about his brain, and he says it has made all the difference. It is tempting to dismiss brain injury at an early age as the cause of years of criminal behavior. It’s certainly true in Mr. Taylor’s case that there were other contributing factors, including ongoing substance abuse, a lack of money and weak social and psychological support. But after spending years researching brain injuries in an effort to understand my own recovery from several and as a friend of Mr. Taylor’s, I’m reckoning with the fact that experts are only now beginning to recognize the connection between brain injury and incarceration. While such trauma may not offer a tidy explanation for histories like his, growing insight into this connection offers an opportunity to change the grim legacy of incarceration and mental illness in this country by treating an underlying factor that can fuel recidivism. © 2024 The New York Times Company

Keyword: Aggression; Brain Injury/Concussion
Link ID: 29585 - Posted: 12.04.2024

By Claudia López Lloreda For decades, researchers have considered the brain “immune privileged”—protected from the vagaries of the body’s immune system. But building evidence suggests that the brain may be more immunologically active than previously thought, well beyond its own limited immune response. The choroid plexus in particular—the network of blood vessels and cerebrospinal-fluid (CSF)-producing epithelial cells that line the organ’s ventricles—actively recruits immune cells from both the periphery and the CSF, according to a new study in mice. The epithelial layer of the choroid plexus shields the rest of the brain from toxic substances, pathogens and other molecules that circulate in the blood. Dysfunction and neuroinflammation in the choroid plexus is associated with aging and many neurological conditions, such as amyotrophic lateral sclerosis and Alzheimer’s disease. Even in the absence of inflammation, the choroid plexus harbors immune cells, some of which reside in the space between the vessels and the epithelial layer, and some on the epithelial surface. During an immune response, it also contains recruited cells, such as macrophages and other leukocytes, and pro-inflammatory signals, previous research has shown. But those findings offered only a snapshot of the cells’ locations, says Maria Lehtinen, professor of pathology at Harvard Medical School, who led the new work. “Just because [the cell] is in the tissue doesn’t mean it’s necessarily crossing or has gone in the direction that you anticipate that it would be going in.” How the choroid plexus gatekeeps immune cells remains a big question in the field, says Michal Schwartz, a neuroimmunologist at the Weizmann Institute of Science, who was not involved with the new work. © 2024 Simons Foundation

Keyword: Neuroimmunology
Link ID: 29571 - Posted: 11.23.2024

By Joanne Silberner To describe the destructive effects of intense health anxiety to his young doctors in training at Columbia University Irving Medical Center in New York City, psychiatrist Brian Fallon likes to quote 19th-century English psychiatrist Henry Maudsley: “The sorrow which has no vent in tears may make other organs weep.” That weeping from other parts of the body may come in the form of a headache that, in the mind of its sufferer, is flagging a brain tumor. It may be a rapid heartbeat a person wrongly interprets as a brewing heart attack. The fast beats may be driven by overwhelming, incapacitating anxiety. Hal Rosenbluth, a businessman in the Philadelphia area, says he used to seek medical care for the slightest symptom. In his recent book Hypochondria, he describes chest pains, breathing difficulties and vertigo that came on after he switched from a daily diabetes drug to a weekly one. He ended up going to the hospital by ambulance for blood tests, multiple electrocardiograms, a chest x-ray, a cardiac catheterization and an endoscopy, all of which were normal. Rosenbluth’s worries about glucose levels had led him to push for the new diabetes drug, and its side effects were responsible for many of his cardiac symptoms. His own extreme anxiety had induced doctors to order the extra care. Hypochondria can, in extreme cases, leave people unable to hold down a job or make it impossible for them to leave the house, cook meals, or care for themselves and their families. Recent medical research has shown that hypochondria is as much a real illness as depression and post-traumatic stress disorder. This work, scientists hope, will convince doctors who believed the disorder was some kind of character flaw that their patients are truly ill—and in danger. A study published just last year showed that people with hypochondria have higher death rates than similar but nonafflicted people, and the leading nonnatural cause of death was suicide. It was relatively rare, but the heightened risk was clear.

Keyword: Stress; Attention
Link ID: 29567 - Posted: 11.20.2024

By Miryam Naddaf Humans have evolved disproportionately large brains compared with our primate relatives — but this neurological upgrade came at a cost. Scientists exploring the trade-off have discovered unique genetic features that show how human brain cells handle the stress of keeping a big brain working. The work could inspire new lines of research to understand conditions such as Parkinson’s disease and schizophrenia. The study, which was posted to the bioRxiv preprint server on 15 November1, focuses on neurons that produce the neurotransmitter dopamine, which is crucial for movement, learning and emotional processing. By comparing thousands of laboratory-grown dopamine neurons from humans, chimpanzees, macaques and orangutans, researchers found that human dopamine neurons express more genes that boost the activity of damage-reducing antioxidants than do those of the other primates. The findings, which are yet to be peer-reviewed, are a step towards “understanding human brain evolution and all the potentially negative and positive things that come with it”, says Andre Sousa, a neuroscientist at the University of Wisconsin–Madison. “It's interesting and important to really try to understand what's specific about the human brain, with the potential of developing new therapies or even avoiding disease altogether in the future.” Just as walking upright has led to knee and back problems, and changes in jaw structure and diet resulted in dental issues, the rapid expansion of the human brain over evolutionary time has created challenges for its cells, says study co-author Alex Pollen, a neuroscientist at the University of California, San Francisco. “We hypothesized that the same process may be occurring, and these dopamine neurons may represent vulnerable joints.” © 2024 Springer Nature Limited

Keyword: Development of the Brain; Stress
Link ID: 29565 - Posted: 11.20.2024

By Sara Manning Peskin Seven Deadly Sins: The Biology of Being Human Guy Leschziner William Collins (2024) There is no food in sight in Alex’s house. Even the rubbish bin is fastened closed. The kitchen is like a bank vault, hidden behind a locked door from which staff members bring out portioned meals for Alex and her six housemates, all of whom have a genetic disorder called Prader–Willi syndrome. Although Alex was born underweight, by early adulthood she could eat three servings in a sitting, had gorged on cat food and carried 110 kilograms on her small frame. Her ‘gluttony’, writes neurologist Guy Leschziner in Seven Deadly Sins, is the result of a condition that instils such a voracious appetite that some people have eaten to the point of bursting their stomachs. Whereas marketers of diet programmes have conventionally coupled obesity to a lack of willpower, Leschziner uses Alex’s case to argue that body size is driven less by moralistic factors and more by genetics, hormones and gut microorganisms. Similar themes run throughout the book, as the author examines lust, envy and other supposed infractions, gathering examples of people who exhibit these traits because of neurological disorders. Like his earlier books about sleep and the senses, Seven Deadly Sins educates as much as it entertains, turning complex neuroscientific topics into fodder for cocktail-party conversations. The biology of behaviour Exploring wrath, Leschziner introduces two men with epilepsy. One lurches into rages in the wake of his seizures and finds himself surrounded by shards of broken dishes afterwards. Another, a “gentle giant”, has anger outbursts because of a medication prescribed to control his disease. © 2024 Springer Nature Limited

Keyword: Emotions
Link ID: 29564 - Posted: 11.20.2024

By Claudia López Lloreda Fear memories serve a purpose: A mouse in the wild learns to fear the sound of footsteps, which helps it avoid predators. But in certain situations, those fear memories can also tinge neutral memories with fear, resulting in maladaptive behavior. A mouse or person, for instance, may learn to fear stimuli that should presumably be safe. This shift can occur when an existing fear memory broadens—either by recruiting inappropriate neurons into the cell ensemble that contains it or by linking up to a previously neutral memory, according to two new studies in mice, one published today and another last week. Memories are embodied in the brain through sparse ensembles of neurons, called engrams, that activate when an animal forms a new memory or recalls it later. These ensembles were thought to be “stable and permanent,” says Denise Cai, associate professor of neuroscience at the Icahn School of Medicine at Mount Sinai, who led one of the studies. But the new findings reveal how, during times of fear and stress, memories can become malleable, either as they are brought back online or as the neurons that encode them expand. There is “this really powerful ability of stress to look back and change memories for neutral experiences that have come before by pulling them into the same neural representation or by exciting them more during offline periods,” says Elizabeth Goldfarb, assistant professor of psychiatry at the Yale School of Medicine, who was not involved in the studies. That challenges the previous dogma, Cai says. “We’ve learned that these memory ensembles are actually quite dynamic.” © 2024 Simons Foundation

Keyword: Learning & Memory; Stress
Link ID: 29563 - Posted: 11.16.2024

By Angie Voyles Askham Engrams, the physical circuits of individual memories, consist of more than just neurons, according to a new study published today in Nature. Astrocytes, too, shape how some memories are stored and retrieved, the work shows. The results represent “a fundamental change” in how the neuroscience field should think about indexing memories, says lead researcher Benjamin Deneen, professor of neurosurgery at Baylor College of Medicine. “We need to reconsider the cellular, physical basis of how we store memories.” When mice form a new memory, a specific set of neurons becomes active and expresses the immediate early gene c-FOS, past work has found. Reactivating that ensemble of neurons, the engram, causes the mice to recall that memory. Interactions between neurons and astrocytes are critical for the formation of long-term memory, according to a spatial transcriptomics study from February, and both astrocytes and oligodendrocytes are involved in memory formation, other work has shown. Yet engram studies have largely ignored the activity of non-neuronal cells, says Sheena Josselyn, senior scientist at the Hospital for Sick Children, who was not involved in the new study. But astrocytes are also active alongside neurons as memories are formed and recalled, and disrupting the star-shaped cells’ function interferes with these processes, the new work reveals. The study does not dethrone neurons as the lead engram stars, according to Josselyn. “It really shows that, yes, neurons are important. But there are also other players that we’re just beginning to understand the importance of,” she says. “It’ll help broaden our focus.” © 2024 Simons Foundation

Keyword: Learning & Memory; Glia
Link ID: 29558 - Posted: 11.13.2024

By Angie Voyles Askham Keeping track of social hierarchies is crucial for any animal. Primates in particular must adapt their behaviors based on the status of those around them, or risk losing their own rank. “True, smart social behavior in humans and in monkeys is dependent on a full adjustment to the context,” says Katalin Gothard, professor of physiology and neuroscience at the University of Arizona. Multiple brain areas keep track of social information. Among them, the amygdala—known for processing emotions—responds to faces, facial expressions and social status, and activates as people learn social hierarchies. But the brain adapts this information for different social settings, a new study reveals: Neurons in the macaque amygdala encode knowledge about social status in a context-specific way, Gothard and her colleagues discovered. Just like people, macaques can infer social standing from videos, and the activity of amygdala cells captures information about both the identity of the individual they are watching and how that animal relates to others in the scene. These findings help explain how primates process information about social position, says Ralph Adolphs, professor of psychology and neuroscience at California Institute of Technology, who was not involved in the work. And because the monkeys could successfully learn this information from videos, the results open up a new avenue for studying how the primate brain encodes these relationships in a complex and dynamic way, he adds. “That’s a big step forward.” Like people, macaques have no physical traits that directly convey dominance, Gothard says. “The status of these individuals is inferred.” So she and her colleagues tested two macaques’ ability to understand a hierarchy that the team invented among four unfamiliar monkeys in a series of videos. Each clip simulated status-appropriate interactions between two of the four monkeys on a split screen to convey those two animals’ relative positions: a scene of a higher-ranked animal acting aggressive juxtaposed with one of a lower-ranked monkey smacking its lips in appeasement, for example. © 2024 Simons Foundation

Keyword: Emotions; Attention
Link ID: 29544 - Posted: 11.06.2024

By Claire Murashima What do you think of when you hear the term “OCD”? In pop culture, people with obsessive-compulsive disorder are often portrayed as meticulous to an extreme degree. They’re highly organized, perfectionistic, or germophobic — like Jack Nicholson’s character in the film As Good As It Gets, who tosses out bars of soap after using them once. Depictions like that aren’t inaccurate, but they’re not the whole story. Research shows that 1 in 40 American adults have OCD or will develop it at some point in their lives, according to the International OCD Foundation. Although the term “OCD” is often used casually, the disorder must be diagnosed by a medical professional. We wanted to take a closer look at how people with OCD cope with it every day as OCD Awareness Month wraps up. I live with OCD, and it impacts just about every aspect of my life. Growing up, I had to say a prayer before I ate anything, because I thought I’d vomit if I didn’t. Later in life, I struggled with flying, because I feared that I might vomit on the plane, or that someone might vomit near me. The fear of vomiting is called emetophobia, and it’s a common symptom of OCD — though it’s not talked about as often. People with OCD can experience very specific intrusive thoughts known as obsessions, and then engage in compulsions, which are ritualized behaviors to address them, according to the International OCD Foundation. Anxiety can be the underlying emotion of OCD — but unlike generalized anxiety disorder, the underlying emotion could also be a sense of disgust, wrongness or incompleteness, according to Dr. Christopher Pittenger, the director of the Yale School of Medicine OCD Research Clinic. © 2024 npr

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 29536 - Posted: 11.02.2024

By Claudia López Lloreda Success tends to breed success. For instance, when a mouse dominates its opponents over and over, it becomes increasingly aggressive—helping to ensure victory in future fights. This “winner effect” takes hold thanks to multiple changes in synaptic plasticity, according to new findings published today in Cell. The results begin to reveal the mechanisms behind various forms of aggression seen in animals, says Jacob Nordman, assistant professor of molecular and integrative physiology at Southern Illinois University, who was not involved in the work. “There’s some aggression that is defensive; there’s some aggression that is pathological; there’s some aggression that’s territorial,” he says. “There might be a set of behaviors and, in turn, a set of circuits and possibly plasticity within those circuits, that speak to that.” Innate aggression is controlled by the ventromedial hypothalamus (VMH)—also known as the “attack” center—which shapes an animal’s social behaviors and fear response. But aggression can be learned, too. When paired with a mouse that is naturally docile, a more dominant mouse will eventually attack the other—and if it prevails, it tends to pick even longer fights with rivals over the coming days, thanks to synapse strengthening and increased activity in the VMH, a 2020 study reported. Full-blown and more generalized aggression emerges after even longer winning streaks, and it involves additional mechanisms, the new study suggests: Changes to neuronal excitability and dendritic spine morphology help cement the animal’s hawkishness. “Aggression is malleable—you can shape it,” says Scott Russo, professor of neuroscience at the Icahn School of Medicine at Mount Sinai, who was not involved with the study. “It’s not something that’s defined only by genetics, but that actually these circuits that support aggressive social behavior can change as a consequence of experience.” © 2024 Simons Foundation

Keyword: Aggression; Hormones & Behavior
Link ID: 29524 - Posted: 10.19.2024