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

By Frieda Klotz Up until a couple years ago, an attorney in his late 30s used to repeatedly check his vehicle for signs that he might have injured a pedestrian. The man had no reason to think he had actually hit someone, but his obsessive-compulsive disorder made him fearful. “I spent hours examining the car,” he said. He’d feel the body for dents, take photos, and was never quite done. At its worst, the condition consumed up to 17 hours of his day. “My mind was hijacked for 25 years by a devil that was OCD,” said the man, who asked that his name not be used due to the stigma surrounding mental health disorders and the treatment he’s undergone. He was first diagnosed with the disorder, which is characterized by obsessive preoccupations that interfere with daily life, when he was 15, shortly after his mother died. In the intervening years, he tried numerous forms of therapy, medication, brain stimulation, and residential treatments — all of which, he estimated, cost him hundreds of thousands of dollars. None of them helped long-term. In 2022, his father heard about a brain surgery intended to relieve OCD symptoms and found it was offered by two hospitals affiliated with Brown University. In December 2023, a neurosurgeon created a small hole in the man’s skull and deployed heat to burn away brain tissue. The resulting lesion is thought to disrupt the interaction between parts of the brain associated with OCD symptoms. “I didn’t think it would work at all, because nothing had worked on me,” he told Undark on a Zoom call with his neuropsychologist at Brown, Nicole McLaughlin, and a communications officer from the health system where the attorney had his surgery. “It was a complete miracle.” He added that he was still aware of his repeating thoughts after the surgery, but they no longer bothered him: “It was unbelievable.”

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 29748 - Posted: 04.16.2025

By Matt Richtel So sharp are partisan divisions these days that it can seem as if people are experiencing entirely different realities. Maybe they actually are, according to Leor Zmigrod, a neuroscientist and political psychologist at Cambridge University. In a new book, “The Ideological Brain: The Radical Science of Flexible Thinking,” Dr. Zmigrod explores the emerging evidence that brain physiology and biology help explain not just why people are prone to ideology but how they perceive and share information. What is ideology? It’s a narrative about how the world works and how it should work. This potentially could be the social world or the natural world. But it’s not just a story: It has really rigid prescriptions for how we should think, how we should act, how we should interact with other people. An ideology condemns any deviation from its prescribed rules. You write that rigid thinking can be tempting. Why is that? Ideologies satisfy the need to try to understand the world, to explain it. And they satisfy our need for connection, for community, for just a sense that we belong to something. There’s also a resource question. Exploring the world is really cognitively expensive, and just exploiting known patterns and rules can seem to be the most efficient strategy. Also, many people argue — and many ideologies will try to tell you — that adhering to rules is the only good way to live and to live morally. I actually come at it from a different perspective: Ideologies numb our direct experience of the world. They narrow our capacity to adapt to the world, to understand evidence, to distinguish between credible evidence and not credible evidence. Ideologies are rarely, if ever, good. Q: In the book, you describe research showing that ideological thinkers can be less reliable narrators. Can you explain? Remarkably, we can observe this effect in children. In the 1940s, Else Frenkel-Brunswik, a psychologist at the University of California, Berkeley, interviewed hundreds of children and tested their levels of prejudice and authoritarianism, like whether they championed conformity and obedience or play and imagination. When children were told a story about new pupils at a fictional school and asked to recount the story later, there were significant differences in what the most prejudiced children remembered, as opposed to the most liberal children. © 2025 The New York Times Company

Keyword: Emotions; Attention
Link ID: 29737 - Posted: 04.09.2025

Ian Sample Science editor Researchers who tracked cases of dementia in Welsh adults have uncovered the strongest evidence yet that the shingles vaccination reduces the risk of developing the devastating brain disease. Health records of more than 280,000 older adults revealed that those who received a largely discontinued shingles vaccine called Zostavax were 20% less likely to be diagnosed with dementia over the next seven years than those who went without. Pascal Geldsetzer, at Stanford University, said: “For the first time we are able to say much more confidently that the shingles vaccine causes a reduction in dementia risk. If this truly is a causal effect, we have a finding that’s of tremendous importance.” The researchers took advantage of a vaccination rollout that took place in Wales more than a decade ago. Public health policy dictated that from 1 September 2013, people born on or after 2 September 1933 became eligible for the Zostavax shot, while those who were older missed out. The policy created a natural experiment where the older population was sharply divided into two groups depending on their access to the vaccine. This allowed the researchers to compare dementia rates in older people born weeks apart but on either side of the vaccine eligibility divide. After accounting for the fact that not all those eligible for the vaccine received it, the researchers found vaccination led to a 20% reduction in dementia risk, with the strongest effect in women. Anupam Jena, a professor of healthcare policy at Harvard Medical School, said the implications were profound. © 2025 Guardian News & Media Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 29732 - Posted: 04.05.2025

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