By Andrew Jacobs and Jacey Fortin News reports detailing Elon Musk’s drug use have prompted renewed attention to ketamine, a powerful anesthetic that has become increasingly popular as a therapy for treatment-resistant depression and other mental health issues. Although Mr. Musk has acknowledged using ketamine in the past to treat depression, he has denied suggestions that he is currently using ketamine — or any other drug. “I am NOT taking drugs!” he wrote last week in a social media post following the publication of an article in The New York Times that described reports of his use of drugs on the campaign trail last year. Those drugs included ketamine and other psychedelic compounds, among them MDMA and psilocybin mushrooms. Mr. Musk left the White House last week. Since then, he and President Trump have traded barbs on social media over the president’s domestic policy bill and have mentioned government contracts with Mr. Musk’s companies and Mr. Musk’s relationship to the White House. Mr. Trump, who was briefed on the article in The Times, has been telling associates in the last day or so that Musk’s “crazy” behavior is linked to his drug use, according to a Times report citing two people with knowledge of Mr. Trump’s private conversations. But later on Friday, Mr. Trump told reporters he did not want to comment on Mr. Musk’s drug use. The very public feud between the two men has once again drawn unflattering attention to ketamine, a drug that has become increasingly available at legal clinics across the country. It is also used recreationally and can be dangerous when misused. What is ketamine, and is it legal? Ketamine is an injectable, short-acting dissociative anesthetic that can have hallucinogenic effects at certain doses. It distorts perceptions of sight and sound and makes users feel detached from pain and their surroundings. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29824 - Posted: 06.07.2025

By Calli McMurray The hunt for a soulmate can be hard work—particularly for naive neurons. During development, the cells’ axons snake through burgeoning brain areas in search of the perfect dendrite to form a synapse with. Cell surface proteins serve as molecular identification tags to help axons distinguish “Mr. Wrong” dendrite from “Mr. Right,” according to the chemoaffinity hypothesis. But there are too many cells and too few cell surface proteins for this to be the only strategy, says Claude Desplan, professor of biology and neural science at New York University. “There is no way you can find your partner in a big mess of many different thousands of types of neurons. So you do need to reduce the issue.” In this brain region, 50 types of olfactory receptor neurons link up with 50 types of neurons that project to a sensory integration hub called the mushroom body; each synapse type bunches together inside the lobe to form its own distinct glomerulus. The axons of olfactory receptor neurons do not search the entire structure for their postsynaptic partner. Instead, the projection neurons inside the lobe send their dendrites to meet axons traveling along the surface. Once the two join up, they descend to their proper place in the lobe, imaging experiments show. “Axons don’t need to delve deep. They only need to survey the surface in order to find their target,” says the study’s principal investigator, Liqun Luo, professor of biology at Stanford University. To make matters even simpler, the axons stick to a narrow, genetically determined trajectory, Luo says. Cortical regions may achieve a similar simplification through columns and layers: Axons travel to a certain brain region and then plunge to a particular depth, Luo suggests. Genetically altering these trajectories precludes the olfactory receptor neurons from finding their proper mate, additional experiments show. Dendrites from the postsynaptic cell still wait for their partner at the surface, but “they will be sitting there waiting forever,” Luo says. Some cells “are still sticking their dendrites out” in adulthood, and in at least one case the team observed, a cell eventually matched with another partner. © 2025 Simons Foundation

Keyword: Development of the Brain
Link ID: 29823 - Posted: 06.07.2025

Anna Bawden Health and social affairs correspondent Weight loss drugs could at least double the risk of diabetic patients developing age-related macular degeneration, a large-scale study has found. Originally developed for diabetes patients, glucagon-like peptide-1 receptor agonist (GLP-1 RA) medicines have transformed how obesity is treated and there is growing evidence of wider health benefits. They help reduce blood sugar levels, slow digestion and reduce appetite. But a study by Canadian scientists published in Jama Ophthalmology has found that after six months of use GLP-1 RAs are associated with double the risk of older people with diabetes developing neovascular age-related macular degeneration compared with similar patients not taking the drugs. Academics at the University of Toronto examined medical data for more than 1 million Ontario residents with a diagnosis of diabetes and identified 46,334 patients with an average age of 66 who were prescribed GLP-1 RAs. Nearly all (97.5%) were taking semaglutide, while 2.5% were on lixisenatide. The study did not exclude any specific brand of drugs, but since Wegovy was only approved in Canada in November 2021, primarily for weight loss, it is likely the bulk of semaglutide users in the study were taking Ozempic, which is prescribed for diabetes. Each patient on semaglutide or lixisenatide was matched with two patients who also had diabetes but were not taking the drugs, who shared similar characteristics such as age, gender and health conditions. The researchers then compared how many patients developed neovascular age-related macular degeneration over three years. © 2025 Guardian News & Media Limited

Keyword: Vision; Obesity
Link ID: 29822 - Posted: 06.07.2025

David Farrier Charles Darwin suggested that humans learned to speak by mimicking birdsong: our ancestors’ first words may have been a kind of interspecies exchange. Perhaps it won’t be long before we join the conversation once again. The race to translate what animals are saying is heating up, with riches as well as a place in history at stake. The Jeremy Coller Foundation has promised $10m to whichever researchers can crack the code. This is a race fuelled by generative AI; large language models can sort through millions of recorded animal vocalisations to find their hidden grammars. Most projects focus on cetaceans because, like us, they learn through vocal imitation and, also like us, they communicate via complex arrangements of sound that appear to have structure and hierarchy. Sperm whales communicate in codas – rapid sequences of clicks, each as brief as 1,000th of a second. Project Ceti (the Cetacean Translation Initiative) is using AI to analyse codas in order to reveal the mysteries of sperm whale speech. There is evidence the animals take turns, use specific clicks to refer to one another, and even have distinct dialects. Ceti has already isolated a click that may be a form of punctuation, and they hope to speak whaleish as soon as 2026. The linguistic barrier between species is already looking porous. Last month, Google released DolphinGemma, an AI program to translate dolphins, trained on 40 years of data. In 2013, scientists using an AI algorithm to sort dolphin communication identified a new click in the animals’ interactions with one another, which they recognised as a sound they had previously trained the pod to associate with sargassum seaweed – the first recorded instance of a word passing from one species into another’s native vocabulary. The prospect of speaking dolphin or whale is irresistible. And it seems that they are just as enthusiastic. In November last year, scientists in Alaska recorded an acoustic “conversation” with a humpback whale called Twain, in which they exchanged a call-and-response form known as “whup/throp” with the animal over a 20-minute period. In Florida, a dolphin named Zeus was found to have learned to mimic the vowel sounds, A, E, O, and U. © 2025 Guardian News & Media Limited

Keyword: Language; Evolution
Link ID: 29821 - Posted: 06.04.2025

Kristel Tjandra For two decades, Ann Johnson has been unable to walk or talk after she experienced a stroke that impaired her balance and her breathing and swallowing abilities. But in 2022, Johnson was finally able to hear her voice through an avatar, thanks to a brain implant. The implant is an example of the neurotechnologies that have entered human trials during the past five years. These devices, developed by research teams and firms including entrepreneur Elon Musk’s Neuralink, can alter the nervous system’s activity to influence functions such as speech, touch and movement. Last month, they were the topic of a meeting in Paris, hosted by the United Nations scientific and cultural agency UNESCO, at which delegates finalized a set of ethical principles to govern neurotechnologies. The recommendations focus on protecting users from technology misuse that could infringe on their human rights, including their autonomy and freedom of thought. The delegates, who included scientists, ethicists and legal specialists, decided on nine principles. These include recommendations that technology developers disclose how neural information is collected and used, and that they ensure the long-term safety of a product on people’s mental states. “This document clarifies how to protect human rights, especially in relation to the nervous system,” says Pedro Maldonado, a neuroscientist at the University of Chile in Santiago who was one of 24 experts who drafted the recommendations in 2024. The principles are not legally binding, but nations and organizations can use them to develop their own policies. In November, UNESCO’s 194 member states will vote on whether to adopt the standards. The meeting considered a range of neurotechnology applications, including devices designed to be implanted into the body and non-invasive devices, which are being explored in medicine, entertainment and education. © 2025 Springer Nature Limited

Keyword: Brain imaging
Link ID: 29820 - Posted: 06.04.2025

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

By Lina Zeldovich When Catherine Lord was a psychology student a half century ago, she took part in a pioneering effort to move kids with autism from psychiatric institutions into the community. Lord was inspired by positive changes in the kids and devoted her life to developing therapies for people with autism and understanding the biology of the condition. Today, Lord is a professor of psychiatry at the University of California, Los Angeles, and renowned worldwide for developing tools to diagnose autism, which have become clinical standards, and for her efforts to improve the lives of people with autism and their families. Along with her research, Lord maintains a clinical practice where she works with people with autism, from toddlers to adults. So I couldn’t think of a better scientist to address the views of autism espoused by Robert F. Kennedy, Jr. Since being appointed as the United States Secretary of Health and Human Services, Kennedy has continued to spread misinformation about the condition, a pattern that began two decades ago when he claimed childhood vaccines cause autism, a charge long ago proven to be false. Earlier this year, Kennedy announced the National Institutes of Health would launch a new study to investigate the causes of autism. To conduct its study, he said, the NIH would gather medical records of Americans with autism from federal and commercial databases. In conversation, Lord spoke with authority and concern as she pointed out the mendacity and danger of Kennedy’s comments, and clarified the state of autism research and science. He has made a variety of statements about autism that suggests he doesn’t really know what he’s talking about. © 2025 NautilusNext Inc.,

Keyword: Autism
Link ID: 29818 - Posted: 06.04.2025

By Lauren Schenkman Addiction may be known as a disease of “more,” but drug-taking also taps a powerful drive for less that can suppress reward in the brain, even at low doses, according to a new study of nicotine responses in mice. The results suggest that the systems of reward and aversion that regulate addiction are more intertwined than previously thought. “That’s absolutely fascinating, because the field has been dominated by this notion of the go, the drive to get drug, but the drive is moderated by the stop,” says Paul Kenny, professor of neuroscience at the Icahn School of Medicine at Mount Sinai, who was not involved in the work. A faulty “stop” signal could be one of the culprits in addiction, he adds. Recent studies have begun to explore this stop signal. Intravenous nicotine activates nicotinic acetylcholine receptors on dopamine neurons in the midbrain’s ventral tegmental area (VTA), generating a rewarding effect that promotes more drug consumption. And high doses activate a tiny adjacent area, the interpeduncular nucleus (IPN), which drives aversion, previous studies have suggested. But doses too low to excite the VTA also activate the IPN in mice, the new work shows. In another experiment, the team used fluorescent proteins to find where axons from the IPN terminate and to identify the intermediate player connecting the IPN and the VTA: the laterodorsal tegmental nucleus (LDTg). The findings were published in Neuron in April. “This was very thrilling,” says the study’s principal investigator, Alexandre Mourot, research director in brain plasticity at the Institut National de la Santé et de la Recherche Médicale (INSERM). It suggests that at very low doses, the VTA does not respond because the IPN “erases the rewarding properties of the drug,” he says. © 2025 Simons Foundation

Keyword: Drug Abuse
Link ID: 29817 - Posted: 06.04.2025

By Abby Ellin Sally Odenheimer starved herself because she was an athlete and thought she’d run faster on an empty stomach. Karla Wagner starved herself because she wanted to be in charge of at least one aspect of her life. Janice Bremis simply felt too fat. They all sought perfection and control. Not eating helped. They are women in their 60s and 70s who have struggled with anorexia nervosa since childhood or adolescence. Years later, their lives are still governed by calories consumed, miles run, laps swum, pounds lost. “It’s an addiction I can’t get rid of,” said Ms. Odenheimer, 73, a retired teacher who lives outside Denver. For decades, few people connected eating disorders with older people; they were seen as an affliction of teenage girls and young women. But research suggests that an increasing number of older women have been seeking treatment for eating disorders, including bulimia, binge eating disorder (known as BED) and anorexia, which has the highest mortality rate of any psychiatric disorder, and brings with it an elevated risk of suicide. In a 2017 paper in the journal BMC Medicine, researchers reported that more than 15 percent of 5,658 women surveyed met the criteria for a lifetime eating disorder while in their 30s and 40s. A 2023 review of recent research reported that the prevalence rates among women 40 and older with full diagnoses of eating disorders were between 2.1 and 7.7 percent. (For men, they were less than 1 percent.) © 2025 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 29816 - 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

By Laura Dattaro One of Clay Holroyd’s mostly highly cited papers is a null result. In 2005, he tested a theory he had proposed about a brain response to unexpected rewards and disappointments, but the findings—now cited more than 600 times—didn’t match his expectations, he says. In the years since, other researchers have run similar tests, many of which contradicted Holroyd’s results. But in 2021, EEGManyLabs announced that it would redo Holroyd’s original experiment across 13 labs. In their replication effort, the researchers increased the sample size from 17 to 370 people. The results—the first from EEGManyLabs—published in January in Cortex, failed to replicate the null result, effectively confirming Holroyd’s theory. “Fundamentally, I thought that maybe it was a power issue,” says Holroyd, a cognitive neuroscientist at Ghent University. “Now this replication paper quite nicely showed that it was a power issue.” The two-decade tale demonstrates why pursuing null findings and replications—the focus of this newsletter—is so important. Holroyd’s 2002 theory proposed that previously observed changes in dopamine associated with unexpectedly positive or negative results cause neural responses that can be measured with EEG. The more surprising a result, he posited, the larger the response. To test the idea, Holroyd and his colleagues used a gambling-like task in which they told participants the odds of correctly identifying which of four choices would lead to a 10-cent reward. In reality, the reward was random. When participants received no reward, their neural reaction to the negative result was equally strong regardless of which odds they had been given, contradicting the theory. © 2025 Simons Foundation

Keyword: Attention; Learning & Memory
Link ID: 29814 - Posted: 05.31.2025

Jon Hamilton Joe Walsh, 79, is waiting to inhale. He's perched on a tan recliner at the Center for Alzheimer Research and Treatment at Brigham and Women's Hospital in Boston. His wife, Karen Walsh, hovers over him, ready to depress the plunger on a nasal spray applicator. "One, two, three," a nurse counts. The plunger plunges, Walsh sniffs, and it's done. The nasal spray contains an experimental monoclonal antibody meant to reduce the Alzheimer's-related inflammation in Walsh's brain. He is the first person living with Alzheimer's to get the treatment, which is also being tested in people with diseases including multiple sclerosis, ALS and COVID-19. Sponsor Message Health A man genetically destined to develop Alzheimer's isn't showing any symptoms And the drug appears to be reducing the inflammation in Walsh's brain, researchers report in the journal Clinical Nuclear Medicine. "I think this is something special," says Dr. Howard Weiner, a neurologist at Mass General Brigham who helped develop the nasal spray, along with its maker, Tiziana Life Sciences. Whether a decrease in inflammation will bring improvements in Walsh's thinking and memory, however, remains unclear. The experimental treatment is part of a larger effort to find new ways to interrupt the cascade of events in the brain that lead to Alzheimer's dementia. Two drugs now on the market clear the brain of sticky amyloid plaques, clumps of toxic protein that accumulate between neurons. Other experimental drugs have targeted the tau tangles, a different protein that builds up inside nerve cells. © 2025 npr

Keyword: Alzheimers
Link ID: 29813 - Posted: 05.31.2025

Danielle Wilhour Cerebrospinal fluid, or CSF, is a clear, colorless liquid that plays a crucial role in maintaining the health and function of your central nervous system. It cushions the brain and spinal cord, provides nutrients and removes waste products. Despite its importance, problems related to CSF often go unnoticed until something goes wrong. Recently, cerebrospinal fluid disorders drew public attention with the announcement that musician Billy Joel had been diagnosed with normal pressure hydrocephalus. In this condition, excess CSF accumulates in the brain’s cavities, enlarging them and putting pressure on surrounding brain tissue even though diagnostic readings appear normal. Because normal pressure hydrocephalus typically develops gradually and can mimic symptoms of other neurodegenerative diseases, such as Alzheimer’s or Parkinson’s disease, it is often misdiagnosed. I am a neurologist and headache specialist. In my work treating patients with CSF pressure disorders, I have seen these conditions present in many different ways. Here’s what happens when your cerebrospinal fluid stops working. What is cerebrospinal fluid? CSF is made of water, proteins, sugars, ions and neurotransmitters. It is primarily produced by a network of cells called the choroid plexus, which is located in the brain’s ventricles, or cavities. The choroid plexus produces approximately 500 milliliters (17 ounces) of CSF daily, but only about 150 milliliters (5 ounces) are present within the central nervous system at any given time due to constant absorption and replenishment in the brain. This fluid circulates through the ventricles of the brain, the central canal of the spinal cord and the subarachnoid space surrounding the brain and spinal cord. © 2010–2025, The Conversation US, Inc.

Keyword: Biomechanics; Stroke
Link ID: 29812 - Posted: 05.31.2025

Alison Abbott Daiza Gordon watched her two younger brothers die when they were adolescents. They had Hunter syndrome, a rare, incurable disease — predominantly affecting boys — in which a gene for an important enzyme is missing. Guilt compounded her grief when her attempts to resuscitate her youngest brother failed. She was just 19 years old. Gordon went on to discover how merciless genetics can be. Her own three sons were all born with the condition. When her two eldest hit their second birthdays, the symptoms started to emerge: a thickening of facial features, loss of language, hearing and movement and other impacts to mental and physical development. But she sees hope for her sons that was denied to her brothers. Her children are enrolled in a clinical trial testing a technology to carry a replacement for the missing enzyme, called iduronate-2-sulfatase (IDS), into the brain. Early results indicate improvement in some of the condition’s cognitive and physical symptoms. Gordon’s eldest sons are no longer deaf and they have started to run around. They are meeting developmental milestones she’d never dared to hope for. Her two-year-old, who started the therapy when he was just three months old, is showing none of the early symptoms. “When I look at them, I realize they have a chance of an actual future,” says Gordon. Regular infusions of replacement IDS has been the standard of care for the past two decades, and it protects important organs such as the liver and kidneys from damage. But without help, the large enzyme can’t make it through the protective barrier that separates the blood from one of the most important organs — the brain. For Gordon’s children, that help comes from an innovative molecular transport system, a chemical tag attached to IDS that shuttles it through the tightly joined cells that make up the blood–brain barrier. Several such shuttles, which take advantage of natural transport systems in the brain, are now being developed. With the ability to move large biological drugs — including antibodies, proteins and the viruses used in gene therapy — these shuttles promise to revolutionize neuropharmacology. And that’s not just for rare diseases such as Hunter syndrome, but also for cancer, Alzheimer’s disease and other common brain disorders. © 2025 Springer Nature Limited

Keyword: Drug Abuse; Alzheimers
Link ID: 29811 - Posted: 05.28.2025

By Sydney Wyatt Donald Hebb famously proposed in 1949 that when neurons fire together, the synaptic connections between them strengthen, forming the basis for long-term memories. That theory—which held up in experiments in rat hippocampal slice cultures—has shaped how researchers understand synaptic plasticity ever since. But a new computational modeling study adds to mounting evidence that Hebbian plasticity does not always explain how changing neuronal connections enable learning. Rather, behavioral timescale synaptic plasticity (BTSP), which can strengthen synapses even when neurons fire out of sync, better captures the changes seen in CA1 hippocampal cells as mice learn to navigate a new environment, the study suggests. Hebbian spike-timing-dependent plasticity occurs when a neuron fires just ahead of one it synapses onto, leading to a stronger connection between the two cells. BTSP, on the other hand, relies on a complex spike, or a burst of action potentials, in the postsynaptic cell, which triggers a calcium signal that travels across the dendritic arbor. The signal strengthens synaptic connections with the presynaptic cell that were active within seconds of that spike, causing larger changes in synaptic strength. BTSP helps hippocampal cells establish their place fields, the positions at which they fire, previous work suggests. But it was unclear whether it also contributes to learning, says Mark Sheffield, associate professor of neurobiology at the University of Chicago, who led the new study. The new findings suggest that it does—challenging how researchers traditionally think about plasticity mechanisms in the hippocampus, says Jason Shepherd, associate professor of neurobiology at the University of Utah, who was not involved in the research. “The classic rules of plasticity that we have been sort of thinking about for decades may not be actually how the brain works, and that’s a big deal.” © 2025 Simons Foundation

Keyword: Learning & Memory
Link ID: 29810 - Posted: 05.28.2025

By Chris Berdik Yale psychiatrist Albert Powers didn’t know what to expect as he strolled among the tarot card readers, astrologers, and crystal vendors at the psychic fair held at the Best Western outside North Haven, Connecticut, on a cloudy November Saturday in 2014. At his clinic, Powers worked with young people, mostly teenagers, who had started hearing voices. His patients and their families were worried that the voices might be precursors of psychosis such as schizophrenia. Sometimes, they were. But Powers also knew that lots of people occasionally heard voices — between 7 and 15 percent of the population, according to studies — and about 75 percent of those people lived otherwise normal lives. WHAT I LEFT OUT is a recurring feature in which book authors are invited to share anecdotes and narratives that, for whatever reason, did not make it into their final manuscripts. In this installment, journalist Chris Berdik shares a story that didn’t make it into his recent book “Clamor: How Noise Took Over the World and How We Can Take It Back” (Norton, 272 pages). He wanted to study high-functioning voice hearers, and a gathering of psychics seemed like a good place to find them. If clinicians could better distinguish voice hearers who develop psychosis and lose touch with reality from those who don’t, he thought, then maybe he could help steer more patients down a healthier path. Powers introduced himself to the fair’s organizer and explained the sort of person he hoped to find. The organizer directed him to a nearby table where he met a smiley, middle-aged medium. The woman had a day job as an emergency services dispatcher, but the voices made frequent appearances in her daily life, and her side hustle was communicating with the dead.

Keyword: Schizophrenia; Attention
Link ID: 29809 - Posted: 05.28.2025

By Paula Span & KFF Health News Kristin Kramer woke up early on a Tuesday morning 10 years ago because one of her dogs needed to go out. Then, a couple of odd things happened. When she tried to call her other dog, “I couldn’t speak,” she said. As she walked downstairs to let them into the yard, “I noticed that my right hand wasn’t working.” But she went back to bed, “which was totally stupid,” said Kramer, now 54, an office manager in Muncie, Indiana. “It didn’t register that something major was happening,” especially because, reawakening an hour later, “I was perfectly fine.” So she “just kind of blew it off” and went to work. It’s a common response to the neurological symptoms that signal a TIA, a transient ischemic attack or ministroke. At least 240,000 Americans experience one each year, with the incidence increasing sharply with age. Because the symptoms disappear quickly, usually within minutes, people don’t seek immediate treatment, putting them at high risk for a bigger stroke. Kramer felt some arm tingling over the next couple of days and saw her doctor, who found nothing alarming on a CT scan. But then she started “jumbling” her words and finally had a relative drive her to an emergency room. By then, she could not sign her name. After an MRI, she recalled, “my doctor came in and said, ‘You’ve had a small stroke.’” Did those early-morning aberrations constitute a TIA? Might a 911 call and an earlier start on anticlotting drugs have prevented her stroke? “We don’t know,” Kramer said. She’s doing well now, but faced with such symptoms again, “I would seek medical attention.” © 2025 SCIENTIFIC AMERICAN,

Keyword: Stroke
Link ID: 29808 - Posted: 05.28.2025

Sofia Marie Haley I approach a flock of mountain chickadees feasting on pine nuts. A cacophony of sounds, coming from the many different bird species that rely on the Sierra Nevada’s diverse pine cone crop, fill the crisp mountain air. The strong “chick-a-dee” call sticks out among the bird vocalizations. The chickadees are communicating to each other about food sources – and my approach. Mountain chickadees are a member of the family Paridae, which is known for its complex vocal communication systems and cognitive abilities. Along with my advisers, behavioral ecologists Vladimir Pravosudov and Carrie Branch, I’m studying mountain chickadees at our study site in Sagehen Experimental Forest, outside of Truckee, California, for my doctoral research. I am focusing on how these birds convey a variety of information with their calls. The chilly autumn air on top of the mountain reminds me that it will soon be winter. It is time for the mountain chickadees to leave the socially monogamous partnerships they had while raising their chicks to form larger flocks. Forming social groups is not always simple; young chickadees are joining new flocks, and social dynamics need to be established before the winter storms arrive. I can hear them working this out vocally. There’s an unusual variety of complex calls, with melodic “gargle calls” at the forefront, coming from individuals announcing their dominance over other flock members. Examining and decoding bird calls is becoming an increasingly popular field of study, as scientists like me are discovering that many birds – including mountain chickadees – follow systematic rules to share important information, stringing together syllables like words in a sentence. © 2010–2025, The Conversation US, Inc.

Keyword: Language; Evolution
Link ID: 29807 - Posted: 05.28.2025

By Frieda Klotz In 2006, a new study on antidepressants was making headlines with its promising results: Two-thirds of participants who tried various antidepressants recovered from their depression symptoms within less than a year. The findings seemed to offer hope to the tens of millions of Americans who suffer from depression. But Henry Edmund “Ed” Pigott, then a psychologist in private practice, wasn’t buying it. After further exploring the study — a major National Institutes of Health trial that enrolled 4,000 patients — he was convinced that the researchers’ methods greatly inflated their results, almost doubling them. In other words, the drugs may work, but not for as many people as the study suggested. Henry Edmund Pigott, now a retired psychologist, began investigating a major National Institutes of Health trial on depression in 2006. Decades later, after many studies based on the landmark trial have been published, he still has questions. “Once I got started on it, it was like, ‘Okay, this really needs to be exposed,’” said Pigott, who is now retired. His suspicion sparked a two-decade quest to correct the record and obtain a retraction from the authors of the NIH study, whose work had received $35 million of federal funding. In 2023, Pigott and colleagues published a reanalysis of the NIH data in BMJ Open, finding that the original study’s remission rates were roughly half of what was reported. Pigott isn’t against antidepressants wholesale — he said he just wants patients to understand the complete risks and benefits. And many experts and clinicians stress that antidepressants are lifesaving medications. David Matuskey, a psychiatrist and associate professor at Yale University, described them as vital tools to help patients in desperate need: “Is it a perfect tool? No, but it’s an important one.”

Keyword: Depression
Link ID: 29806 - Posted: 05.28.2025

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