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

Keyword: Alzheimers
Link ID: 29767 - Posted: 04.30.2025

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

By Michael Erard In many Western societies, parents eagerly await their children’s first words, then celebrate their arrival. There’s also a vast scientific and popular attention to early child language. Yet there is (and was) surprisingly little hullabaloo sparked by the first words and hand signs displayed by great apes. 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, author and linguist Michael Erard shares a story that didn’t make it into his recent book “Bye Bye I Love You: The Story of Our First and Last Words” (MIT Press, 344 pages.) As far back as 1916, scientists have been exploring the linguistic abilities of humans’ closest relatives by raising them in language-rich environments. But the first moments in which these animals did cross a communication threshold created relatively little fuss in both the scientific literature and the media. Why? Consider, for example, the first sign by Washoe, a young chimpanzee that was captured in the wild and transported in 1966 to a laboratory at the University of Nevada, where she was studied by two researchers, Allen Gardner and Beatrice Gardner. Washoe was taught American Sign Language in family-like settings that would be conducive to communicative situations. “Her human companions,” wrote the Gardners in 1969, “were to be friends and playmates as well as providers and protectors, and they were to introduce a great many games and activities that would be likely to result in maximum interaction.” When the Gardners wrote about the experiments, they did note her first uses of specific signs, such as “toothbrush,” that didn’t seem to echo a sign a human had just used. These moments weren’t ignored, yet you have to pay very close attention to their writings to find the slightest awe or enthusiasm. Fireworks it is not.

Keyword: Language; Evolution
Link ID: 29753 - Posted: 04.23.2025

By Jacek Krywko edited by Allison Parshall There are only so many colors that the typical human eye can see; estimates put the number just below 10 million. But now, for the first time, scientists say they’ve broken out of that familiar spectrum and into a new world of color. In a paper published on Friday in Science Advances, researchers detail how they used a precise laser setup to stimulate the retinas of five participants, making them the first humans to see a color beyond our visual range: an impossibly saturated bluish green. Our retinas contain three types of cone cells, photoreceptors that detect the wavelengths of light. S cones pick up relatively short wavelengths, which we see as blue. M cones react to medium wavelengths, which we see as green. And L cones are triggered by long wavelengths, which we see as red. These red, green and blue signals travel to the brain, where they’re combined into the full-color vision we experience. But these three cone types handle overlapping ranges of light: the light that activates M cones will also activate either S cones or L cones. “There’s no light in the world that can activate only the M cone cells because, if they are being activated, for sure one or both other types get activated as well,” says Ren Ng, a professor of electrical engineering and computer science at the University of California, Berkeley. Ng and his research team wanted to try getting around that fundamental limitation, so they developed a technicolor technique they call “Oz.” “The name comes from the Wizard of Oz, where there’s a journey to the Emerald City, where things look the most dazzling green you’ve ever seen,” Ng explains. On their own expedition, the researchers used lasers to precisely deliver tiny doses of light to select cone cells in the human eye. First, they mapped a portion of the retina to identify each cone cell as either an S, M or L cone. Then, using the laser, they delivered light only to M cone cells. © 2025 SCIENTIFIC AMERICAN,

Keyword: Vision
Link ID: 29752 - Posted: 04.19.2025

Smriti Mallapaty Two hotly anticipated clinical trials using stem cells to treat people with Parkinson’s disease have published encouraging results. The early-stage trials demonstrate that injecting stem-cell-derived neurons into the brain is safe1,2. They also show hints of benefit: the transplanted cells can replace the dopamine-producing cells that die off in people with the disease, and survive long enough to produce the crucial hormone. Some participants experienced visible reductions in tremors. The studies, published by two groups in Nature today, are “a big leap in the field”, says Malin Parmar, a stem-cell biologist at Lund University, Sweden. “These cell products are safe and show signs of cell survival.” Japan’s big bet on stem-cell therapies might soon pay off with breakthrough therapies The trials were mainly designed to test safety and were small, involving 19 individuals in total, which is not enough to indicate whether the intervention is effective, says Parmar. “Some people got slightly better and others didn’t get worse,” says Jeanne Loring, a stem-cell researcher at Scripps Research in La Jolla, California. This could be due to the relatively small number of cells transplanted in these first early-stage trials. Parkinson’s is a progressive neurological condition driven by the loss of dopamine-producing neurons, which causes tremors, stiffness and slowness in movement. There is currently no cure for the condition, which is projected to affect 25 million people globally by 2050. Cell therapies are designed to replace damaged neurons, but previous trials using fetal tissue transplants have had mixed results. The latest findings are the first among a handful of global trials testing more-advanced cell therapies. © 2025 Springer Nature Limited

Keyword: Parkinsons; Stem Cells
Link ID: 29751 - Posted: 04.19.2025

By Jan Hoffman Fentanyl overdoses have finally begun to decline over the past year, but that good news has obscured a troubling shift in illicit drug use: a nationwide surge in methamphetamine, a powerful, highly addictive stimulant. This isn’t the ’90s club drug or even the blue-white tinged crystals cooked up in “Breaking Bad.” As cartels keep revising lab formulas to make their product more addictive and potent, often using hazardous chemicals, many experts on addiction think that today’s meth is more dangerous than older versions. Here is what to know. What is meth? Meth, short for methamphetamine, is a stimulant, a category of drugs that includes cocaine. Meth is far stronger than coke, with effects that last many hours longer. It comes in pill, powder or paste form and is smoked, snorted, swallowed or injected. Meth jolts the central nervous system and prompts the brain to release exorbitant amounts of reinforcing, feel-good neurotransmitters such as dopamine, which help people experience euphoria and drive them to keep seeking it. Meth is an amphetamine, a category of stimulant drugs perhaps best known to the public as the A.D.H.D. prescription medications Adderall and Vyvanse. Those stimulants are milder and shorter-lasting than meth but, if misused, they too can be addictive. What are meth’s negative side effects? They vary, depending on the tolerance of the person taking it and the means of ingestion. After the drug’s rush has abated, many users keep bingeing it. They forget to drink water and are usually unable to sleep or eat for days. In this phase, known as “tweaking,” users can become hyper-focused on activities such as taking apart bicycles — which they forget to reassemble — or spending hours collecting things like pebbles and shiny gum wrappers. They may become agitated and aggressive. Paranoia, hallucinations and psychosis can set in. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29750 - Posted: 04.19.2025

By Erin Blakemore Consuming more than eight alcoholic drinks a week is associated with brain injuries linked to Alzheimer’s disease and cognitive decline, a recent study in the journal Neurology suggests. The analysis looked for links between heavy drinking and brain health. Researchers used autopsy data from the Biobank for Aging Studies at the University of São Paulo Medical School in Brazil collected between 2004 and 2024. The team analyzed data from 1,781 people ages 50 or older at death. The average age at death was 74.9. With the help of surveys of the deceased’s next of kin, researchers gathered information about the deceased’s cognitive function and alcohol consumption in the three months before their death. Among participants, 965 never drank, 319 drank up to seven drinks per week (moderate drinking), and 129 had eight or more drinks per week (heavy drinking). Another 368 were former heavy drinkers who had stopped drinking before their last three months of life. The analysis showed that heavy drinkers and former heavy drinkers, respectively, had 41 percent and 31 percent higher odds of neurofibrillary tangles — clumps of the protein tau that accumulate inside brain neurons and have been associated with Alzheimer’s disease. Moderate, heavy and former heavy drinkers also had a higher risk of hyaline arteriolosclerosis, which thickens the walls of small blood vessels in the brain, impeding blood flow and causing brain damage over time. Though 40 percent of those who never drank had vascular brain lesions, they were more common in moderate (44.6 percent), heavy (44.1 percent) and former heavy drinkers (50.2 percent), the study found.

Keyword: Drug Abuse; Alzheimers
Link ID: 29749 - Posted: 04.19.2025

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