Bobbi-Jean MacKinnon A new scientific study has found no evidence of a mystery brain disease in New Brunswick, says a report published Wednesday in the Journal of the American Medical Association, known as JAMA. Instead, an independent reassessment of 25 of 222 patients diagnosed by Moncton neurologist Alier Marrero as having a "neurological syndrome of unknown cause" concluded that all of the cases were attributable to well-known conditions. These include common neurodegenerative diseases, such as Alzheimer's and Parkinson's, functional neurological disorder, traumatic brain injury, and metastatic cancer, says the report. Despite the small sample size, "when we did the statistics … the chances of any of those other individuals having a mystery disease was less than one in a million," said Dr. Anthony Lang, a senior neurologist and neuroscientist in Toronto, and one of the 13 co-authors. The researchers, affiliated with the University of Toronto, New Brunswick's Horizon Health Network and other Canadian institutions, do not believe exposure to something in the environment, such as the herbicide glyphosate or heavy metals, made the patients ill either, said Lang, director of the Edmund J Safra Program in Parkinson's Disease at the University Health Network. "The neurological problems varied a great deal. Some had neurodegenerative diseases, but others had other neurological problems and therefore a single environmental toxin … could never have explained this broad variety of neurological abnormalities." Lang, who got involved in the study because he started hearing about a mystery disease but wasn't seeing any publications in medical literature, is not surprised by the results. ©2025 CBC/Radio-Canada.

Keyword: Movement Disorders; Alzheimers
Link ID: 29779 - Posted: 05.10.2025

Freda Kreier Some people can function well on little sleep.Credit: Oleg Breslavtsev/Getty Most people need around eight hours of sleep each night to function, but a rare genetic condition allows some to thrive on as little as three hours. In a study published today in the Proceedings of the National Academy of Sciences1, scientists identified a genetic mutation that probably contributes to some people’s limited sleep needs. Understanding genetic changes in naturally short sleepers — people who sleep for three to six hours every night without negative effects — could help to develop treatments for sleep disorders, says co-author Ying-Hui Fu, a neuroscientist and geneticist at the University of California, San Francisco. “Our bodies continue to work when we go to bed”, detoxifying themselves and repairing damage, she says. “These people, all these functions our bodies are doing while we are sleeping, they can just perform at a higher level than we can.” In the 2000s, Fu and her colleagues were approached by people who slept six hours or less each night. After analysing the genomes of a mother and daughter, the team identified a rare mutation in a gene that helps to regulate humans’ circadian rhythm, the internal clock responsible for our sleep–wake cycle. The researchers suggested that this variation contributed to the duo’s short sleep needs. That discovery prompted others with similar sleeping habits to contact the laboratory for DNA testing. The team now knows several hundred naturally short sleepers. Fu and her colleagues have so far identified five mutations in four genes that can contribute to the trait — although different families tend to have different mutations. Short sleeper In the latest study, the researchers searched for new mutations in the DNA of a naturally short sleeper. They found one in SIK3, a gene encoding an enzyme that, among other things, is active in the space between neurons. Researchers in Japan had previously found another mutation in Sik3 that caused mice to be unusually sleepy2. © 2025 Springer Nature Limited

Keyword: Sleep; Genes & Behavior
Link ID: 29778 - Posted: 05.07.2025

By Lizzie Wade As John Rick excavated one of the many underground chambers at the ancient Peruvian site of Chavín de Huántar in 2017 his trowel hit something intriguing, and exceedingly delicate. It was a cigarette-size tube made of animal bone and packed full of sediment. The following year, his team found almost two dozen more. Rick, an archaeologist at Stanford University, suspected these bone tubes were pieces of ancient drug paraphernalia. Now, a chemical analysis of plant material preserved inside the bone tubes confirms ancient people used them to inhale snuffs made of tobacco and a hallucinogenic plant known as vilca. Rick and colleagues say the rituals involving these drugs may have helped the people of Chavín consolidate their power and influence some 2500 years ago, a time when complex social and political hierarchies were first taking shape in Peru. Although researchers have long suspected rituals at Chavín involved hallucinogenic drugs, “What’s exciting about this paper is that, for first time, we have actual evidence,” says José Capriles, an archaeologist at Pennsylvania State University who wasn’t involved in the research but has studied psychoactive drugs used by ancient people. Chavín de Huántar, which was occupied in the first millennium B.C.E., is renowned for its intricate stone carvings, often depicting animal-human hybrids or transformations of human into beast, and an extensive network of underground chambers. It also had a broad cultural reach. The site in Peru’s north-central highlands abounds with seashells and obsidian, neither found locally, and Chavín-style art shows up in many places throughout the Andes and on the Peruvian coast. “Chavín was part of the first big moment in Andean prehistory when people, ideas, and goods were circulating quite extensively,” says Dan Contreras, an archaeologist at the University of Florida and a co-author of the new paper.

Keyword: Drug Abuse
Link ID: 29775 - Posted: 05.07.2025

By Carl Zimmer Consciousness may be a mystery, but that doesn’t mean that neuroscientists don’t have any explanations for it. Far from it. “In the field of consciousness, there are already so many theories that we don’t need more theories,” said Oscar Ferrante, a neuroscientist at the University of Birmingham. If you’re looking for a theory to explain how our brains give rise to subjective, inner experiences, you can check out Adaptive Resonance Theory. Or consider Dynamic Core Theory. Don’t forget First Order Representational Theory, not to mention semantic pointer competition theory. The list goes on: A 2021 survey identified 29 different theories of consciousness. Dr. Ferrante belongs to a group of scientists who want to lower that number, perhaps even down to just one. But they face a steep challenge, thanks to how scientists often study consciousness: Devise a theory, run experiments to build evidence for it, and argue that it’s better than the others. “We are not incentivized to kill our own ideas,” said Lucia Melloni, a neuroscientist at the Max Planck Institute for Empirical Aesthetics in Frankfurt, Germany. Seven years ago, Dr. Melloni and 41 other scientists embarked on a major study on consciousness that she hoped would break this pattern. Their plan was to bring together two rival groups to design an experiment to see how well both theories did at predicting what happens in our brains during a conscious experience. The team, called the Cogitate Consortium, published its results on Wednesday in the journal Nature. But along the way, the study became subject to the same sharp-elbowed conflicts they had hoped to avoid. Dr. Melloni and a group of like-minded scientists began drawing up plans for their study in 2018. They wanted to try an approach known as adversarial collaboration, in which scientists with opposing theories join forces with neutral researchers. The team chose two theories to test. © 2025 The New York Times Company

Keyword: Consciousness
Link ID: 29773 - Posted: 05.03.2025

By Anil Seth On stage in New York a couple years ago, noted neuroscientist Christof Koch handed a very nice bottle of Madeira wine to philosopher David Chalmers. Chalmers had won a quarter-century-long bet about consciousness—or at least our understanding of it. Nautilus Members enjoy an ad-free experience. Log in or Join now . The philosopher had challenged the neuroscientist in 1998—with a crate of fine wine on the line—that in 25 years, science would still not have located the seat of consciousness in the brain. The philosopher was right. But not without an extraordinary—and revealing—effort on the part of consciousness researchers and theorists. Backing up that concession were the results of a long and thorough “adversarial collaboration” that compared two leading theories about consciousness, testing each with rigorous experimental data. Now we finally learn more about the details of this work in a new paper in the journal Nature. Nicknamed COGITATE, the collaboration pitted “global neuronal workspace theory” (GNWT)—an idea advocated by cognitive neuroscientist Stanislas Dehaene, which associates consciousness with the broadcast of information throughout large swathes of the brain—against “integrated information theory” (IIT)—the idea from neuroscientist Giulio Tononi, which identifies consciousness with the intrinsic cause-and-effect power of brain networks. The adversarial collaboration involved the architects of both theories sitting down together, along with other researchers who would lead and execute the project (hats off to them), to decide on experiments that could potentially distinguish between the theories—ideally supporting one and challenging the other. Deciding on the theory-based predictions, and on experiments good enough to test them, was never going to be easy. In consciousness research, it is especially hard since—as philosopher Tim Bayne and I noted—theories often make different assumptions, and attempt to explain different things even if, on the face of it, they are all theories of “consciousness.” © 2025 NautilusNext Inc.,

Keyword: Consciousness
Link ID: 29772 - Posted: 05.03.2025

By Allison Parshall ] Where in the brain does consciousness originate? Theories abound, but neuroscientists still haven’t coalesced around one explanation, largely because it’s such a hard question to probe with the scientific method. Unlike other phenomena studied by science, consciousness cannot be observed externally. “I observe your behavior. I observe your brain, if I do an intracranial EEG [electroencephalography] study. But I don’t ever observe your experience,” says Robert Chis-Ciure, a postdoctoral researcher studying consciousness at the University of Sussex in England. Scientists have landed on two leading theories to explain how consciousness emerges: integrated information theory, or IIT, and global neuronal workspace theory, or GNWT. These frameworks couldn’t be more different—they rest on different assumptions, draw from different fields of science and may even define consciousness in different ways, explains Anil K. Seth, a consciousness researcher at the University of Sussex. To compare them directly, researchers organized a group of 12 laboratories called the Cogitate Consortium to test the theories’ predictions against each other in a large brain-imaging study. The result, published in full on Wednesday in Nature, was effectively a draw and raised far more questions than it answered. The preliminary findings were posted to the preprint server bioRxiv in 2023. And only a few months later, a group of scholars publicly called IIT “pseudoscience” and attempted to excise it from the field. As the dust settles, leading consciousness researchers say that the Cogitate results point to a way forward for understanding how consciousness arises—no matter what theory eventually comes out on top. “We all are very good at constructing castles in the sky” with abstract ideas, says Chis-Ciure, who was not involved in the new study. “But with data, you make those more grounded.” © 2025 SCIENTIFIC AMERICAN,

Keyword: Consciousness
Link ID: 29771 - Posted: 05.03.2025

Logan S. James It is late at night, and we are silently watching a bat in a roost through a night-vision camera. From a nearby speaker comes a long, rattling trill. The bat briefly perks up and wiggles its ears as it listens to the sound before dropping its head back down, uninterested. Next from the speaker comes a higher-pitched “whine” followed by a “chuck.” The bat vigorously shakes its ears and then spreads its wings as it launches from the roost and dives down to attack the speaker. Bats show tremendous variation in the foods they eat to survive. Some species specialize on fruits, others on insects, others on flower nectar. There are even species that catch fish with their feet. At the Smithsonian Tropical Research Institute in Panama, we’ve been studying one species, the fringe-lipped bat (Trachops cirrhosus), for decades. This bat is a carnivore that specializes in feeding on frogs. Male frogs from many species call to attract female frogs. Frog-eating bats eavesdrop on those calls to find their next meal. But how do the bats come to associate sounds and prey? We were interested in understanding how predators that eavesdrop on their prey acquire the ability to discriminate between tasty and dangerous meals. We combined our expertise on animal behavior, bat cognition and frog communication to investigate. © 2010–2025, The Conversation US, Inc.

Keyword: Hearing; Development of the Brain
Link ID: 29768 - Posted: 05.03.2025

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

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

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 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

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

The devastating stimulant has been hitting Portland, Maine hard, even competing with fentanyl as the street drug of choice. Although a fentanyl overdose can be reversed with Narcan, no medicine can reverse a meth overdose. Nor has any been approved to treat meth addiction. Unlike fentanyl, which sedates users, meth can make people anxious and violent. Its effects can overwhelm not just users but community residents and emergency responders. John once fielded customer complaints for a telecommunications company. Now he usually hangs out with friends in the courtyard of a center offering services to help people who use drugs, hitting his pipe, or as he calls it, “getting methicated.” He usually lives outdoors, though he can sometimes handle a few days at a shelter. By noon, he tries to stop smoking meth, so he can get to sleep later that night. Quitting is not on his radar: meth rules his life. “We cannot ride on the railroad, the railroad rides upon us,” he said, with a nod to Henry David Thoreau. Most weekdays, Bill Burns, an addiction and mental health specialist with the Portland police, walks the Bayside neighborhood, checking in on folks. On Thursdays, he rewards the regulars he drives to addiction treatment clinics with his own homemade jolts of dopamine: sugar-dense, Rice Krispie-style treats. Recently, he encountered a young man in full meth psychosis, wild-eyed, bare-chested and bleeding, flinging himself against concrete barriers in an alley. Mr. Burns slipped between the man and a brick wall and wrapped his arms protectively around him. Even as the man flailed uncontrollably, smacking Mr. Burns and smearing blood on his shirt, he managed to stammer, “Sorry!” Speaking softly, Mr. Burns kept repeating, “You’re going to be safe. You’re OK. We’re here because we just want to make sure you’re safe. No, you’re not in trouble. Nobody wants to hurt you. ” © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29747 - Posted: 04.16.2025

By Rachel Brazil Drugs that mimic glucagonlike peptide-1 (GLP-1), such as semaglutide—marketed as Ozempic or Wegovy—have revolutionized the treatment of obesity and type 2 diabetes, but they have major drawbacks. “[They] are expensive to manufacture, they have to be refrigerated, and they often have to be injected because they cannot go through the gastrointestinal tract without being degraded,” explains Alejandra Tomas, a cell biologist at Imperial College London who studies the cellular receptor GLP-1 drugs target. That’s all because they consist of peptides, or long chains of amino acids. A small-molecule version of the therapy, on the other hand, could be given as a daily pill and would be much cheaper to produce. Companies including Eli Lilly, Pfizer, and Roche have launched clinical trials of such compounds. Results from Lilly’s first phase 3 trial of its oral drug are expected later this year. But Pfizer announced this week it was halting development of its candidate after signs of liver injury in a trial participant. The candidates furthest along in development activate the same receptors as peptide drugs do, in much the same way. But several firms are exploring more innovative small molecules that target different sites on those receptors—and could lead to even more effective treatments with fewer side effects. “In the next 4 or 5 years, this field will mature and more patients ultimately should be able to get these medicines,” says Kyle Sloop, a molecular biologist at Lilly Research Laboratories. By mimicking a natural hormone, semaglutide and other drugs in its class help regulate blood sugar by increasing insulin secretion from the pancreas in response to glucose, and suppress appetite by slowing down digestion. The first generation of peptide drugs were essentially copies of GLP-1, with modifications to prevent the peptide from quickly degrading once in the body. Novo Nordisk first won U.S. approval for semaglutide to treat type 2 diabetes in 2017. It needed to be injected, but in 2019 the company added a pill form, which includes an absorption-enhancing ingredient that allows the peptide to penetrate the stomach wall. However, it requires a high dose and has to be taken while fasting, with minimal liquid.

Keyword: Obesity
Link ID: 29746 - Posted: 04.16.2025

By Azeen Ghorayshi The percentage of American children estimated to have autism spectrum disorder increased in 2022, continuing a long-running trend, according to data released on Tuesday by the Centers for Disease Control and Prevention. Among 8-year-olds, one in 31 were found to have autism in 2022, compared with 1 in 36 in 2020. That rate is nearly five times as high as the figure in 2000, when the agency first began collecting data. The health agency noted that the increase was most likely being driven by better awareness and screening, not necessarily because autism itself was becoming more common. That diverged sharply from the rhetoric of the nation’s health secretary, Robert F. Kennedy Jr., who on Tuesday said, “The autism epidemic is running rampant.” Mr. Kennedy has repeatedly tried to connect rising autism rates with vaccines, despite dozens of studies over decades that failed to establish such a link. The health secretary nonetheless has initiated a federal study that will revisit the possibility and has hired a well-known vaccine skeptic to oversee the effort. Mr. Kennedy recently announced an effort by the Department of Health and Human Services to pinpoint the “origins of the epidemic” by September, an initiative that was greeted with skepticism by many autism experts. “It seems very unlikely that it is an epidemic, in the way that people define epidemics,” said Catherine Lord, a psychologist and autism researcher at the David Geffen School of Medicine at the University of California, Los Angeles. A significant part of the increase instead can be attributed to the expansion of the diagnosis over the years to capture milder cases, Dr. Lord said, as well as decreased stigma and greater awareness of support services. Still, she left open the possibility that other factors are contributing to more children developing autism. “We can account for a lot of the increase but perhaps not all of it,” Dr. Lord said. “But whatever it is, it’s not vaccines,” she added. © 2025 The New York Times Company

Keyword: Autism
Link ID: 29744 - Posted: 04.16.2025