Hannah Critchlow About 2 billion years ago, evolution performed an improbable experiment. A larger ancestral cell engulfed a smaller bacterium. It should have been a meal. Instead, it became a merger. The bacterium survived inside its host, and together they forged one of the most consequential partnerships in the history of life. The host offered shelter and access to oxygen. The bacterium supplied something revolutionary: a vastly more efficient way to generate energy. From this intimate alliance emerged the eukaryotic cell – and with it, the possibility of complex life. Every plant, animal and thinking being traces its lineage back to that ancient symbiosis. Our capacity for reflection, imagination and doubt rests upon what was once a free-living microbe. We call these descendants mitochondria. They persist in nearly every cell of our bodies, hundreds to thousands at a time. In total, we carry an estimated 10 million billion of them – collectively accounting for roughly a 10th of our body mass. Red blood cells are the exception: they lack mitochondria, which maximises oxygen transport. Almost every other cell depends on them absolutely. Neurons are especially demanding hosts. Each contains thousands of mitochondria, occupying up to 40 per cent of its volume. These rod-shaped structures are often described as the cell’s powerhouses. Through aerobic metabolism, they generate most of the chemical energy that keeps cells alive and functioning – the molecular fuel that sustains every biological process. Although the brain represents just 2 per cent of body weight, it consumes about 20 per cent of our energy at rest. Every perception, memory, emotion and idea is metabolically expensive. Thought itself is an energy-hungry act. Weight for weight, our brains are more mitochondrial than neural. This is more than a biological curiosity. It suggests that cognition is inseparable from metabolism – that the mind is not only shaped by networks of neurons but by networks of energy. © Aeon Media Group Ltd. 2012-2026.

Keyword: Biomechanics; Evolution
Link ID: 30213 - Posted: 04.22.2026

Ian Sample Science editor A married couple who met over a dissected brain and went on to create the first approved gene therapy for blindness have been awarded one of the most lucrative prizes in science. Molecular biologist Jean Bennett and ophthalmologist Albert Maguire share the $3m (£2.2m) Breakthrough prize for life sciences with physician Katherine High for the 25-year-long project, during which the couple adopted a pair of dogs they had treated for blindness. The therapy, named Luxturna, was approved in the US in 2017 and has transformed the lives of people born with Leber congenital amaurosis (LCA), a genetic disorder that typically causes total blindness by early adulthood. Proof that the therapy worked came in a clinical trial in which one patient described seeing their child’s face for the first time, the fine grain in wooden furniture and branches waving in the wind. Other patients reported similar profound improvements. Nine slices of bread toasted and burned to different degrees, from white to blackened. “I was overwhelmed,” said Bennett, who is now retired from the University of Pennsylvania. “It was one of the most miraculous eureka moments you can imagine.” Bennett said it was a “tremendously exciting time” for scientific and medical research, but warned that the US administration’s attacks on science could “cause damage for generations to come”, leading her to fear a brain drain that the country would struggle to recover from. “Agendas have become politicised, government agencies that support basic and applied research have been undermined, knowledgable advisers and experts have been dismissed or have fled and revised guidelines contradict decades of rigorous research,” she said. © 2026 Guardian News & Media Limited

Keyword: Vision
Link ID: 30212 - Posted: 04.22.2026

By Chand Chandrasekaran Decisions emerge from coordinated activity patterns across many brain areas. The challenge we face as neuroscientists is figuring out how. Technologies such as Neuropixels and optical imaging enable recordings from populations of neurons across many brain areas, leading to enormously impressive datasets with thousands of neurons. But making sense of these data to uncover the computations underlying decision-making has proved elusive. I think it is a great time for the field to design experiments that match the ambition of our tools. By designing decision-making tasks that vary along multiple dimensions and truly challenge our animals, we might finally understand how multiple brain areas coordinate to drive decisions. The starting point of most decision-making experiments is to get animals to perform a task for rewards, such as juice or food. It is often tempting to train the animal to do “something simple” because the training is easy and quick. Later we can get to the “exciting stuff”: Go in with a kitchen sink of experimental tools to collect neurophysiological data and/or perturb the system and use mathematical tools to uncover how activity in the brain leads to the behavior of interest. Though this approach sounds great in principle, analyzing the neural data associated with simple behavioral tasks can be challenging for multiple reasons. First, when the behavior is too simple, the brain does not need to compute much. When many areas could solve a problem, often they do: Relevant signals pop up all over the brain, leaving us with the somewhat puzzling conclusion that the behavior is global. But some tasks may be too trivial to require different computations from different areas, so it’s unsurprising that many areas look similar in such contexts. Second, animals perform simple tasks quickly, generating only a narrow window of neural activity from which to try to make sense of how they reached a decision. You might be left with just 50 milliseconds of potentially very noisy neural data from which to understand decision-related computations. © 2026 Simons Foundation

Keyword: Attention
Link ID: 30211 - Posted: 04.22.2026

Jon Hamilton It's often called the mind's eye. "I can look at an object in the world around me, but I can also close my eyes and imagine the object," says Varun Wadia, a brain scientist at Cedars-Sinai Medical Center and the California Institute of Technology. That sort of visual imagination, Wadia says, is what allows most people to conjure the face of a loved one or navigate to work using a mental map. For 'time cells' in the brain, what matters is what happens in the moment Shots - Health News For 'time cells' in the brain, what matters is what happens in the moment But its neural underpinnings were a mystery until Wadia and a team reported in the journal Science that imagined and perceived objects appear to activate the same neurons and use the same neural code. "This has not been demonstrated before at the neural level," says Kalanit Grill-Spector, a psychology professor at Stanford University's Wu Tsai Neurosciences Institute, who was not involved in the research. With these insights, she says, scientists are one step closer to building computer models that can simulate vision as well as vision disorders like macular degeneration. These models, in turn, could help researchers develop prosthetic devices to restore sight. The research also helps explain how the brain uses imagination to augment visual information, says Thomas Naselaris, a neuroscientist at the University of Minnesota. © 2026 npr

Keyword: Vision; Consciousness
Link ID: 30210 - Posted: 04.22.2026

Ian Sample Science editor Changes to microbes that live in the gut can identify people at greater risk of Parkinson’s disease long before symptoms develop, according to work that also raises hopes for new therapies. Researchers discovered signature changes in the gut microbiome that are more pronounced in people with a genetic risk for Parkinson’s and even more stark in those diagnosed with the disease. The signature could help doctors spot patients at risk of Parkinson’s years before they display clear symptoms and suggests that healthier diets and treatments that reshape the microbiome might prevent or delay the disease. Prof Anthony Schapira, the head of clinical and movement neurosciences at University College London and lead investigator on the study, said it was the first time a microbial signature in Parkinson’s patients had been seen in people with a genetic susceptibility but had yet to develop symptoms. The signature appears to become stronger as the disease progresses. “These same changes can be found in a small proportion of the general population that may put them at increased risk,” Schapira said. Cases of Parkinson’s have doubled in the past 25 years, with more than 8.5 million people globally now living with the condition. The disease causes progressive brain damage, leading to tremors, slow movement and stiff and inflexible muscles. Patients often experience depression, anxiety, sleep and memory problems, and difficulty with balance. © 2026 Guardian News & Media Limited

Keyword: Parkinsons
Link ID: 30209 - Posted: 04.22.2026

By Bethany Brookshire It’s easy to think of the human body as a single, fully integrated unit. After all, stub your toe all the way at one end of your body, and your brain registers it at the other. A suite of muscles works together to hop up-and-down and the lungs fill with air to expel curses from your mouth. In this moment, your body is one organism, one set of cells all pulling together against the world — and whatever it was that hurt your toe. But while our cells all work together to help us walk, eat and argue with each other on the internet, they are not all pulling together toward the same goal all the time. Each one of the body’s 30 trillion to 40 trillion human cells is its own world, with its own set of DNA that accumulates its own changes over time. These mutations can mean nothing, but they can also mean everything. While many mutations are inert, others cause harm. Still others bring hope, and could correct some of the body’s problems, science writer Roxanne Khamsi explains in Beyond Inheritance. The book draws on the latest research across multiple fields of science to show that mutations are with us throughout our lives, shaping our health and our lifespans. Many people might think of mutations as things that arise and take over only in times of trouble such as cancer. Otherwise, mutation is something that matters only if it’s passed down to the next generation — whether it produces a new eye color or a serious genetic disorder. But mutations do far more than determine what we look like when we’re born and the manner in which we die, Khamsi argues. “Our genetic destinies are not necessarily defined by what we inherit from our biological parents,” she writes. © Society for Science & the Public 2000–2026.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 30208 - Posted: 04.22.2026

Miryam Naddaf By analysing more than a million brain cells, researchers have uncovered widespread differences in patterns of gene activity between male and female brains. The work, which defined sex on the basis of a person’s combination of sex chromosomes, could help to explain why the risk of developing some brain conditions — such as schizophrenia and Alzheimer’s disease — differs between males and females. Although the differences were subtle, the team identified more than 100 genes that showed consistent variation in their expression between males and females across several brain regions. The work was published on 16 April in Science1. “Having these gene-expression signatures provides a molecular handle to understanding the biology of how the brains of men and women might be functioning slightly differently in the context of the different hormonal environments that their bodies produce,” says Jessica Tollkuhn, a neuroscientist and molecular biologist at Cold Spring Harbor Laboratory in New York. She adds that “understanding sex differences in disease susceptibility could lead to better treatments to benefit everyone”. Subtle differences Previous studies2,3 have documented sex differences when it comes to a person’s risk of developing various neurological conditions. For example, schizophrenia, attention deficit hyperactivity disorder (ADHD) and Parkinson’s disease are more common in biological males — who typically have XY sex chromosomes. By contrast, Alzheimer’s disease and mood disorders such as depression and anxiety tend to be more common in females, whose sex chromosomes are usually XX. © 2026 Springer Nature Limited

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 30207 - Posted: 04.18.2026

By Pam Belluck Since the approval of new Alzheimer’s drugs in recent years, there has been a lingering question: While data indicated that they could modestly slow cognitive decline for some patients, would that effect be meaningful or too slight to make difference? A new review of research spanning a decade, published on Wednesday, concluded that the clinical benefit of these and similar drugs is negligible. But the way the review was conducted spurred heated criticism from many Alzheimer’s experts, including some who had been skeptical of some of them. The review, published by Cochrane, an international network of health researchers, evaluated studies that were conducted on seven monoclonal antibody drugs developed over the last two decades to target amyloids, proteins that form plaques in the brains of people who have Alzheimer’s disease. Some Alzheimer’s experts said the conclusions were meaningless because the review swept under one umbrella drugs that had shown very dissimilar results and worked differently. The experts noted that data from the two most recent drugs studied — Leqembi and Kisunla — showed they could slow cognitive decline, which led to approval from the Food and Drug Administration and made them the only anti-amyloid drugs available to patients. But a vast majority of the studies analyzed in the review involved four earlier drugs that had failed clinical trials or were never approved and a fifth drug that was pulled from the market. “The problem with the review is the mix of ingredients,” said Dr. Jason Karlawish, a director of the Penn Memory Center at the University of Pennsylvania, who has been skeptical or cautious toward some of the drugs over the years. “They took some of the rotten ingredients and mixed it in with the fresh food, and the result is a stinky stew.” © 2026 The New York Times Company

Keyword: Alzheimers
Link ID: 30206 - Posted: 04.18.2026

By Angie Voyles Askham When Shan Siddiqi arrived in Australia in February to speak at the 2026 Noosa Brain Workshop, he was still thinking about a paper published in Nature Neuroscience three weeks prior. The work had criticized lesion network mapping (LNM), a neuroimaging method that Siddiqi uses as the basis for much of his work. LNM uses the location of brain lesions in various health conditions to infer information about networks of brain activity altered in those conditions. But the January paper claimed the approach produces biased results, and points to largely the same brain networks no matter the condition. After reading the full paper, however, Siddiqi, associate professor of psychiatry at Harvard Medical School, decided the authors’ criticism was toothless—it highlighted issues that he and his colleagues were aware of, and had already developed methods to address. Yet to his dismay, in the following days and weeks the criticism kept coming, both on social media and in news articles, including one by The Transmitter. The issue hung over the conference, too. During a social event on the first night of the Noosa meeting, other attendees asked Siddiqi, as a leading proponent of the method, for his thoughts, and he decided he needed to address the criticism in his talk the following day. The next afternoon, he told the audience of senior neuroimaging researchers that he took the challenge raised in the paper seriously, and said it had caused him and his co-author Michael D. Fox to reanalyze their data in collaboration with neuroimaging statisticians. He then presented the two competing hypotheses to the audience—LNM findings are disease specific versus LNM is mathematically flawed—and explained how he and Fox tested both with real data. The results seemed to validate LNM, Siddiqi said, leading him to conclude that the critique rested on incorrect assumptions about how the method is implemented. © 2026 Simons Foundation

Keyword: Brain imaging
Link ID: 30205 - Posted: 04.18.2026

Nicholas Humphrey In his novel Penguin Island (1908), Anatole France spins a wonderful tale about a blind old monk who sets off from Brittany on a mission to the Hebrides and lands on an island inhabited only by penguins. Though the birds speak a strange language, he assumes they must be human beings. So he proceeds to baptise them. When the news of this reaches heaven, it causes a major stir. God himself is embarrassed. He gathers an assembly of clerics and doctors, and asks them for an opinion on the delicate question of whether the birds must now be given souls. It is a matter of more than theoretical importance. ‘The Christian state,’ St Cornelius points out, ‘is not without serious inconveniences for a penguin … The habits of birds are, in many points, contrary to the commandments of the Church …’ After lengthy discussion, they settle on a compromise. The baptised penguins are indeed to be granted souls – but, on St Catherine’s recommendation, their souls are to be of small size. For the penguins, souls were an unexpected bonus. As René Descartes, the philosopher-scientist of the 17th century, had explained, nonhuman animals in general, in a state of nature, are mere soulless machines. Here’s a sketch of a Cartesian penguin, without even a smidgen of a soul. Descartes believed that humans too are machines of a kind. But he held that, with humans, thankfully, God has arranged the addition of a soul as standard practice. Early in infancy, the material substance of the human brain is put into communication via the pineal gland with the separate substance of the mind: res extensa (extended stuff) is joined by res cogitans (thinking stuff). The consciousness that results lays the foundation for the soul. © Aeon Media Group Ltd. 2012-2026

Keyword: Consciousness; Language
Link ID: 30204 - Posted: 04.18.2026

By Ellen Barry Edna Foa, an Israeli American psychologist who pressed her field — and her patients — to more directly confront fear and anxiety, revolutionizing the treatment of post-traumatic stress disorder, died on March 24 at a hospital in Philadelphia. She was 88. Her death, from complications of pneumonia, was confirmed by her daughter Yael Foa. Dr. Foa completed her training in the late 1960s, when clinicians tended to treat people with severe anxiety disorders cautiously and gradually. One of her first patients, a woman with an intense fear of objects related to death, had been prescribed a course of “systematic desensitization.” Dr. Foa was instructed to visit her every day carrying a small stone from a cemetery, bringing the stone a little closer each time until at long last the patient would be able to hold it. “We started to feel that she will never get better at that rate,” Dr. Foa recalled in a 2018 podcast interview. Dr. Foa decided to move faster, driving the patient to a funeral home and bringing her inside so that the woman was forced to deal with her distress. Avoiding those feelings, Dr. Foa posited, was actually holding the patient back. This theory culminated, about a decade later, in Dr. Foa’s landmark innovation. In the 1980s, she developed prolonged exposure therapy, a structured protocol of eight to 12 90-minute sessions in which the patient recounts a traumatic event in the present tense, lingering on the most vivid and upsetting elements. Then the patient undertakes real life exposure to reminders of the event. These sessions could be uncomfortable, Dr. Foa acknowledged. But they served to ease the patient’s sensitivity and correct flawed thinking, demonstrating that there was no harm in confronting the feared object, place or event. Over the years that followed, a series of studies supported the approach’s effectiveness. © 2026 The New York Times Company

Keyword: Stress
Link ID: 30203 - Posted: 04.18.2026

By Katie Engelhart The doctor told her that her husband was just a vegetable now. “And he’s always just going to be a vegetable.” Did he really say it like that? Vegetable? And, just? Well, that’s how she remembers it. In his notes, the doctor wrote that his patient’s prognosis was “Poor/Grave.” A few weeks earlier, on Oct. 4, 2024, while on a trip out of town, Aaron Williams said that his stomach hurt. Then he started vomiting and couldn’t stop, and then he started screaming. His wife, Tabitha, tried to drive him back home to Aiken, S.C. — and she was almost there, maybe 30 minutes away, when Aaron’s body stiffened and his limbs flung out and he went quiet. At the hospital, Aaron, who was 30, was found to be in cardiac arrest. Doctors performed CPR, and when it did not work, they did it again and again; Aaron’s small, lithe body — just 5-foot-8, 135 pounds — heaved under the force of it, until after five rounds of compressions his heart started beating again. Doctors inserted a breathing tube and attached it to a ventilator next to Aaron’s bed. Sitting at her comatose husband’s side, Tabitha could hear its quiet mechanical hiss. As it turned out, Aaron, who has Type 1 diabetes, had not been taking his insulin. Part of it, maybe, was hubris; he had been a diabetic since forever, and he thought he knew his body well enough to know when his glucose levels were really off-kilter. Also, he didn’t have a prescription; Aaron and Tabitha had recently moved, with five of their children, and he still hadn’t found a new family doctor who would take Medicaid. Doctors did a CT scan, an electroencephalogram (EEG) and later an M.R.I., and they saw evidence of a global anoxic brain injury and “severe cortical dysfunction.” There was cerebral swelling too: so much that his brain pushed outward against his skull, partly flattening the folds and ridges that covered its surface. When he was examined, Aaron had no blink reflex, and he didn’t respond to sound. © 2026 The New York Times Company

Keyword: Consciousness
Link ID: 30202 - Posted: 04.15.2026

Oliver Milman We may appear to have little in common with sperm whales – enormous, ocean-dwelling animals that last shared a common ancestor with humans more than 90 million years ago. But the whales’ vocalized communications are remarkably similar to our own, researchers have discovered. Not only do sperm whale have a form of “alphabet” and form vowels within their vocalizations but the structure of these vowels behaves in the same way as human speech, the new study has found. Sperm whales communicate in a series of short clicks called codas. Analysis of these clicks shows that the whales can differentiate vowels through the short or elongated clicks or through rising or falling tones, using patterns similar to languages such as Mandarin, Latin and Slovenian. The structure of the whales’ communication has “close parallels in the phonetics and phonology of human languages, suggesting independent evolution”, the paper, published in the Proceedings B journal, states. Sperm whale coda vocalizations are “highly complex and represent one of the closest parallels to human phonology of any analyzed animal communication system”, it added. The findings are the latest discovery about the lives of sperm whales by Project Ceti (standing for Cetacean Translation Initiative), an organization that has studied whales off the coast of Dominica in an attempt to find out what they are saying. Last month, the project released video of a sperm whale giving birth while other whales supported it. © 2026 Guardian News & Media Limited

Keyword: Animal Communication; Language
Link ID: 30201 - Posted: 04.15.2026

By Elie Dolgin Two U.S. states and more than a dozen cities and counties have moved in the past year to stop adding fluoride to community drinking water, citing research suggesting the mineral could harm children’s brain development. But a new analysis of cognitive outcomes tracked over decades finds no evidence that water fluoridation is associated with lower adolescent IQ or diminished mental abilities later in life, researchers report April 13 in the Proceedings of the National Academy of Sciences. The results, based on standardized intelligence testing of more than 10,000 people in Wisconsin followed since their senior year of high school in 1957, challenge the idea that typical fluoridation levels in public drinking water pose a neurodevelopmental risk, a central point of contention in ongoing policy debates. “It’s very strong data,” says Steven Levy, a dentist and public health researcher at the University of Iowa in Iowa City who was not involved in the research. “There’s no strong signal at all coming through that should give us concern.” However, given the politically charged nature of water fluoridation and continued differences in how researchers interpret the available evidence, the findings are unlikely to be the last word on the issue. © Society for Science & the Public 2000–2026

Keyword: Intelligence; Neurotoxins
Link ID: 30200 - Posted: 04.15.2026

Brian Mann Earlier this year, Naida Rutherford, the coroner in Richland County, South Carolina, was helping investigate what appeared to be a mysterious overdose. The case had many of the hallmarks of a typical fentanyl death. "Every sort of physical manifestation, like the foam coming from the mouth and nose, as if they had an overdose," Rutherford said. "Their blood tested negative for any substance, which was very odd." Her team was stumped, so Rutherford expanded the testing, looking for new compounds. "That's where we found the cychlorphine," she told NPR, referring to one of the incredibly potent synthetic opioids spreading fast in the U.S. street drug supply. Sponsor Message The state of Virginia has seen drug overdose deaths plunge by more than 40% in a single year. Many other states are seeing improvements above 30%. Why is this happening? Researchers say it may be a combination of factors, some hopeful and some painful. "This is the first time we've seen it in South Carolina, which is very scary because none of us knew to test for it." Experts say the U.S. addiction crisis is evolving fast, in ways that appear both hopeful and incredibly dangerous. The peril comes from a street drug supply that chemists now describe as a "synthetic soup." Where once most drug users mostly consumed plant-based substances such as cocaine and heroin, drug gangs and cartels have shifted to producing and selling synthetic substances made from industrial chemicals. © 2026 npr

Keyword: Drug Abuse
Link ID: 30199 - Posted: 04.15.2026

By Michael S. Rosenwald Thomas S. Langner, a sociologist who helped lead a landmark study of New Yorkers that revealed striking insights about the social, cultural and economic forces that shape mental illness, died on March 16 at his home in Sandy Hook, Conn. He was 102. His wife, Susan Kassirer, confirmed the death. When “Mental Health in the Metropolis: The Midtown Manhattan Study” was published in 1962, headline writers had a field day with the top-line finding: that only 18.5 percent of Manhattan residents could be considered psychologically well adjusted, while 23 percent showed significant impairment in daily functioning. “City Gets Mental Test, Results Are Real Crazy,” Newsday declared. The Daytona Beach Morning Journal wondered: “New York Living for ‘Nuts’ Only?” The actual substance of the two-part study — the second installment appeared in 1963 — was the challenge it posed to the widely held view in psychiatry that biological and individual factors are the primary drivers of mental illness. Professor Langner, along with a team of psychiatrists, anthropologists and social workers at Cornell University Medical College (now Weill Cornell Medicine), spent more than a decade studying 1,660 people who lived on the East Side of Manhattan, between 59th and 96th Streets. The researchers concluded that developing mental illness didn’t simply come down to a genetic lottery. © 2026 The New York Times Company

Keyword: Stress; Schizophrenia
Link ID: 30198 - Posted: 04.15.2026

By Jonathan Corum and Matt Richtel Illicit labs are creating new synthetic drugs at breakneck speed. Dangerous, untested compounds are reaching users long before health agencies know they exist. Older drugs are regularly modified to create novel threats. Ecstasy is a prime example. The party drug MDMA has been illegal since 1985. Its molecular structure can be drawn like this: But what if you could add one atom to this molecule to change both the experience of taking the drug and its legal status? You can. A single oxygen atom changes the molecule to methylone, which provides an Ecstasy-like euphoria. The discovery of what this simple change could do has had a profound consequence. When methylone reached the U.S. market in 2010 the drug could be sold legally in corner stores and smoke shops as “bath salts.” But methylone wasn’t the end of the story. Illicit chemists now use methylone’s structure as a template for modern-day alchemy. New drug laws push them to invent new variants, which emerge in the illicit drug market with untested potencies and effects — a vicious cycle that has been impossible to contain. These chemists are located in unregulated labs around the globe, from big enterprises in China and India that produce drugs and their precursor compounds in huge volumes, to single-person and small domestic operations that cut and package drugs for retail sale. Some of the most-used drugs, such as fentanyl, are mixed in Mexico and exported north. © 2026 The New York Times Company

Keyword: Drug Abuse
Link ID: 30197 - Posted: 04.11.2026

By Siddhant Pusdekar Deer mice, common across North America, come in two varieties: One lives in prairies, whereas the other inhabits forests. The life of the forest mouse requires greater dexterity—a skill it possesses thanks to its higher number of corticospinal tract axons, according to a January preprint. The existence of “genetically tractable subspecies of deer mice with different behavioral niches” made the discovery possible, says Eiman Azim, associate professor of molecular neurobiology at the Salk Institute for Biological Studies, who wasn’t involved in the study. It enabled the researchers to link genetically driven changes in corticospinal abundance and morphology to dexterity. The new work reveals one way dexterous skill may emerge, while also suggesting neuroscience should investigate “behaviors that evolved for the natural niches” to discover fresh insights, says Ariel Levine, a senior investigator at the U.S. National Institute of Neurological Disorders and Stroke, who wasn’t involved in the study. Dexterity in primates coevolved with direct connections between layer 5 cortical neurons and motor neurons in the spinal cord, Levine says. In rodents, cats and less dexterous monkeys, however, corticospinal neurons connect to motor neurons via interneurons. Direct cortical-motor neuron connections exist in juvenile mice, but they are pruned during development, a 2017 paper showed. Artificially stopping the pruning process created adult lab mice with greater skill at gathering food pellets.

Keyword: Evolution; Development of the Brain
Link ID: 30196 - Posted: 04.11.2026

By Diana Kwon The ability to conjure pictures in the mind’s eye enables us to remember the past and imagine the future. It also allows us to plan, navigate and create works of art. In a study published April 9 in Science, researchers report that imagining an object reactivates some of the same neurons involved in seeing it in the first place, providing new insight into how mental imagery is produced in the brain. Previous research had hinted that the neurons involved in perceiving and imagining images overlapped. These studies used various methods, such as asking participants to view and then imagine pictures while lying in a functional MRI scanner, to show that the same brain regions were involved in these processes. But whether the same individual neurons were involved remained an open question, says Ueli Rutishauser, a neuroscientist at Cedars-Sinai Medical Center in Los Angeles. Because measuring neuronal activity requires electrodes in the brain, Rutishauser and colleagues studied 16 adults with epilepsy who had already had electrodes temporarily implanted into their brains to identify the origin of their seizures. Participants viewed hundreds of images from five categories — faces, text, plants, animals and everyday objects — while researchers recorded activity from over 700 neurons in the ventral temporal cortex, a region involved in representing visual objects. Of those, about 450 selectively responded to individual categories. Machine learning then revealed that 80 percent of those category-responsive neurons were selective to specific visual features within the images. © Society for Science & the Public 2000–2026.

Keyword: Attention; Vision
Link ID: 30195 - Posted: 04.11.2026

Alison Abbott The development of the human brain, with its extraordinary range of cognitive abilities, is an awe-inspiring feat of evolution. Each of its tens of billions of cells must be born at precisely the right time, migrate to the correct locations, differentiate into as many as 3,000 distinct cell types, and form exquisitely specific synaptic connections with one another. Most of this happens before birth, but development continues for nearly three more decades. None of this is easy to study. Conventionally, scientists have relied on animal models and scarce human brain tissue. But the advent of tiny laboratory-grown models of human brains called organoids has transformed their options. First created more than a decade ago, these organoids started off as very simple models. But in the past few years, scientists have refined the technology to grow more-intricate systems that represent more brain regions. Research has snowballed as scientists have used organoids to probe brain development, model neurodevelopmental conditions such as autism and schizophrenia and test new treatments for brain diseases. These tiny spheres are helping researchers to get at difficult-to-answer questions such as why the human brain develops so much more slowly than other mammalian brains do. And this year, researchers are hoping to run the first clinical trial of a brain-disorder treatment developed entirely in organoids. “The field is at an inflection point,” says developmental biologist Jürgen Knoblich at the Institute for Molecular Biotechnology in Vienna. But organoids are not without their limitations. It’s hard to sustain them in the lab for more than a few months, for instance. And they lack complexity. © 2026 Springer Nature Limited

Keyword: Development of the Brain
Link ID: 30194 - Posted: 04.08.2026