By Simon Makin A new tool makes it possible to probe brain circuit function without the kind of external stimulation required in optogenetics and chemogenetics. The method uses engineered electrical synapses to edit brain circuits. These designer synapses function in living mice, altering activity in cells, circuits and networks, with corresponding effects on behavior. In contrast to tools that involve external stimulation, the result is autonomous. “Here, all the information is completely natural; it’s only how the brain manipulates this information that’s being altered,” says Ithai Rabinowitch, assistant professor of neurobiology at the Hebrew University of Jerusalem, who was not involved in the work. “This is really important, in my view.” The technique, called LinCx (long-term integration of circuits using connexins) could be used to investigate relationships between circuit structure and function, as well as the duties of natural electrical synapses. “It’s potentially a useful tool if it’s used intelligently and thoughtfully to ask questions about the role of electrical synapses in brain circuits,” says Eve Marder, professor of biology at Brandeis University, who was not involved in the study. Electrical synapses consist of gap junctions that, in vertebrates, are composed of connexin proteins, of which there are 21 isoforms in humans. These proteins sit in the membranes of touching cells, docked together to create channels that ions pass through, coupling the cells’ activity. Gap junctions in invertebrates are composed of innexins, which don’t interact with connexins, so expressing a mammalian connexin in Caenorhabditis elegans enabled researchers to rewire an olfactory circuit and flip the worms’ behavior from odor attraction to avoidance, according to a 2014 study. © 2026 Simons Foundation

Keyword: Drug Abuse; Brain imaging
Link ID: 30293 - Posted: 06.24.2026

Max Kozlov In the fraction of a second before a person speaks, their brain weaves together complex grammar, precise vocabulary and the underlying meaning of the language. Now, researchers have tracked the electrical crackle of individual brain cells in real time during unscripted conversations, capturing how sentences are built before a single word is spoken. By observing these neurons in a region of the human brain called the frontotemporal cortex, scientists have discovered that individual brain cells act as specialized linguistic building blocks. “We used to think language was this diffuse, whole-network phenomenon,” says Ziv Williams, a neurosurgeon at Massachusetts General Hospital (MGH) in Boston and co-author of the study. “But it turns out you have specific neurons that only care if a word is a noun, or only care if a phrase is ending.” The work was published today in Nature1. To capture this activity, Williams and his colleagues used electrodes that were temporarily implanted in people with epilepsy to monitor their seizures. Because these participants were awake and speaking freely, the team could observe how the brain operated as they spoke. Neuroscientist Jing Cai, also at MGH, says that this set-up provided a rare opportunity to eavesdrop on the cellular processes that underlie speech, capturing details that standard brain-imaging devices cannot obtain. Access to such data provides a “rare” glimpse into the biological machinery that governs speech, says Angela Friederici, a neuropsychologist at the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig, Germany. © 2026 Springer Nature Limited

Keyword: Language
Link ID: 30291 - Posted: 06.20.2026

By Jennie Erin Smith Like a stadium full of sports fans doing the wave, neurons coordinate their electrical signals in rhythmic patterns that sweep across the cortex, the brain’s outermost layer. Recent studies in humans and animals have shown these patterns, called traveling waves, can take on complex shapes, among them a rotating spiral that has been observed during deep sleep, memory retrieval, and other brain processes. A new study has now captured the fast-spinning waves spanning whole brains, offering clues to how they’re organized and what they might do. The study, published today in Science, examined the brains of mice using multiple recording and imaging methods to reveal brainwide patterns that unite disparate regions from the cortex to the deep brain. The research suggests rotating waves have a key role in coordinating the flow of information across the brain to support perception and behavior. It also offers an explanation for the waves’ spiral pattern by showing that they move along a circular path laid by axons—the long projections of neurons. “This is very exciting work,” says neuroscientist Earl Miller of the Massachusetts Institute of Technology, whose team recently reported that rotating waves in the prefrontal cortex appeared to help monkeys regain their focus after a distraction. The new paper shows the waves are “highly organized across the [mouse] cortex and amazingly, across the hemispheres. When you see this kind of organization, it means something fundamental to function.” It’s been hard to see brainwide patterns of rotating waves because most previous studies have captured them with grids of electrodes that sit on the cortex and gauge signals from nearby neurons. Neuroscientists Nick Steinmetz and Zhiwen Ye of the University of Washington got a broader and more precise sense of the waves’ timing and structure by combining two approaches: rapid widefield calcium imaging, which can record the activity of large populations of neurons in the cortex, and Neuropixels probes, ultrathin microelectrodes that can penetrate brain layers, to record deeper regions such as the thalamus and striatum. © 2026 American Association for the Advancement of Science.

Keyword: Brain imaging; Attention
Link ID: 30290 - Posted: 06.20.2026

By Claudia López Lloreda Neurons in the visual cortex decode an object’s orientation—horizontal, vertical or anything in between—using information from non-orientation-tuned neurons in the thalamus, according to David Hubel and Torsten Wiesel’s Nobel Prize-winning work in cats in the 1950s and ’60s. In other species, though, the process remained unclear. Thalamic neurons in mice, for example, show orientation selectivity, subsequent studies suggested. New mouse findings—realized by imaging individual synapses on cortical neurons and distinguishing which inputs come from the thalamus versus the neighboring cortex during visual processing—help resolve the discrepancy. Signals coming into the primary visual cortex, or V1, from the thalamus are not orientation tuned, but those from other parts of the cortex are, confirming that orientation tuning occurs in the visual cortex, the new study reveals. This study is the first “to get a map of thalamic receptive field location at the level of seeing almost all the spines that receive thalamic input,” says Jose Manuel Alonso, professor of biological and vision sciences at the State University of New York College of Optometry, who was not involved with the work. “This is unbelievably beautiful.” What’s more, the Hubel and Wiesel model of orientation selectivity “is preserved through evolution,” Alonso adds. “In the mouse, this pathway from the thalamus to the V1 is really organized as the Hubel and Wiesel suggested it should be,” says Anton Arkhipov, investigator at the Allen Institute, who was not involved with the study. © 2026 Simons Foundation

Keyword: Vision; Evolution
Link ID: 30262 - Posted: 05.30.2026

Diana Kwon It is a dogma in neuroscience that certain brain cells respond in the same way to the same thing. Specific neurons always fire, for example, when we see particular shapes and colours; other neurons activate to swing an arm or wiggle a nose. The brain needs this stability, the theory goes, to respond to the outside world in a consistent way. So, when neuroscientist Laura Driscoll began her doctoral research at Harvard University in Cambridge, Massachusetts in 2012, her first task was to establish this baseline by tracking the activity of individual mouse neurons over time. To Driscoll’s surprise, the baseline kept moving. Over the course of several days, many of the cells’ responses had shifted noticeably. Neurons that had fired when a mouse was in a specific location on day one were barely responding in the same spot after a few weeks. “It absolutely defied all of our expectations,” recalls Driscoll, who is now at the Allen Institute in Seattle, Washington. “This was so surprising that my whole project changed.” In 2017, she and her colleagues reported findings from that project that flew in the face of neuroscience dogma. Over a single day, neurons in the parietal cortex, a hub for processing sensory information, fired predictably in response to specific things, such as the position of the mouse in a virtual maze. But over the course of a few weeks, even though the task of navigating the maze remained the same, these activity patterns underwent major reorganization1. Some of the neurons stopped firing in response to stimuli that had previously activated them; others did the reverse. In groups of cells, however, patterns of neuronal activity remained more consistent over time. The results suggested that individual neurons might not have fixed roles, and that the response of single cells might be less important than the activity of whole populations. © 2026 Springer Nature Limited

Keyword: Learning & Memory; Brain imaging
Link ID: 30251 - Posted: 05.20.2026

Xiaoying You Chinese companies are racing to develop and deploy artificial-intelligence powered brain–computer interfaces (BCIs) that can help people to move, speak and control devices. BCIs, which link a person’s brain to an external device or a computer using sensors placed around or inside the head, have been used in people who are paralysed and those with neurodegenerative diseases over the past decade. In the past few years, companies, mostly in China and the United States, have added large language models to their brain devices. This enables scientists to decode brain activity more accurately than can be achieved using conventional signal-processing and data-analysing technologies, says Li Haifeng, a neuro-computing scientist at Harbin Institute of Technology in China. In China, trials in small numbers of people are underway and some AI-powered brain devices will soon be sold to the public. First trials in people NeuroXess in Shanghai is one company in China that has run small clinical trials, including on their AI-powered brain implant can assist people with paralysis. The implant is placed in a shallow recess in the skull, and its sensors are fitted on the brain’s outer layer, called the cerebral cortex. The system is then connected by wire to a data transmitter that doubles as a battery, which is embedded in the recipient’s chest. In a trial in October, a 28-year-old man with a spinal cord injury who was fitted with the brain implant was able to control appliances by moving a computer cursor with his thoughts to turn them on and off using an app. © 2026 Springer Nature Limited

Keyword: Robotics; Brain imaging
Link ID: 30249 - Posted: 05.20.2026

By Alonso Daboub Brain cells that help make us human are also uniquely vulnerable to multiple sclerosis. A newfound cellular repair kit can’t keep up with the disease’s damage, leading to the cell death that’s a hallmark of progressive MS, researchers report April 1 in two papers in Nature. The discovery uncovers an important and underexplored mechanism behind how the condition progressively shrinks the brain. By better understanding how MS kills brain cells, scientists can design treatments aimed at preventing cognitive decline, says David Rowitch, a developmental neuroscientist at the University of Cambridge. Each year, 10,000 people in the United States are diagnosed with MS. The body’s immune system attacks neurons in the brain, causing inflammation and unpredictable flare-ups of muscle weakness, tingling and pain. Research has primarily focused on the way the disease causes nerve fibers to lose myelin, the fatty insulation that helps them send messages. But in a second, progressive phase, neurons in the brain begin to die. Patients experience sharper declines in their cognitive ability, leading to difficulties in memory and reasoning as their brains shrink. “There’s no treatment really for that part,” says Steve Fancy, a neuroscientist at the University of California, San Francisco Previous research identified a specific group of neurons in the human cortex, the brain’s wrinkly outermost layer, that are particularly vulnerable to degeneration in progressive MS. Called CUX2 neurons, these brain cells help make up two layers of the cortex thought to play an important role in things like cognition and computation. These layers in the brain are “really very important for making us human,” Fancy says. © Society for Science & the Public 2000–2026.

Keyword: Multiple Sclerosis
Link ID: 30238 - Posted: 05.09.2026

By Jennie Erin Smith Seizures are the most dramatic symptom of epilepsy, but they’re not the only type of abnormal brain activity in people with the condition. Brief electrical bursts called interictal epileptiform discharges, or interictal spikes, can occur hundreds or thousands of times a day, usually without a person noticing. Though not as dangerous as seizures, they can cause temporary confusion and contribute to long-term cognitive problems even in those whose seizures are controlled. A new study of highly detailed recordings from human brains reveals these spikes occur in a choreographed sequence of events that is consistent and predictable. The research, published today in Nature Neuroscience, also shows spikes recruit some of the same neurons involved in speech perception, pulling them briefly off their jobs. The new findings are “impactful,” says Jennifer Gelinas, a neurologist and epilepsy researcher at the University of California (UC), Irvine who was not involved with the study. The work, she says, opens the door to a new generation of brain stimulation technologies that might anticipate and abort spikes before they can cause harm. Named for the distinct peaks they form on electroencephalography readings, spikes were once dismissed by clinicians as benign. But they’re increasingly recognized as far from it. In 2023, a team led by neurologist Jonathan Kleen of UC San Francisco (UCSF) reported that people with temporal lobe epilepsy could not remember or repeat back a word spoken to them during a spike: They went blank. “Imagine this happening when you’re in class, or giving a presentation,” Kleen says. One 2025 study went so far as to conclude that spikes occurring during sleep are the major culprit in long-term memory issues among people with temporal lobe epilepsy. Implantable brain stimulation devices used to suppress seizures can detect spikes and react to them, but they can’t predict them. And this type of treatment, known as closed-loop responsive neurostimulation, can take years to calm epileptic activity. Some antiseizure drugs can also reduce spikes, but treating them “is not as easy as it sounds,” says epileptologist Dániel Fabó of the University of Szeged, who was not involved in the study. Antiepilepsy drugs are tested for their effect on seizures, not spikes, he notes, and using too much of them can affect cognitive function.

Keyword: Epilepsy; Brain imaging
Link ID: 30227 - Posted: 05.02.2026

By Rachel E. Gross The first question Sophie Davies had was: Will it affect my memory? In the three weeks since giving birth, Ms. Davies had been in a downward spiral. She checked herself into the mother-and-baby unit of her hospital in East Anglia, England, where doctors ratcheted up the dose of Prozac she took to manage her obsessive-compulsive disorder. But every morning she woke up in tears, and every time she looked at her baby boy, she felt hollow with guilt. “I’m never going to be able to be a mom,” she recalled thinking, “or if I am, I’m not going to be able to be a good one.” A month in, a hospital worker suggested she try a headset that used an electric current to treat depression. The word “electric” gave Ms. Davies, then 34, pause. It sounded like electroconvulsive therapy, or ECT, the scary-sounding treatment that triggers seizures and can result in memory loss. This therapy was different. Transcranial direct-current stimulation, or tDCS, uses a weak electric current to shock the brain and does not produce seizures. “This is as far from ECT as a jet engine is from my bicycle,” Dr. Mark George, of the Medical University of South Carolina, where he is a leading expert in neuromodulation, a term that encompasses all therapies that use electricity to modify brain function. Ms. Davies did an internet search and confirmed that the side effects of tDCS — ringing in the ears, headaches and mild burns or irritation where the electrode pads touched the forehead — were generally transient and didn’t include amnesia. She decided to give it a try. In England, the brain stimulation device has been approved for treating depression since 2019. It can be prescribed by a doctor or purchased over the counter, where it sells for around $530. © 2026 The New York Times Company

Keyword: Depression; Brain imaging
Link ID: 30225 - Posted: 04.29.2026

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

Max Kozlov For decades, scientists have struggled to understand exactly how years of taking hits to the head while playing sports can translate into severe memory loss and dementia later in life. Now, a study1 published today in Science Translational Medicine reveals that the protective shield known as the blood–brain barrier can be damaged and leaky decades after an athlete retires from sport. This persistent leakiness seems to trigger a long-lasting immune response that is closely tied to cognitive decline, the study finds. The work is a “very important study that finds the disruption of the blood–brain barrier many years after head trauma”, says Katerina Akassoglou, a neuroimmunologist at the Gladstone Institutes in San Francisco, California, who was not involved in the research. Part of the difficulty in studying the long-term effects of head trauma is that some neurodegenerative conditions, such as chronic traumatic encephalopathy (CTE), can be diagnosed only by examining neuronal tissue after death, says Matthew Campbell, a specialist in neurovascular genetics at Trinity College Dublin, who co-authored the paper. Campbell and his colleagues wanted to see whether they could spot warning signs in living athletes by looking at the blood–brain barrier, a dense layer of cells lining the blood vessels that supply the brain. This layer usually keeps harmful substances from leaking out of the blood and into brain tissue. To investigate, the researchers scanned the brains of 47 athletes who had retired from playing contact sports with a high risk of concussion and repetitive head impact, such as rugby and boxing. They also examined a control group of non-athletes and athletes who had played non-contact sports. © 2026 Springer Nature Limited

Keyword: Brain Injury/Concussion
Link ID: 30170 - Posted: 03.21.2026

By Jennie Erin Smith In 2017, physicist Nir Grossman made a discovery that promised a versatile new way to manipulate the living brain. Working in mice, he and his collaborators applied two high-frequency electrical currents to the skull. At the spot in the rodents’ brains where the currents collided, the electric field altered neural activity. Other noninvasive methods typically reach no further than the cortex, the brain’s outer layer. The new approach, called temporal interference (TI) stimulation, offered access to deep-brain areas previously only targetable with surgery. Neuroscientists were quick to see TI’s potential for studying the brain and treating its disorders, and they are now testing it in a variety of human trials. Although the studies are still small and many have not been replicated, they hint that TI may have potential to ease epilepsy symptoms, help stroke patients recover movement, boost memory in people with Alzheimer’s disease, and treat psychiatric conditions. Many say TI—which uses two pairs of head-mounted electrodes linked to portable current generators—is nimbler and likely safer than transcranial focused ultrasound, another emerging technology that can modulate deep-brain regions without surgery. And because TI equipment is inexpensive and widely available, it’s been easy for labs to try out. “What [TI] should be is an open-source therapy,” says physicist and epilepsy researcher Adam Williamson of St. Anne’s University Hospital. This year, he and his colleagues showed in a pilot study of people with epilepsy that TI stimulation to the hippocampus, a deep-brain structure that is often the source of hard-to-treat seizures, could both suppress spikes of abnormal brain activity and improve participants’ sleep. His group and another at Duke University are collaborating on a larger clinical trial of the approach. In TI, two high-frequency electrical currents applied to the brain meet or interfere to form a low-frequency focal area, or “envelope,” that can boost or suppress the rate of neurons’ electrical signaling. “It’s a powerful way to entrain neuronal activity,” says Melanie Boly, an epilepsy researcher at the University of Wisconsin–Madison. © 2026 American Association for the Advancement of Science.

Keyword: Brain imaging
Link ID: 30165 - Posted: 03.19.2026

By Simon Makin A brain repair kit that helps yaks and other animals naturally cope with low oxygen levels at high altitudes may point to a new way to treat brain diseases such as multiple sclerosis. In mice with brain damage that mimics MS, the kit’s tools lessened signs of damage in young mice exposed to low oxygen and improved symptoms of MS in adult mice, researchers report March 13 in Neuron. Previous research found that animals living on the Tibetan Plateau, such as yaks and antelopes, carry a mutation in a gene called Retsat. Their lowland counterparts lack the mutation, leading scientists to suspect that it helps protect the brain in low-oxygen environments. “People usually think it’s because of better lung capability, but I wondered whether evolutionary adaptation changes the brain,” says Liang Zhang, a neuroscientist at Shanghai Jiao Tong University. In particular, he was intrigued that these animals have normal white matter in their brains. White matter makes up about half the brain; it consists of bundles of nerve fibers that allow different brain regions to communicate. This neural wiring is wrapped in myelin, a fatty substance that ensures nerve fibers conduct signals efficiently. In MS, the immune system attacks myelin, leading to neurological symptoms and problems with balance and coordination. Myelin production requires a lot of energy, which the brain gets from oxygen. Low oxygen levels, known as hypoxia, can therefore disrupt myelination. During gestation, such disruption can lead to conditions such as cerebral palsy in newborns. © Society for Science & the Public 2000–2026.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 30160 - Posted: 03.14.2026

By Calli McMurray In 2010, Ardem Patapoutian unmasked a piece of cellular machinery that had long evaded identification: PIEZO channels, pores wrenched open by changes in a cell’s membrane tension to allow ions to flow through, thereby converting mechanical force into electrical activity. The discovery marked a turning point for the field of mechanosensation—a process that can be unwieldy to study, says Arthur Beyder, associate professor of physiology and medicine at the Mayo Clinic, because “it reaches its fingers into everything.” The field needed “something to grab onto,” he says, to untangle these processes from other sensory ones—and PIEZO channels provided the first handhold. The PIEZO discovery garnered much attention, and since then, a flurry of studies have outlined how the channels contribute to touch, itch and proprioception. In 2021, Patapoutian shared the Nobel Prize in Physiology or Medicine for his contributions to this work. Now, a growing cadre of researchers is using these receptors as a tool to explore interoception, or the brain’s sense of what the internal organs are doing. “We’re seeing a resurgence and an expansion of research in this area,” says Miriam Goodman, professor of molecular and cellular physiology at Stanford University. The field, she adds, is in the middle of a “PIEZO-driven renaissance.” Even a body at rest is in constant motion: The heart pumps blood, the lungs expand and contract, the gut squeezes food, and the bladder stretches with urine. Biologists had intuited that mechanical force was a key part of these processes—and also part of how organs communicate with the brain—but for decades they did not have a way to dive into the molecular mechanisms behind them. © 2026 Simons Foundation

Keyword: Pain & Touch
Link ID: 30101 - Posted: 01.31.2026

By Alessio Cozzolino After a heart attack, the heart “talks” to the brain. And that conversation may make recovery worse. Shutting down nerve cells that send messages from injured heart cells to the brain boosted the heart’s ability to pump and decreased scarring, experiments in mice show. Targeting inflammation in a part of the nervous system where those “damage” messages wind up also improved heart function and tissue repair, scientists report January 27 in Cell. “This research is another great example highlighting that we cannot look at one organ and its disease in isolation,” says Wolfram Poller, an interventional cardiologist at Massachusetts General Hospital and Harvard Medical School who was not involved in the study. “And it opens the door to new therapeutic strategies and targets that go beyond the heart.” Someone in the United States has a heart attack about every 40 seconds, according to the U.S. Centers for Disease Control and Prevention. That adds up to about 805,000 people each year. A heart attack is a mechanical problem caused by the obstruction of a coronary artery, usually by a blood clot. If the blockage lasts long enough, the affected cells may start to die. Heart attacks can have long-term effects such as a weakened heart, a reduced ability to pump blood, irregular heart rhythms, and a higher risk of heart failure or another heart attack. Although experts knew from previous research that the nervous and immune systems could amplify inflammation and slow healing, the key players and pathways involved were unknown, says Vineet Augustine, a neurobiologist at the University of California, San Diego. © Society for Science & the Public 2000–2026

Keyword: Neuroimmunology
Link ID: 30098 - Posted: 01.28.2026

Andrew Gregory Health editor Scientists have discovered two new subtypes of multiple sclerosis with the aid of artificial intelligence, paving the way for personalised treatments and better outcomes for patients. Millions of people have the disease globally – but treatments are mostly selected on the basis of symptoms, and may not be effective because they don’t target the underlying biology of the patient. Now, scientists have detected two new biological strands of MS using AI, a simple blood test and MRI scans. Experts said the “exciting” breakthrough could revolutionise treatment of the disease worldwide. In research involving 600 patients, led by University College London (UCL) and Queen Square Analytics, researchers looked at blood levels of a special protein called serum neurofilament light chain (sNfL). The protein can help indicate levels of nerve cell damage and signal how active the disease is. The sNfL results and scans of the patients’ brains were interpreted by a machine learning model, called SuStaIn. The results, published in medical journal Brain, revealed two distinct types of MS: early sNfL and late sNfL. In the first subtype, patients had high levels of sNfL early on in the disease, with visible damage in a part of the brain called the corpus callosum. They also developed brain lesions quickly. This type appears to be more aggressive and active, scientists said. In the second subtype, patients showed brain shrinkage in areas like the limbic cortex and deep grey matter before sNfL levels went up. This type seems to be slower, with overt damage occurring later. Researchers say the breakthrough will enable doctors to more precisely understand which patients are at higher risk of different complications, paving the way for more personalised care. © 2025 Guardian News & Media Limited

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 30058 - Posted: 12.31.2025

By Kelly Servick In the past 20 years, mice with glowing cables sprouting from their heads have become a staple of neuroscience. They reflect the rise of optogenetics, in which neurons are engineered to contain light-sensitive proteins called opsins, allowing pulses of light to turn them on or off. The method has powered thousands of basic experiments into the brain circuits that drive behavior and underlie disease. As this research tool matured, hopes arose for using it as a treatment, too. Compared with the electrical or magnetic brain stimulation approaches already in use, optogenetics offers a way to more precisely target and manipulate the exact cell types underlying brain disorders. So far only one optogenetic application—addressing certain kinds of vision loss by introducing opsins into cells in the eye—has made it into human trials. But its promising early results, along with the discovery of more sensitive and sophisticated opsins, are inspiring researchers to look beyond the eye, developing treatments that would act on peripheral nerves or deep in the brain. Initial tests of these strategies in animal models of epilepsy, amyotrophic lateral sclerosis (ALS), and other neurological disorders have been encouraging, researchers reported last month at the annual meeting of the Society for Neuroscience (SfN) in San Diego. One company is hoping to launch a human trial for an optogenetic pain treatment by 2027. “We definitely don’t want to oversell the idea of using optogenetics [on human brains] any time soon, but we also are firmly convinced that this is now the right moment to be thinking about this seriously,” University of Geneva neurologist and neuroscientist Christian Lüscher told an SfN session he chaired, in which participants presented a newly published road map for bringing optogenetics to the clinic. Still, the presenters acknowledged major remaining challenges, including possible risks of inserting genes for opsins—many of which are derived from algae or other microbes—into a person’s nerves or brain cells. © 2025 American Association for the Advancement of Science.

Keyword: Pain & Touch; Epilepsy
Link ID: 30046 - Posted: 12.13.2025

By Claudia López Lloreda A new commentary calls into question a 2024 paper that described a universal pattern of cortical brain oscillations. But that team has provided a more expansive analysis in response and stands by its original conclusions. Both articles were published today in “Matters Arising” in Nature Neuroscience. Ultimately, the back-and-forth suggests that a frequency “motif” may exist, but it may not be as general as the original study proposed, says Aitor Morales-Gregorio, a postdoctoral researcher at Charles University, who was not involved with any of the work. “The [2024] conclusions are way too optimistic about how general and how universal this principle might be.” The 2024 study identified a brain-wave motif in 14 cortical areas in macaques: Alpha and beta rhythms predominated in the deeper layers, whereas gamma bands appeared in the more superficial layers. Because this motif also showed up in marmosets and humans, the researchers speculated that it may be a universal mechanism for cortical computation in primates. “Results typically come with a level of variability, of noise, of uncertainty,” says 2024 study investigator Diego Mendoza-Halliday, assistant professor of neuroscience at the University of Pittsburgh. But this pattern “was just there the whole time, at all times, in many, many of the recordings.” The team leveraged the findings to create an algorithm that detects Layer 4 of the cortex. But the pattern is “by no means universal,” according to the new commentary, which found the motif in about 60 percent of the recordings in an independent monkey dataset. Further, the algorithm trained to identify Layer 4 of the cortex is unreliable, the commentary shows. © 2025 Simons Foundation

Keyword: Attention
Link ID: 30044 - Posted: 12.13.2025

By Sarah DeWeerdt A temporary increase in neuronal activity in the cortex of newborn mice leads to social deficits in adulthood, according to a new preprint. Those adult rodents also show changes in brain electrical activity, gene expression and connectivity that are reminiscent of autism. The analysis lends support to a prominent hypothesis of autism’s origins, which holds that the condition can arise from an excess of excitatory signaling or insufficient inhibitory signaling in the brain, the study investigators write in their paper. Over the years, support for this signaling imbalance hypothesis has come from other studies in mice and observations that some people with autism have seizures or display excess neuronal activity in electroencephalography (EEG) recordings relative to people without the condition. Postmortem analysis suggests autistic people have more excitatory synapses in the prefrontal cortex than non-autistic people. But determining causality and the role of inhibitory signaling has been difficult. In contrast with most earlier work, the new study “really underscore[s] a different way of looking at excitation-inhibition imbalance, which is looking at it during development as a cause of subsequent changes in brain function that could be associated with autism,” says Vikaas Sohal, professor of psychiatry and behavioral science at the University of California, San Francisco, who was not involved in the work. The study was posted on bioRxiv last month. © 2025 Simons Foundation

Keyword: Development of the Brain; Autism
Link ID: 29994 - Posted: 11.01.2025

By Gina Kolata For the first time, researchers restored some vision to people with a common type of eye disease by using a prosthetic retinal implant. If approved for broader use in the future, the treatment could improve the lives of an estimated one million, mostly older, people in the United States who lose their vision to the condition. The patients’ blindness occurs when cells in the center of the retina start to die, what is known as geographic atrophy resulting from age-related macular degeneration. Without these cells, patients see a big black spot in the center of their vision, with a thin border of sight around it. Although their peripheral vision is preserved, people with this form of advanced macular degeneration cannot read, have difficulty recognizing faces or forms and may have trouble navigating their surroundings. In a study published Monday in The New England Journal of Medicine, vision in 27 out of 32 participants improved so much that they could read with their artificial retinas. The vision that is restored is not normal: It’s black and white, blurry, and the field of view is small. But after getting the retinal implant, patients who could barely see gained on average five lines on a standard eye chart. The implant gets signals from glasses and a camera that projects infrared images to the artificial retina. The camera has a zoom feature that can magnify images like letters, allowing people to read, albeit slowly because with the zoom they don’t see many letters at a time. “This is at the forefront of science,” said Dr. Demetrios Vavvas, director of the retina service at Massachusetts Eye and Ear, a specialty hospital in Boston. He was not involved in the study and emphasized that the implant was not a cure for macular degeneration. But he called it the dawn of a new technology that he predicted will significantly advance. The treatment is only for people with a loss of retinal photoreceptors, so it would not work for other forms of blindness. The study participants had an average age of 79 and had been told that once vision was lost, it was gone forever. © 2025 The New York Times Company

Keyword: Vision; Robotics
Link ID: 29981 - Posted: 10.22.2025