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

By Yasemin Saplakoglu From Santiago Ramón y Cajal’s hand came branches and whorls, spines and webs. Now-famous drawings by the neuroanatomist in the late 19th and early 20th centuries showed, for the first time, the distinctiveness and diversity of the fundamental building blocks of the mammalian brain that we call neurons. In the century or so since, his successors have painstakingly worked to count, track, identify, label and categorize these cells. There is now a dizzying number of ways to put neurons in buckets, often presented in colorful, complex brain cell atlases. With such catalogs, you might organize neurons based on function by separating motor neurons that help you move from sensory neurons that help you see or number neurons that help you estimate quantities. You might distinguish them based on whether they have long axons or short ones, or whether they’re located in the hippocampus or the olfactory bulb. But the vast majority of neurons, regardless of function, form or location, fall into one of two fundamental categories: excitatory neurons that trigger other neurons to fire and inhibitory neurons that stop others from firing. Maintaining the correct proportion of excitation to inhibition is critical for keeping the brain healthy and harmonious. “Imbalances in either direction can be really catastrophic,” said Mark Cembrowski (opens a new tab), a neuroscientist at the University of British Columbia, or lead to neurological conditions. Too much excitation and the brain can produce epileptic seizures. Too little excitation can be associated with conditions such as autism. Neuroscientists are working to uncover how these two classes of cells work — and specifically, how they interact with a rarer third category of cells that influence their behavior. These insights could eventually help reveal how to restabilize networks that get out of balance, which can even occur as a result of normal aging. © 2025 Simons Foundation

Keyword: Epilepsy; Attention
Link ID: 29952 - Posted: 10.01.2025

By Holly Barker When scientists produced the first map of all synaptic connections in the roundworm Caenorhabditis elegans in 1986, many hailed it as a blueprint for the flow of brain signals. As it turned out, though, models of neuronal activity based on this wiring diagram bore little resemblance to the functional maps of brain activity measured in living worms. This disconnect isn’t limited to worms. Mice, for instance, appear to have widespread silent synapses—wired connections that don’t send signals—and the actual responses of some cells in the fruit fly’s visual system do not match the responses the connectome predicts. A new preprint helps to explain why: Most network features, in C. elegans at least, are not conserved between the anatomical and functional connectomes. Yet the anatomical connectome can still forecast—albeit in a complex way—observed neuronal activity in the worms, according to a second preprint by the same team, because “most signaling is happening along the wires,” says Andrew Leifer, associate professor of physics and neuroscience at Princeton University and principal investigator on both preprints. The findings begin to address the long-standing challenge of reconciling structure and function, and show that “we weren’t entirely wrong” about the importance of synaptic connectivity, says Jihong Bai, professor of basic sciences at the Fred Hutchinson Cancer Center, who was not involved in the work. The debut of a color-coded map of cell types in the worm brain in 2021 split the neuroscience community. It made it possible to identify individual neurons in whole-brain recordings and compare annotated recordings with the connectome—an exercise that revealed no correlation between the two. © 2025 Simons Foundation

Keyword: Brain imaging
Link ID: 29907 - Posted: 08.30.2025

Anna Bawden Health and social affairs correspondent Researchers have developed ultra-powerful scans that could enable surgery for previously treatment-resistant epilepsy. Globally, about 50 million people have epilepsy. In England, epileptic seizures are the sixth most common reason for hospital admission. About 360,000 people in the UK have focal epilepsy, which causes recurring seizures in a specific part of the brain. Many patients successfully treat their condition with medication but for more than 100,000 patients, their symptoms do not improve with drugs, leaving surgery as the only option. Finding brain lesions, a significant cause of epilepsy, can be tricky. Ultra-powerful MRI scanners are capable of identifying even tiny lesions in patients’ brains. These 7T MRI scanners produce much more detailed resolution on brain scans, enabling better detection of lesions. If surgeons can see the lesions on MRI scans, this can double the chances of the patient being free of seizures after surgery. But 7T scanners are also susceptible to “dark patches” known as signal dropouts. Now researchers in Cambridge and Paris have developed a new technique to overcome the problem. Scientists at the University of Cambridge’s Wolfson Brain Imaging Centre, and the Université Paris-Saclay, used eight transmitters around the brain, rather than the usual one, to “parallel transmit” MRI images, which significantly reduced the number of black spots. The first study to use this approach, doctors at Addenbrooke’s hospital, Cambridge, then trialled the technique with 31 drug-resistant epilepsy patients to see whether the parallel transmit 7T scanner was better than conventional 3T scanners at detecting brain lesions. The research, published in the journal Epilepsia, found that the parallel transmit 7T scanner identified previously unseen structural lesions in nine patients. © 2025 Guardian News & Media Limited

Keyword: Brain imaging; Epilepsy
Link ID: 29716 - Posted: 03.22.2025

By Jyoti Madhusoodanan In June 2021, 63-year-old Lisa Daurio was making the two-hour drive from her hometown of Pueblo, Colorado, to a doctor’s appointment in Denver when she settled on a life-changing decision: She would tell her doctor she was ready to stop taking her weekly injections to treat her multiple sclerosis. Daurio was not cured, but her condition had remained stable for more than a decade. As she got older, her doctor had periodically asked if she wanted to consider halting her medication. It’s an unusual question in modern medicine: Clinicians don’t typically ask people with arthritis, high cholesterol, diabetes, or other chronic conditions whether they’d like to stop taking their medication as they get older. But MS is an unusual disease, the result of immune cells attacking a person’s brain, optic nerves and spinal cord. The subsequent nerve injuries trigger burning pain, numbness, loss of balance, and a range of other symptoms. These hallmark immune assaults and symptoms flare up sporadically in younger adults and, for some people, seem to quiet down as they age into their 50s and beyond. Still, Daurio’s decision to stop wasn’t straightforward. Her MS symptoms began when she was in her late 30s, with a sense of overwhelming fatigue, a numbness in her legs, and a “feeling of fire ants” that ran “from the back of my neck around the front of my face,” she said. She was diagnosed with MS in 2003, when her entire left side went numb, and she thought she was having a stroke. The weekly injections had kept all of those symptoms at bay for more than a decade. When her doctor broached the idea of stopping them, Daurio’s reaction was “it’s working, let’s not mess with what’s not broken,” she said. Staying on her medication wasn’t always easy. For about 10 years, every dose made her feel like she had the flu. After each shot, she spent two days on Tylenol and a steroid named prednisone to cope with the side effects. But Daurio stuck with the regimen because the injection seemed to help; she had not had a single relapse since 2009, and periodic MRI scans showed no new signs of immune attacks on her brain.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 29692 - Posted: 03.05.2025

By Laura Sanders Depression can affect not just the mind, but the body, too. Inner experiences of mental struggles are private. But in this episode, Jon Nelson and another volunteer, Amanda, let listeners in. Woven into their stories is a brief history of deep brain stimulation, the experimental treatment that involves permanent brain implants. You’ll hear how that research — with its ups and downs — carried the experiments to where they are today. Laura Sanders: This episode deals with mental illness, depression, and suicide. Please listen with care. Previously on The Deep End: Support Science Today. Barbara: He would be up in bed with the lights out or watching like endless hours of television and it was very unpredictable and then there’s a whole life going on downstairs. Jon: That isolation, there’s a little bit of lying involved because you just wanna get out of things, right? Mayberg: I think part of why this kind of treatment resistant depression is so painful and so associated with high rates of suicide, is that you’re suffering. You know exactly what you’re trying to get away from and you can’t move. And if you do move, it follows you. There’s no relief. Jon: I’d be the one standing up in front of everybody leading the champagne toast, and then I’d be driving home and wanting to slam my car into a tree. Sanders: Today we’re going to get into some heavy stuff, but there’s light at the end, I promise. We’re going to pull back the curtain on what depression can do to the body and to the brain. Maybe you know that feeling firsthand. If you don’t, you probably know somebody who does. You’ll also hear the backstory of some people who volunteered for the experiment and the backstory of the science itself. I’m Laura Sanders. Welcome to The Deep End. © Society for Science & the Public 2000–2025.

Keyword: Depression
Link ID: 29676 - Posted: 02.19.2025

By Laura Sanders Meet Jon Nelson. He’s a dad, a husband, a coach and a professional who works in marketing. But underneath it all, he suffered – for years – from severe depression. His suffering was so great that he volunteered for an experimental treatment called deep brain stimulation, in which electrodes are permanently implanted in his brain. In this episode, you’ll hear from Jon about his life before the surgery, and you’ll be introduced to the neuroscience designed to save him. Laura Sanders: This podcast touches on mental illness, depression, and suicide. There are moments of darkness. There are moments of lightness, too. Please keep that in mind before you listen. Jon Nelson is a guy who’s probably a lot like a guy you know. He lives in Newtown, a picturesque small town northeast of Philadelphia. He has three kids, a loving wife, a dog, a cat, and a bearded dragon named Lizzie. He works in marketing. He coaches his kids in softball and hockey, and he’s a ride-or-die Steelers fan. The Nelsons are, in fact, so perfect that they’re almost a caricature, like a sitcom family with a zany dad who’s fond of the phrase, “I’m going to give you some life advice.” Jon Nelson: You know, we try to do the standard sit down and cook together and have meals together. We’re the messy house in the neighborhood with basketballs outside and, you know, we’re constantly playing and doing stuff like that. But, you know, truly we like to spend time together. Sanders: But the view from the outside was a lot different than what Jon felt on the inside. On the outside, Jon lived a charmed life, but inside, he had been fighting with everything he had to stay alive for years. Jon: I would literally read a newspaper article about a plane wreck and I would have instantaneous, like, “Oh, like why couldn’t I have been on that?” Right? Or, you know, you, somebody died in a car wreck, like, “Why couldn’t that have been me?” © Society for Science & the Public 2000–2025

Keyword: Depression
Link ID: 29668 - Posted: 02.12.2025

By Laura Sanders Brain implants for depression: It sounds like science fiction but it’s real. The Deep End, a new podcast from Science News, will give you a glimpse of what it’s like to live with electrodes in your brain. It might change how you think about mental health, the brain and what makes you you. Transcript Laura Sanders: Inside your brain, there are billions of nerve cells that form trillions of connections. These connections make your thoughts, movements, emotions, and memories. Your first kiss, your favorite song, your dreams. Our brains make us who we are. But sometimes they can betray us. Support Science Today. Thank you for being a subscriber to Science News! Interested in more ways to support STEM? Consider making a gift to our nonprofit publisher, the Society for Science, an organization dedicated to expanding scientific literacy and ensuring that every young person can strive to become an engineer or scientist. Donate Now This is a story about four people whose brains turned against them, plunging their lives into the darkness of severe depression. This is also a story about an experiment designed to pull them back out. Amanda: My initial response was a little bit of skepticism, like, “OK, we’re gonna put a box in you, we’re gonna hook it up to some wires, we’re gonna shove them down in your brain and then electrocute you, and it’s gonna make you feel great.” Like, this doesn’t seem like a, like a safe thing to be doing. Sanders: This experiment sounds like science fiction, but it’s real. This is the Deep End, a new podcast from Science News. I’m Laura Sanders. On this podcast, you’ll hear what led people to sign up for this unconventional experiment and what it was like for them. © Society for Science & the Public 2000–202

Keyword: Depression
Link ID: 29655 - Posted: 02.05.2025

Nicola Davis Science correspondent Standing patiently on a small fluffy rug, Calisto the flat-coated retriever is being fitted with some hi-tech headwear. But this is not a new craze in canine fashion: she is about to have her brainwaves recorded. Calisto is one of about 40 pet dogs – from newfoundlands to Tibetan terriers – taking part in a study to explore whether their brainwaves synchronise with those of their owners when the pair interact, a phenomenon previously seen when two humans engage with each other. The researchers behind the work say such synchronisation would suggest person and pet are paying attention to the same things, and in certain circumstances interpreting moments in a similar way. In other words, owner and dog really are on the same wavelength. Dr Valdas Noreika of Queen Mary, University of London said he got the idea for the study after working on similar experiments with mothers and their babies, where such synchronisation has also been seen. “Owners modulate their language in a similar way as parents modulate when they speak to children,” he said. “There are lots of similarities. That could be one of the reasons why we get so attached to dogs – because we already have these cognitive functions and capacities to attach with someone who is smaller or requires help or attention.” Hints of an emotional bond between humans and their dogs stretch into the distant past: researchers have previously discovered the 14,000-year-old remains of a puppy buried in Germany alongside a man and a woman: the analysis suggested the young dog had been nursed through several periods of illness, despite having no particular use. © 2025 Guardian News & Media Limited o

Keyword: Brain imaging; Attention
Link ID: 29613 - Posted: 01.04.2025

' By Sofia Quaglia Flip open any neuroscience textbook and the depiction of a neuron will be roughly the same: a blobby, amoebalike cell body shooting out a long, thick strand. That strand is the axon, which conducts electrical signals to terminals where the cell communicates with other neurons. Axons have long been depicted as smooth and cylindrical, but a new study of mouse neurons challenges that view. Instead, it suggests their natural shape is more like a string of pearls. Even more provocatively, the authors propose those pearly bumps serve as control knobs, influencing how quickly and precisely the cell fires its signals. The study, published today in Nature Neuroscience, should “100%” change how we’ve been thinking about neurons and their signals, says senior author Shigeki Watanabe, a molecular neuroscientist at John Hopkins University. Some outsiders agree. The findings are “highly significant and I think have been overlooked for quite some time,” says evolutionary biologist Pawel Burkhardt of the University of Bergen, who recently spotted similar pearl structures in neurons from tiny marine invertebrates known as comb jellies. Yet several experts in the field contest the findings. Some cite potential confounding effects of the preparation and freezing method used to preserve cells before imaging. And some doubt the work totally upends what’s known about the true shape of the axon. “I think it’s true that [the axon is] not a perfect tube, but it’s not also just this kind of accordion that they show,” says neuroscientist Christophe Leterrier from Aix-Marseille University, who calls the study “a controversial addition to the literature.” Since the mid-1960s, microscopists have seen that axons can scrunch up to form beads when they are diseased or under other stress. Leterrier has called these temporary beads “stress balls for the brain” and found evidence that they prevent cellular damage from spreading. Other studies suggest even normal axons bulge temporarily when cargo traveling to and from the cell nucleus forms a traffic jam, like the elephant bulging inside the body of a boa in the children’s book The Little Prince.

Keyword: Brain imaging
Link ID: 29586 - Posted: 12.04.2024

Does a whiff of pollen trigger a sneeze or a cough? Scientists have discovered nerve cells that cause one response versus another: ‘sneeze neurons’ in the nasal passages relay sneeze signals to the brain, and separate neurons send cough messages, according to a study1 performed in mice. The findings could lead to new and improved treatments for conditions such as allergies and chronic coughs. That’s welcome news because these conditions can be “incredibly frustrating” and the side effects of current treatments can be “incredibly problematic”, says pulmonologist Matthew Drake at Oregon Health & Science University in Portland, who was not involved in the work. The study was published today in Cell. Previous work2 categorized neurons in the mouse airway on the basis of the proteins complexes, called ion channels, that are carried on the cell surfaces. To work out which nose neurons cause sneezing, researchers exposed mice to various compounds, each known to activate specific types of ion channel. They struck gold when a substance called BAM 8-22 left the mice sneezing. The compound is known to activate an ion channel called MrgprC11, leading the researchers to suspect that neurons carrying MrgprC11 cause sneezing. Indeed, when the researchers deleted MrgprC11 from the suspected sneeze neurons and then gave mice the flu, they found themselves with sick, but sneezeless, mice. Even with the sneeze neurons out of the picture, the sick mice continued to have cough-like reactions to influenza infection. Using methods similar to those that homed in on the sneeze neurons, the researchers tracked the cough response to a set of neurons in the trachea that express a signalling chemical called somatostatin. Viruses “evolve very quickly”, says neuroscientist and study co-author Qin Liu at Washington University in St. Louis, Missouri. That could explain why there are two separate systems capable of detecting and clearing them from the airways. © 2024 Springer Nature Limited

Keyword: Neuroimmunology
Link ID: 29466 - Posted: 09.07.2024

By Holly Barker Machine-learning models can predict a neuron’s location based on recorded bursts of activity, a new preprint suggests. The findings may provide novel insights into how the brain integrates signals from different regions, the researchers say. The algorithm—trained on electrode recordings of neurons in mice—appeared to learn a cell’s whereabouts from its interspike interval, the sequence of delays between blips of activity. And after deciphering the spike pattern from one mouse, the tool predicted neuronal locations based on recordings from another rodent. That conservation between animals suggests the information serves some useful brain function, or at least doesn’t get in the way, says lead investigator Keith Hengen, assistant professor of biology at Washington University in St. Louis. Although more research is needed, the anatomical information embedded in interspike intervals could—in theory—provide contextual information for neuronal computations. For example, the brain might process signals from thalamic neurons differently from those in the hippocampus, says study investigator Aidan Schneider, a graduate student in Hengen’s lab. Schneider and his colleagues trained the model using tens of thousands of Neuropixels probe recordings from 58 awake mice, published by the Allen Institute. When Schneider’s team presented the algorithm with fresh data, it could decipher whether a given neuron resided in the hippocampus, midbrain, thalamus or visual cortex 89 percent of the time, once the team removed noise from the data. (Random guesses would be correct 25 percent of the time.) But the tool was less able to pinpoint specific substructures within those regions. It’s a great example of the kinds of insights that labs poring over huge datasets can produce, says Drew Headley, assistant professor of molecular and behavioral neuroscience at Rutgers University, who was not involved in the study. But the findings may simply echo published reports of variations in spiking activity across different brain regions, he says. © 2024 Simons Foundation

Keyword: Brain imaging
Link ID: 29452 - Posted: 08.28.2024

Hannah Devlin Science correspondent A UK teenager with severe epilepsy has become the first person in the world to be fitted with a brain implant aimed at bringing seizures under control. Oran Knowlson’s neurostimulator sits under the skull and sends electrical signals deep into the brain, reducing his daytime seizures by 80%. His mother, Justine, said that her son had been happier, chattier and had a much better quality of life since receiving the device. “The future looks hopeful, which I wouldn’t have dreamed of saying six months ago,” she said. Martin Tisdall, a consultant paediatric neurosurgeon who led the surgical team at Great Ormond Street hospital (Gosh) in London, said: “For Oran and his family, epilepsy completely changed their lives and so to see him riding a horse and getting his independence back is absolutely astounding. We couldn’t be happier to be part of their journey.” Oran, who is 13 and lives in Somerset, had the surgery in October as part of a trial at Gosh in partnership with University College London, King’s College hospital and the University of Oxford. Oran has Lennox-Gastaut syndrome, external, a treatment-resistant form of epilepsy which he developed at the age of three. Between then and having the device fitted, he hasn’t had a single day without a seizure and sometimes suffered hundreds in a day. He often lost consciousness and would stop breathing, needing resuscitation. This means Oran needed round-the-clock care, as seizures could happen at any time of day, and he was at a significantly increased risk of sudden unexpected death in epilepsy (Sudep). © 2024 Guardian News & Media Limited

Keyword: Epilepsy; Robotics
Link ID: 29367 - Posted: 06.24.2024

By Shaena Montanari Five years ago, while working to develop a tool to label neurons active during seizures in mice, Quynh Anh Nguyen noticed something she had not seen before. “There was a particular region in the brain that seemed to light up really prominently,” she says. Nguyen, assistant professor of pharmacology at Vanderbilt University, had induced seizures in the animals by injecting kainic acid into the hippocampus—a common strategy to model temporal lobe epilepsy. The condition often involves hyperactivity in the anterior and middle regions of the hippocampus, but Nguyen’s mice also showed the activation in a tiny posterior part of the hippocampus that she was not familiar with. Nguyen brought the data to her then-supervisor Ivan Soltesz, professor of neurosciences and neurosurgery at Stanford University. Together they realized that these neurons were in an area called the fasciola cinereum—a subregion of the hippocampus so understudied, Soltesz says, that when Nguyen first asked him what it was, he had “no idea.” Despite the subregion’s obscurity, it looks to be an important and previously overlooked contributor to epilepsy in people who do not respond to anti-seizure medications or tissue ablation in the hippocampus, Nguyen and her colleagues say. Fasciola cinereum neurons were active during seizures in six people with drug-resistant epilepsy, the team reported in April. © 2024 Simons Foundation

Keyword: Epilepsy
Link ID: 29360 - Posted: 06.15.2024

Jon Hamilton A flexible film bristling with tiny sensors could make surgery safer for patients with a brain tumor or severe epilepsy. The experimental film, which looks like Saran wrap, rests on the brain’s surface and detects the electrical activity of nerve cells below. It’s designed to help surgeons remove diseased tissue while preserving important functions like language and memory. “This will enable us to do a better job,” says Dr. Ahmed Raslan, a neurosurgeon at Oregon Health and Science University who helped develop the film. The technology is similar in concept to sensor grids already used in brain surgery. But the resolution is 100 times higher, says Shadi Dayeh, an engineer at the University of California, San Diego, who is leading the development effort. In addition to aiding surgery, the film should offer researchers a much clearer view of the neural activity responsible for functions including movement, speech, sensation, and even thought. “We have these complex circuits in our brains,” says John Ngai, who directs the BRAIN Initiative at the National Institutes of Health, which has funded much of the film’s development. “This will give us a better understanding of how they work.” Mapping an ailing brain The film is intended to improve a process called functional brain mapping, which is often used when a person needs surgery to remove a brain tumor or tissue causing severe epileptic seizures. © 2024 npr

Keyword: Brain imaging; Epilepsy
Link ID: 29357 - Posted: 06.13.2024

By Yasemin Saplakoglu György Buzsáki first started tinkering with waves when he was in high school. In his childhood home in Hungary, he built a radio receiver, tuned it to various electromagnetic frequencies and used a radio transmitter to chat with strangers from the Faroe Islands to Jordan. He remembers some of these conversations from his “ham radio” days better than others, just as you remember only some experiences from your past. Now, as a professor of neuroscience at New York University, Buzsáki has moved on from radio waves to brain waves to ask: How does the brain decide what to remember? By studying electrical patterns in the brain, Buzsáki seeks to understand how our experiences are represented and saved as memories. New studies from his lab and others have suggested that the brain tags experiences worth remembering by repeatedly sending out sudden and powerful high-frequency brain waves. Known as “sharp wave ripples,” these waves, kicked up by the firing of many thousands of neurons within milliseconds of each other, are “like a fireworks show in the brain,” said Wannan Yang, a doctoral student in Buzsáki’s lab who led the new work, which was published in Science in March. They fire when the mammalian brain is at rest, whether during a break between tasks or during sleep. Sharp wave ripples were already known to be involved in consolidating memories or storing them. The new research shows that they’re also involved in selecting them — pointing to the importance of these waves throughout the process of long-term memory formation. It also provides neurological reasons why rest and sleep are important for retaining information. Resting and waking brains seem to run different programs: If you sleep all the time, you won’t form memories. If you’re awake all the time, you won’t form them either. “If you just run one algorithm, you will never learn anything,” Buzsáki said. “You have to have interruptions.” © 2024 the Simons Foundation.

Keyword: Learning & Memory
Link ID: 29322 - Posted: 05.23.2024

Ian Sample Science editor A device that stimulates the spinal nerves with electrical pulses appears to boost how well people recover from major spinal cord injuries, doctors say. An international trial found that patients who had lost some or all use of their hands and arms after a spinal cord injury regained strength, control and sensation when the stimulation was applied during standard rehabilitation exercises. The improvements were small but were described by doctors and patients as life-changing because of the impact they had on the patients’ daily routines and quality of life. “It actually makes it easier for people to move, including people who have complete loss of movement in their hands and arms,” said Prof Chet Moritz, in the department of rehabilitation medicine at the University of Washington in Seattle. “The benefits accumulate gradually over time as we pair this spinal stimulation with intensive therapy of the hands and arms, such that there are benefits even when the stimulator is turned off.” Rather than being implanted, the Arc-Ex device is worn externally and uses electrodes that are placed on the skin near the section of the spinal cord responsible for controlling a particular movement or function. The researchers believe that electrical stimulation helps nerves that remain intact after the injury to send signals and ultimately partially restore some communication between the brain and paralysed body part. More than half of patients who suffer spinal cord injuries still have some intact nerves that cross the injury site. © 2024 Guardian News & Media Limited

Keyword: Robotics; Movement Disorders
Link ID: 29315 - Posted: 05.21.2024