By Sara Reardon By eavesdropping on the brains of living people, scientists have created the highest-resolution map yet of the neurons that encode the meanings of various words1. The results hint that, across individuals, the brain uses the same standard categories to classify words — helping us to turn sound into sense. The study is based on words only in English. But it’s a step along the way to working out how the brain stores words in its language library, says neurosurgeon Ziv Williams at the Massachusetts Institute of Technology in Cambridge. By mapping the overlapping sets of brain cells that respond to various words, he says, “we can try to start building a thesaurus of meaning”. The brain area called the auditory cortex processes the sound of a word as it enters the ear. But it is the brain’s prefrontal cortex, a region where higher-order brain activity takes place, that works out a word’s ‘semantic meaning’ — its essence or gist. Previous research2 has studied this process by analysing images of blood flow in the brain, which is a proxy for brain activity. This method allowed researchers to map word meaning to small regions of the brain. But Williams and his colleagues found a unique opportunity to look at how individual neurons encode language in real time. His group recruited ten people about to undergo surgery for epilepsy, each of whom had had electrodes implanted in their brains to determine the source of their seizures. The electrodes allowed the researchers to record activity from around 300 neurons in each person’s prefrontal cortex. © 2024 Springer Nature Limited

Keyword: Language; Brain imaging
Link ID: 29383 - Posted: 07.06.2024

By Simon Makin Most of us have an “inner voice,” and we tend to assume everybody does, but recent evidence suggests that people vary widely in the extent to which they experience inner speech, from an almost constant patter to a virtual absence of self-talk. “Until you start asking the right questions you don’t know there’s even variation,” says Gary Lupyan, a cognitive scientist at the University of Wisconsin–Madison. “People are really surprised because they’d assumed everyone is like them.” A new study, from Lupyan and his colleague Johanne Nedergaard, a cognitive scientist at the University of Copenhagen, shows that not only are these differences real but they also have consequences for our cognition. Participants with weak inner voices did worse at psychological tasks that measure, say, verbal memory than did those with strong inner voices. The researchers have even proposed calling a lack of inner speech “anendophasia” and hope that naming it will help facilitate further research. The study adds to growing evidence that our inner mental worlds can be profoundly different. “It speaks to the surprising diversity of our subjective experiences,” Lupyan says. Psychologists think we use inner speech to assist in various mental functions. “Past research suggests inner speech is key in self-regulation and executive functioning, like task-switching, memory and decision-making,” says Famira Racy, an independent scholar who co-founded the Inner Speech Research Lab at Mount Royal University in Calgary. “Some researchers have even suggested that not having an inner voice may impact these and other areas important for a sense of self, although this is not a certainty.” Inner speech researchers know that it varies from person to person, but studies have typically used subjective measures, like questionnaires, and it is difficult to know for sure if what people say goes on in their heads is what really happens. “It’s very difficult to reflect on one’s own inner experiences, and most people aren’t very good at it when they start out,” says Charles Fernyhough, a psychologist at Durham University in England, who was not involved in the study. © 2024 SCIENTIFIC AMERICAN,

Keyword: Consciousness
Link ID: 29382 - Posted: 07.06.2024

By Charles Q. Choi Chimeroids—brain organoids grown from the cells of multiple people—offer scientists a novel way to compare individual differences in response to drugs, infections or pathogenic variants, according to a new study in Nature. “The possibilities are endless,” says lead investigator Paola Arlotta, professor and chair of stem cell and regenerative biology at Harvard University. The approach overcomes a longstanding issue that has plagued any comparison of organoids derived from different people: Disparities between the organoids might reflect genetic dissimilarities between individual people but could also result just from inadvertent variations in how each organoid was grown, says Aparna Bhaduri, assistant professor of biological chemistry at the University of California, Los Angeles, who did not contribute to the new study. Mixing cells from multiple donors into a single organoid makes it possible to grow all the cells under the same conditions and makes it more likely that any differences seen between the cells are rooted in genetic variations between the people, Bhaduri says. Initially, Arlotta’s team tried to produce chimeroids by mixing pluripotent stem cells from multiple donors. But one person’s cells usually outgrew the others to make up most of each organoid. Even small differences in the stem cells’ extremely high growth rates easily led one person’s cells to overshadow the others, the team noted. So instead, the researchers grew the stem cells independently in organoids until they began to proliferate more slowly as neural stem cells or neural progenitor cells. They then broke these organoids apart and mixed them together, producing the chimeroids that developed with balanced numbers of up to five donors’ cells. Each cell line in the chimeroids could produce all the cell types normally found in the cerebral cortex, Arlotta and her colleagues discovered using DNA and RNA sequencing techniques. © 2024 Simons Foundation

Keyword: Development of the Brain; Genes & Behavior
Link ID: 29381 - Posted: 07.06.2024

By Rodrigo Pérez Ortega It starts with blind spots, flashing lights, and blurry vision—a warning of what’s to come. About an hour later, the dreadful headache kicks in. This pairing, a shining visual experience called an aura and then a headache, happens in about one-third of people who live with migraine. But researchers haven’t been able to figure out exactly how the two are linked at the molecular level. Now, a new study in mice, published today in Science, establishes a direct mechanism: molecules traveling in the fluid that bathes the brain. The finding could lead to new targets for much-needed migraine treatments. “It’s exciting,” says Rami Burstein, a translational neuroscientist at Harvard Medical School who was not involved in the new study. “It takes a very large step into understanding how something that happened in the brain can alter sensation or perception,” he says. It may also explain why the pain of migraine is experienced only in the head, he adds. Migraine, a debilitating neurological disorder, affects about 148 million people worldwide. Recently developed medications can help reduce headaches but are not effective for everyone. Although exact causes remain elusive, research has shown migraines most likely start with a pathological burst of neural activity. During an aura before a migraine, researchers have observed a seizurelike phenomenon called cortical spreading depression (CSD), in which a wave of abnormal neural firing slowly travels throughout the brain’s outer layer, or cortex. But because the brain itself contains no pain-sensing neurons, signals from the brain would have to somehow reach the peripheral nervous system—the nerves that communicate between the body parts and the brain—to cause a headache. In particular, they’d have to get to the two lumps of neurons below the brain called the trigeminal ganglia, which innervate the two sides of our face and head. Scientists knew that pain fibers from the trigeminal ganglion were nested in the meninges—the thin, delicate membranes that envelop and protect the brain.

Keyword: Pain & Touch
Link ID: 29380 - Posted: 07.06.2024

By Paula Span About a month ago, Judith Hansen popped awake in the predawn hours, thinking about her father’s brain. Her father, Morrie Markoff, was an unusual man. At 110, he was thought to be the oldest in the United States. His brain was unusual, too, even after he recovered from a stroke at 99. Although he left school after the eighth grade to work, Mr. Markoff became a successful businessman. Later in life, his curiosity and creativity led him to the arts, including photography and sculpture fashioned from scrap metal. He was a healthy centenarian when he exhibited his work at a gallery in Los Angeles, where he lived. At 103, he published a memoir called “Keep Breathing.” He blogged regularly, pored over The Los Angeles Times daily, discussed articles in Scientific American and followed the national news on CNN and “60 Minutes.” Now he was nearing death, enrolled in home hospice care. “In the middle of the night, I thought, ‘Dad’s brain is so great,’” said Ms. Hansen, 82, a retired librarian in Seattle. “I went online and looked up ‘brain donation.’” Her search led to a National Institutes of Health web page explaining that its NeuroBioBank, established in 2013, collected post-mortem human brain tissue to advance neurological research. Through the site, Ms. Hansen contacted the nonprofit Brain Donor Project. It promotes and simplifies donations through a network of university brain banks, which distribute preserved tissue to research teams. Tish Hevel, the founder of the project, responded quickly, putting Ms. Hansen and her brother in touch with the brain bank at the University of California, Los Angeles. Brain donors may have neurological and other diseases, or they may possess healthy brains, like Mr. Markoff’s. “We’re going to learn so much from him,” Ms. Hevel said. “What is it about these superagers that allows them to function at such a high level for so long?” © 2024 The New York Times Company

Keyword: Development of the Brain; Brain imaging
Link ID: 29379 - Posted: 07.06.2024

By Dave Philipps David Metcalf’s last act in life was an attempt to send a message — that years as a Navy SEAL had left his brain so damaged that he could barely recognize himself. He died by suicide in his garage in North Carolina in 2019, after nearly 20 years in the Navy. But just before he died, he arranged a stack of books about brain injury by his side, and taped a note to the door that read, in part, “Gaps in memory, failing recognition, mood swings, headaches, impulsiveness, fatigue, anxiety, and paranoia were not who I was, but have become who I am. Each is worsening.” Then he shot himself in the heart, preserving his brain to be analyzed by a state-of-the-art Defense Department laboratory in Maryland. The lab found an unusual pattern of damage seen only in people exposed repeatedly to blast waves. The vast majority of blast exposure for Navy SEALs comes from firing their own weapons, not from enemy action. The damage pattern suggested that years of training intended to make SEALs exceptional was leaving some barely able to function. But the message Lieutenant Metcalf sent never got through to the Navy. No one at the lab told the SEAL leadership what the analysis had found, and the leadership never asked. It was not the first time, or the last. At least a dozen Navy SEALs have died by suicide in the last 10 years, either while in the military or shortly after leaving. A grass-roots effort by grieving families delivered eight of their brains to the lab, an investigation by The New York Times has found. And after careful analysis, researchers discovered blast damage in every single one. It is a stunning pattern with important implications for how SEALs train and fight. But privacy guidelines at the lab and poor communication in the military bureaucracy kept the test results hidden. Five years after Lieutenant Metcalf’s death, Navy leaders still did not know. Until The Times told the Navy of the lab’s findings about the SEALs who died by suicide, the Navy had not been informed, the service confirmed in a statement. © 2024 The New York Times Company

Keyword: Brain Injury/Concussion; Depression
Link ID: 29378 - Posted: 07.03.2024

By Adolfo Plasencia Recently, a group of Australian researchers demonstrated a “mind-reading” system called BrainGPT. The system can, according to its creators, convert thoughts (recorded with a non-invasive electrode helmet) into words that are displayed on a screen. Essentially, BrainGPT connects a multitasking EEG encoder to a large language model capable of decoding coherent and readable sentences from EEG signals. Is the mind, the last frontier of privacy, still a safe place to think one’s thoughts? I spoke with Harvard-based behavioral neurologist Alvaro Pascual-Leone, a leader in the study of neuroplasticity and noninvasive brain stimulation, about what it means and how we can protect ourselves. The reality is that the ability to read the brain and influence activity is already here. It’s no longer only in the realm of science fiction. Now, the question is, what exactly can we access and manipulate in the brain? Consider this example: If I instruct you to move a hand, I can tell if you are preparing to move, say, your right hand. I can even administer a precise “nudge” to your brain and make you move your right hand faster. And you would then claim, and fully believe, that you moved it yourself. However, I know that, in fact, it was me who moved it for you. I can even force you to move your left hand—which you were not going to move—and lead you to rationalize why you changed your mind when in fact, our intervention led to that action you perceive as your choice. We have done this experiment in our laboratory. In humans, we can modify brain activity by reading and writing in the brain, so to speak, though we can affect only very simple things right now. In animals, we can do much more complex things because we have much more precise control of the neurons and their timing. But the capacity for that modulation of smaller circuits progressively down to individual neurons in humans is going to come, including much more selective modification with optogenetic alternatives—that is, using light to control the activity of neurons. © 2024 NautilusNext Inc.,

Keyword: Brain imaging
Link ID: 29377 - Posted: 07.03.2024

By Carl Zimmer For thousands of years, philosophers have argued about the purpose of language. Plato believed it was essential for thinking. Thought “is a silent inner conversation of the soul with itself,” he wrote. Many modern scholars have advanced similar views. Starting in the 1960s, Noam Chomsky, a linguist at M.I.T., argued that we use language for reasoning and other forms of thought. “If there is a severe deficit of language, there will be severe deficit of thought,” he wrote. As an undergraduate, Evelina Fedorenko took Dr. Chomsky’s class and heard him describe his theory. “I really liked the idea,” she recalled. But she was puzzled by the lack of evidence. “A lot of things he was saying were just stated as if they were facts — the truth,” she said. Dr. Fedorenko went on to become a cognitive neuroscientist at M.I.T., using brain scanning to investigate how the brain produces language. And after 15 years, her research has led her to a startling conclusion: We don’t need language to think. “When you start evaluating it, you just don’t find support for this role of language in thinking,” she said. When Dr. Fedorenko began this work in 2009, studies had found that the same brain regions required for language were also active when people reasoned or carried out arithmetic. But Dr. Fedorenko and other researchers discovered that this overlap was a mirage. Part of the trouble with the early results was that the scanners were relatively crude. Scientists made the most of their fuzzy scans by combining the results from all their volunteers, creating an overall average of brain activity. © 2024 The New York Times Company

Keyword: Language; Consciousness
Link ID: 29376 - Posted: 07.03.2024

By Abdullahi Tsanni Time takes its toll on the eyes. Now a funky, Hitchcockian video of 64 eyeballs, all rolling and blinking in different directions, is providing a novel visual of one way in which eyes age. A video display of 64 eyeballs, captured using eye trackers, helped researchers compare the size of younger and older study participants’ pupils under differing light conditions, confirming aging affects our eyes. Lab studies have previously shown that the eye’s pupil size shrinks as people get older, making the pupil less responsive to light. A new study that rigged volunteers up with eye-trackers and GoPro videos and sent them traipsing around a university campus has confirmed what happens in the lab happens in real life, too. While pupils remain sensitive to changing light conditions, pupil size can decrease up to about 0.4 millimeters per decade, researchers report June 19 in Royal Society Open Science. “We see a big age effect,” says Manuel Spitschan, a neuroscientist at Max Planck Institute for Biological Cybernetics in Tubingen, Germany. The change helps explain why it can be increasingly harder for people to see in dim light as they age. Light travels through the dark pupil in the center of the eye to the retina, a layer of cells in the back of the eyes that converts the light into images. The pupil’s size can vary from 2 to 8 millimeters in diameter depending on light conditions, getting smaller in bright light and larger in dim light. “With a small pupil, less light enters the eye,” Spitschan says. © Society for Science & the Public 2000–2024.

Keyword: Vision; Development of the Brain
Link ID: 29375 - Posted: 07.03.2024

Richard Luscombe Federal health authorities on Tuesday gave approval to an experimental new drug that has shown to delay the onset of Alzheimer’s disease in trials. Donanemab, manufactured by Eli Lilly, is the second medication that has won the blessing of the Food and Drug Administration (FDA) to treat patients showing early symptoms of the disease, most prominently cognitive impairment. Last year, authorities cleared the drug lecanemab, marketed under the brand name Leqembi, after it demonstrated a similar decline in the progression of Alzheimer’s in a control group. The treatments are not a cure, but the first to physically alter the course of the disease rather than just addressing its symptoms, the FDA said. The video player is currently playing an ad. Indianapolis-based Eli Lilly reported the success of its trial a year ago, and subsequently applied for the FDA authorization that was announced today. Experts at the time said it “could be the beginning of the end of Alzheimer’s disease”, which affects almost 7 million people, mostly older Americans, according to the Alzheimer’s Association. “Kisunla demonstrated very meaningful results for people with early symptomatic Alzheimer’s disease, who urgently need effective treatment options,” Anne White, executive vice-president of Eli Lilly said on Tuesday, referring to donanemab by the brand name it will be sold under. © 2024 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29374 - Posted: 07.03.2024

By Lauren J. Young Kimberly Chauche, a corporate secretary in Lincoln, Neb., says she’s always been overweight. When she was as young as five years old, her doctors started trying to figure out why. Since then her life has involved nutritionists and personal trainers, and eventually she sought therapists to treat her compulsive eating and weight-related anxiety. Yet answers never arrived, and solutions never lasted. At 43, Chauche was prescribed a weight-loss medi­cation called Wegovy—one of a new class of drugs that mimic a hormone responsible for insulin pro­duction. She took her first dose in March 2024, in­jecting it into herself with a needle. Within a couple of months she had lost almost 20 pounds, and that felt great. But the weight loss seemed like a bonus com­pared with a startling change in how she reacted to food. She noticed the shift almost immediately: One day her son was eating popcorn, a snack she could never resist, and she walked right past the bowl. “All of a sudden it was like some part of my brain that was always there just went quiet,” she says. Her eating habits improved, and her anxiety eased. “It felt almost surreal to put an injector against my leg and have happen in 48 hours what decades of intervention could not ac­complish,” she says. “If I had lost almost no weight, just to have my brain working the way it’s working, I would stay on this medication forever.” Chauche is hardly alone in her effusive descriptions of how Wegovy vanquished her intrusive thoughts about food—an experience increasingly referred to as the “quieting of food noise.” Researchers—some of whom ushered in the development of these blockbuster drugs—want to understand why. Among them is biochemist Svetlana Mojsov of the Rockefeller University, who has spent about 50 years investigating gut hormones that could be key to regulating blood glucose levels. In seeking potential treatments for type 2 diabetes, Mojsov ultimately focused on one hormone: glucagonlike peptide 1, or GLP-1. Her sequence of the protein in the 1980s became the initial template for drugs like Wegovy. The medications, called GLP-1 receptor agonists, use a synthetic version of the natural substance to activate the hormone’s receptors. The first ones arrived in 2005. In 2017 the U.S. Food and Drug Administration approved semaglutide—now widely known as Ozempic. © 2024 SCIENTIFIC AMERICAN,

Keyword: Obesity; Hormones & Behavior
Link ID: 29373 - Posted: 06.26.2024

By Meghan Rosen Float like a butterfly, sniff out cancer like a bee? Honeybees can detect the subtle scents of lung cancer in the lab — and even the faint aroma of disease that can waft from a patient’s breath. Inspired by the insects’ exquisite olfactory abilities, scientists hooked the brains of living bees up to electrodes, passed different scents under the insects’ antennae and then recorded their brain signals. “It’s very clear — like day and night — whether [a bee] is responding to a chemical or not,” says Debajit Saha, a neural engineer at Michigan State University in East Lansing. Different odors sparked recognizable brain activity patterns, a kind of neural fingerprint for scent, Saha and colleagues report June 4 in Biosensors and Bioelectronics. One day, he says, doctors might be able to use honeybees in cancer clinics as living sensors for early disease detection. Electronic noses, or e-noses, and other types of mechanical odor-sensing equipment exist, but they’re not exactly the bee’s knees. When it comes to scent, Saha says, “biology has this ability to differentiate between very, very similar mixtures, which no other engineered sensors can do.” Scent is an important part of how many insect species communicate, says chemical ecologist Flora Gouzerh of the French National Research Institute for Sustainable Development in Montpellier. For them, “it’s a language,” she says. The idea that animal senses can get a whiff of disease is nothing new; doctors reported a case of a border collie and a Doberman sniffing out their owner’s melanoma in 1989. More recently, scientists have shown that dogs can detect COVID-19 cases by smelling people’s sweat (SN: 6/1/22). A lot of insects probably have disease-detecting abilities, too, Gouzerh says. Ants, for instance, can be trained to pick out the smell of cancer cells grown in a lab dish. But until now, bees’ abilities haven’t been quite so clear, she says. © Society for Science & the Public 2000–2024.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29372 - Posted: 06.26.2024

By Charles Q. Choi The largest-yet single-cell genomics analysis reveals new details of the molecular pathways and cell types that are altered in the cortex in people with autism. The work, published last month in Science, also hints at how genes linked to the condition contribute to these brain differences. The findings are part of a package of 14 new papers from PsychENCODE, a multi-institution consortium launched in 2015 to study the molecular basis of neuropsychiatric conditions. The initiative’s latest phase of research analyzed human brains at the single-cell level instead of relying on bulk tissue samples as in previous efforts. “Single-cell analysis gives you the ability to really understand a condition in terms of cell-cell interactions, and how a condition might affect different cell types in very different ways,” says PsychENCODE chair Daniel Geschwind, professor of human genetics, neurology and psychiatry at the University of California, Los Angeles, who led the new autism study. Past work by Geschwind and others identified a “molecular signature” in tissue samples of autism brains, characterized by increased expression of immune signaling genes, decreased activity of synaptic and neuronal genes, and a reduction in the regional gene-expression patterns typically seen across the cortex. The first single-cell analysis—involving cells from 15 autistic and 16 non-autistic people, and published in 2019—hinted at a role for microglia and excitatory neurons in layer 2/3 of the cortex. The new study confirms these previous findings and expands autism’s molecular signature to include a subtype of interneurons and layer 5/6 excitatory neurons, which project to other cortical areas. It also adds gene-expression changes, such as heightened immune responses in oligodendrocytes, cells that help produce the myelin sheath insulating the central nervous system. “That suggests there may be something going on broadly with connectivity in autism,” Geschwind says. © 2024 Simons Foundation

Keyword: Autism; Epigenetics
Link ID: 29371 - Posted: 06.26.2024

By Dana G. Smith In July 2016, a heat wave hit Boston, with daytime temperatures averaging 92 degrees for five days in a row. Some local university students who were staying in town for the summer got lucky and were living in dorms with central air-conditioning. Other students, not so much — they were stuck in older dorms without A.C. Jose Guillermo Cedeño Laurent, a Harvard researcher at the time, decided to take advantage of this natural experiment to see how heat, and especially heat at night, affected the young adults’ cognitive performance. He had 44 students perform math and self-control tests five days before the temperature rose, every day during the heat wave, and two days after. “Many of us think that we are immune to heat,” said Dr. Cedeño, now an assistant professor of environmental and occupational health and justice at Rutgers University. “So something that I wanted to test was whether that was really true.” It turns out even young, healthy college students are affected by high temperatures. During the hottest days, the students in the un-air-conditioned dorms, where nighttime temperatures averaged 79 degrees, performed significantly worse on the tests they took every morning than the students with A.C., whose rooms stayed a pleasant 71 degrees. A heat wave is once again blanketing the Northeast, South and Midwest. High temperatures can have an alarming effect on our bodies, raising the risk for heart attacks, heatstroke and death, particularly among older adults and people with chronic diseases. But heat also takes a toll on our brains, impairing cognition and making us irritable, impulsive and aggressive. Numerous studies in lab settings have produced similar results to Dr. Cedeño’s research, with scores on cognitive tests falling as scientists raised the temperature in the room. One investigation found that just a four-degree increase — which participants described as still feeling comfortable — led to a 10 percent average drop in performance across tests of memory, reaction time and executive functioning. © 2024 The New York Times Company

Keyword: Aggression
Link ID: 29370 - Posted: 06.26.2024

Jon Hamilton About 170 billion cells are in the brain, and as they go about their regular tasks, they produce waste — a lot of it. To stay healthy, the brain needs to wash away all that debris. But how exactly it does this has remained a mystery. Now, two teams of scientists have published three papers that offer a detailed description of the brain's waste-removal system. Their insights could help researchers better understand, treat and perhaps prevent a broad range of brain disorders. The papers, all published in the journal Nature, suggest that during sleep, slow electrical waves push the fluid around cells from deep in the brain to its surface. There, a sophisticated interface allows the waste products in that fluid to be absorbed into the bloodstream, which takes them to the liver and kidneys to be removed from the body. One of the waste products carried away is amyloid, the substance that forms sticky plaques in the brains of patients with Alzheimer's disease. This illustration demonstrates how the thin film of sensors could be applied to the brain during surgery. There's growing evidence that in Alzheimer's disease, the brain's waste-removal system is impaired, says Jeffrey Iliff, who studies neurodegenerative diseases at the University of Washington but was not a part of the new studies. The new findings should help researchers understand precisely where the problem is and perhaps fix it, Iliff says. "If we restore drainage, can we prevent the development of Alzheimer's disease?" he asks. The new studies come more than a decade after Iliff and Dr. Maiken Nedergaard, a Danish scientist, first proposed that the clear fluids in and around the brain are part of a system to wash away waste products. The scientists named it the glymphatic system, a nod to the body's lymphatic system, which helps fight infection, maintain fluid levels and filter out waste products and abnormal cells. © 2024 npr

Keyword: Sleep
Link ID: 29369 - Posted: 06.26.2024

By Miryam Naddaf Researchers have developed a four-dimensional model of spinal-cord injury in mice, which shows how nearly half a million cells in the spinal cord respond over time to injuries of varying severity. The model, known as a cell atlas, could help researchers to resolve outstanding questions and develop new treatments for people with spinal-cord injury (SCI). “If you know what every single cell on the spinal cord is doing in response to injury, you could use that knowledge to develop tailor-made and mechanism-based therapies,” says Mark Anderson, a neurobiologist at the Swiss Federal Institute of Technology in Geneva, Switzerland, who worked on the atlas. “Things don’t need to be a shot in the dark.” Anderson and his colleagues used machine-learning algorithms to build the atlas by mapping data from RNA sequencing and other cell-biology techniques. They described the work in a Nature paper published today1 and have made the entire atlas available through an online platform. The atlas is a valuable resource for testing hypotheses about SCI, says Binhai Zheng, who studies spinal-cord regeneration at the University of California, San Diego. “There are a lot of hidden treasures.” The researchers examined sections of the spinal cord, sampled from 52 injured and uninjured mice at 1, 4, 7, 14, 30 and 60 days after injury. Their analysis involved 18 experimental SCI conditions, including different types of injury and levels of severity. They used RNA-sequencing tools to explore how 482,825 cells responded to injury over time. © 2024 Springer Nature Limited

Keyword: Brain imaging; Brain Injury/Concussion
Link ID: 29368 - Posted: 06.26.2024

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 Claire Yuan Men and women experience pain differently, and until now, scientists didn’t know why. New research says it may be in part due to differences in male and female nerve cells. Pain-sensing nerve cells from male and female animal tissues responded differently to the same sensitizing substances, researchers report June 3 in Brain. The results suggest that at the cellular level, pain is produced differently between the sexes. The results might allow researchers “to come up with drugs that would be specific to treat female patients or male patients,” says Katherine Martucci, a neuroscientist who studies chronic pain at Duke University School of Medicine and was not involved in the study. “There’s no debate about it. They’re seeing these differences in the cells.” Some types of chronic and acute pain appear more often in one sex, but it’s unclear why. For instance, about 50 million adults in the United States suffer from chronic pain conditions, many of which are more common in women (SN: 5/22/23). Similar disparities exist for acute conditions. Such differences prompted pain researcher Frank Porreca of the University of Arizona Health Sciences in Tucson and colleagues to study nerve cells called nociceptors, which can act like alarm sensors for the body. The cells’ pain sensors, found in skin, organs and elsewhere in the body, can detect potentially dangerous stimuli and send signals to the brain, which then interprets the information as pain. In some cases, the nerve cells can become more sensitive to outside stimulation, registering even gentle sensations — like a shirt rubbing sunburned skin — as pain. © Society for Science & the Public 2000–2024.

Keyword: Pain & Touch; Sexual Behavior
Link ID: 29366 - Posted: 06.24.2024

By Sara Reardon Specific nerve cells on the penis and clitoris detect vibrations and then become activated, causing sexual behaviours such as erections, a study in mice has revealed1. The findings could lead to new treatments for conditions such as erectile dysfunction, or for restoring sexual function in people with lower-body paralysis. Krause corpuscles — nerve endings in tightly wrapped balls located just under the skin — were first discovered in human genitals more than 150 years ago. The structures are similar to touch-activated corpuscles found on people’s fingers and hands, which respond to vibrations as the skin moves across a textured surface. But there is little research into how the genital corpuscles work and how they are involved in sex, probably because the topic is sometimes considered taboo. “It’s been hard to get people to work on this because some people have a hard time talking about it,” says David Ginty, a sensory neurobiologist at Harvard Medical School in Boston, Massachusetts, who led the team that conducted the latest research. “But I don’t, because the biology is so interesting.” Ginty and other sensory biologists have long wanted to study these mysterious neuron balls. But activating and tracking specific neurons was nearly impossible until advanced molecular techniques emerged in the past 20 years. In a 19 June paper in Nature1, Ginty and his collaborators activated the Krause corpuscles in both male and female mice using various mechanical and electrical stimuli. The neurons fired in response to low-frequency vibrations in the range of 40–80 hertz. Ginty notes that these frequencies are generally used in many sex toys; humans, it seems, realized that this was the best way to stimulate Krause corpuscles before any official experiments were published. © 2024 Springer Nature Limited

Keyword: Sexual Behavior; Pain & Touch
Link ID: 29365 - Posted: 06.24.2024

By Dennis Normile For several decades, evidence has accumulated that animals turn to medicinal plants to relieve their ailments. Chimpanzees (and some other species) swallow leaves to mechanically clear the gut of parasites. Chimps also rely on the ingested pith of an African relative of the daisy, Vernonia amygdalina, to rid themselves of intestinal worms. Dolphins rub against antibacterial corals and sponges to treat skin infections. And recently, a male Sumatran orangutan was observed chewing the leaves of Fibraurea tinctoria, a South Asian plant with antibacterial and anti-inflammatory properties, and dabbing the juice onto a wound. These instances of animals playing doctor with therapeutic plants have typically been identified one by one. Today, in PLOS ONE, a multinational team proposes adding 17 samples from 13 plant species to the chimpanzee pharmacopia. “The paper provides important new findings about self-medication behavior in wild chimpanzees,” a topic that’s still relatively unknown, says Isabelle Laumer, a cognitive biologist at the Max Planck Institute of Animal Behavior and lead author on the orangutan self-medication paper who was not involved in the new chimp research. Observers with the team behind today's paper spent 4 months with each of two chimp communities habituated to human observers in Uganda’s Budongo Forest. The researchers supplemented their own observations with historical data. From the 170 chimps in the two communities, the observers zeroed in on 51 individuals suffering bacterial infections and inflammation as indicated by abnormal urine composition, diarrhea, traces of parasites, or apparent wounds. For 10 hours a day they followed the sick chimps through the forest, noting which plants they ate and when, and watching in particular to see whether the animals went out of their way to find and consume plants not part of their usual diet. In one example, researchers observed an individual suffering from diarrhea very briefly venture outside the group’s safe home territory to eat a small amount of dead wood from Alstonia boonei, a tree in the dogbane family. Chimps rarely eat dead wood, which is not nutritious for them, the team says.

Keyword: Evolution
Link ID: 29364 - Posted: 06.24.2024