By Angie Voyles Askham The primary visual cortex carries, well, visual information — or so scientists thought until early 2010. That’s when a team at the University of California, San Francisco first described vagabond activity in the brain area, called V1, in mice. When the animals started to run on a treadmill, some neurons more than doubled their firing rate. The finding “was kind of mysterious,” because V1 was thought to represent only visual signals transmitted from the retina, says Anne Churchland, professor of neurobiology at the University of California, Los Angeles, who was not involved in that work. “The idea that running modulated neural activity suggested that maybe those visual signals were corrupted in a way that, at the time, felt like it would be really problematic.” The mystery grew over the next decade, as a flurry of mouse studies from Churchland and others built on the 2010 results. Both arousal and locomotion could shape the firing of primary visual neurons, those newer findings showed, and even subtle movements such as nose scratches contribute to variance in population activity, all without compromising the sensory information. A consensus started to form around the idea that sensory cortical regions encode broader information about an animal’s physiological state than previously thought. At least until last year, when two studies threw a wrench into that storyline: Neither marmosets nor macaque monkeys show any movement-related increase in V1 signaling. Instead, running seems to slightly suppress V1 activity in marmosets, and spontaneous movements have no effect on the same cells in macaques. The apparent differences across species raise new questions about whether mice are a suitable model to study the primate visual system, says Michael Stryker, professor of physiology at the University of California, San Francisco, who led the 2010 work. “Maybe the primate’s V1 is not working the same as in the mouse,” he says. “As I see it, it’s still a big unanswered question.” © 2024 Simons Foundation

Keyword: Vision
Link ID: 29153 - Posted: 02.20.2024

Nancy S. Jecker & Andrew Ko Putting a computer inside someone’s brain used to feel like the edge of science fiction. Today, it’s a reality. Academic and commercial groups are testing “brain-computer interface” devices to enable people with disabilities to function more independently. Yet Elon Musk’s company, Neuralink, has put this technology front and center in debates about safety, ethics and neuroscience. In January 2024, Musk announced that Neuralink implanted its first chip in a human subject’s brain. The Conversation reached out to two scholars at the University of Washington School of Medicine – Nancy Jecker, a bioethicst, and Andrew Ko, a neurosurgeon who implants brain chip devices – for their thoughts on the ethics of this new horizon in neuroscience. How does a brain chip work? Neuralink’s coin-size device, called N1, is designed to enable patients to carry out actions just by concentrating on them, without moving their bodies. Subjects in the company’s PRIME study – short for Precise Robotically Implanted Brain-Computer Interface – undergo surgery to place the device in a part of the brain that controls movement. The chip records and processes the brain’s electrical activity, then transmits this data to an external device, such as a phone or computer. The external device “decodes” the patient’s brain activity, learning to associate certain patterns with the patient’s goal: moving a computer cursor up a screen, for example. Over time, the software can recognize a pattern of neural firing that consistently occurs while the participant is imagining that task, and then execute the task for the person. © 2010–2024, The Conversation US, Inc.

Keyword: Robotics; Learning & Memory
Link ID: 29151 - Posted: 02.20.2024

By Claudia López Lloreda By squirting cells from a 3D printer, researchers have created tissue that looks—and acts—like a chunk of brain. In recent years, scientists have learned how to load up 3D printers with cells and other scaffolding ingredients to create living tissues, but making realistic brainlike constructs has been a challenge. Now, one team has shown that, by modifying its printing techniques, it can print and combine multiple subtypes of cells that better mimic signaling in the human brain. “It’s remarkable that [the researchers] can replicate” how brain cells work, says Riccardo Levato, a regenerative medicine researcher at Utrecht University who was not involved with the study. “It’s the first demonstration that, with some simple organization [of cells], you can start getting some interesting functional [responses].” The new technology, described last week in Cell Stem Cell, could offer advantages over existing techniques that neuroscientists use to create 3D brain tissues in the lab. One common approach involves using stem cells to grow miniature brainlike blobs called organoids. But researchers can’t control the types of cells or their precise location in these constructs. Each organoid “is unique,” making it difficult to reproduce research results, says neuroscientist Su-Chun Zhang of the University of Wisconsin–Madison, an author of the new study. With the right kind of 3D printing, however, “you can control where different cell types are placed,” says developmental biologist Francis Szele of the University of Oxford. Past studies have used 3D printers to construct brain tissues that allowed researchers to study how the cells matured and made connections, and even integrate printed tissue into mouse brains. But those constructs had limited functionality. And efforts that produced more functional printed tissue used rat cells, not human cells. © 2024 American Association for the Advancement of Science.

Keyword: Development of the Brain; Robotics
Link ID: 29145 - Posted: 02.10.2024

By Simon Makin A new device makes it possible for a person with an amputation to sense temperature with a prosthetic hand. The technology is a step toward prosthetic limbs that restore a full range of senses, improving both their usefulness and acceptance by those who wear them. A team of researchers in Italy and Switzerland attached the device, called ”MiniTouch,” to the prosthetic hand of a 57-year-old man named Fabrizio, who has an above-the-wrist amputation. In tests, the man could identify cold, cool and hot bottles of liquid with perfect accuracy; tell the difference between plastic, glass and copper significantly better than chance; and sort steel blocks by temperature with around 75 percent accuracy, researchers report February 9 in Med. Thank you for being a subscriber to Science News! Interested in more ways to support STEM? Consider making a gift to our nonprofit publisher, Society for Science, an organization dedicated to expanding scientific literacy and ensuring that every young person can strive to become an engineer or scientist. “It’s important to incorporate these technologies in a way that prosthesis users can actually use to perform functional tasks,” says neuroengineer Luke Osborn of Johns Hopkins University Applied Physics Laboratory in Laurel, Md., who was not involved in the study. “Introducing new sensory feedback modalities could help give users more functionality they weren’t able to achieve before.” The device also improved Fabrizio’s ability to tell whether he was touching an artificial or human arm. His accuracy was 80 percent with the device turned on, compared with 60 percent with it off. “It’s not quite as good as with the intact hand, probably because we’re not giving [information about] skin textures,” says neuroengineer Solaiman Shokur of EPFL, the Swiss Federal Institute of Technology in Lausanne. © Society for Science & the Public 2000–2024.

Keyword: Pain & Touch
Link ID: 29144 - Posted: 02.10.2024

By Ben Guarino Billionaire technologist Elon Musk announced this week that his company Neuralink has implanted its brain-computer interface into a human for the first time. The recipient was “recovering well,” Musk wrote on his social media platform X (formerly Twitter) on Monday evening, adding that initial results showed “promising neuron spike detection”—a reference to brain cells’ electrical activity. Each wireless Neuralink device contains a chip and electrode arrays of more than 1,000 superthin, flexible conductors that a surgical robot threads into the cerebral cortex. There the electrodes are designed to register thoughts related to motion. In Musk’s vision, an app will eventually translate these signals to move a cursor or produce text—in short, it will enable computer control by thinking. “Imagine if Stephen Hawking could communicate faster than a speed typist or auctioneer. That is the goal,” Musk wrote of the first Neuralink product, which he said is named Telepathy. The U.S. Food and Drug Administration had approved human clinical trials for Neuralink in May 2023. And last September the company announced it was opening enrollment in its first study to people with quadriplegia. Monday’s announcement did not take neuroscientists by surprise. Musk, the world’s richest man, “said he was going to do it,” says John Donoghue, an expert in brain-computer interfaces at Brown University. “He had done the preliminary work, built on the shoulders of others, including what we did starting in the early 2000s.” Neuralink’s original ambitions, which Musk outlined when he founded the company in 2016, included meshing human brains with artificial intelligence. Its more immediate aims seem in line with the neural keyboards and other devices that people with paralysis already use to operate computers. The methods and speed with which Neuralink pursued those goals, however, have resulted in federal investigations into dead study animals and the transportation of hazardous material. © 2024 SCIENTIFIC AMERICAN

Keyword: Robotics
Link ID: 29124 - Posted: 01.31.2024

By Ben Guarino Billionaire technologist Elon Musk announced this week that his company Neuralink has implanted its brain-computer interface into a human for the first time. The recipient was “recovering well,” Musk wrote on his social media platform X (formerly Twitter) on Monday evening, adding that initial results showed “promising neuron spike detection”—a reference to brain cells’ electrical activity. Each wireless Neuralink device contains a chip and electrode arrays of more than 1,000 superthin, flexible conductors that a surgical robot threads into the cerebral cortex. There the electrodes are designed to register thoughts related to motion. In Musk’s vision, an app will eventually translate these signals to move a cursor or produce text—in short, it will enable computer control by thinking. “Imagine if Stephen Hawking could communicate faster than a speed typist or auctioneer. That is the goal,” Musk wrote of the first Neuralink product, which he said is named Telepathy. The U.S. Food and Drug Administration had approved human clinical trials for Neuralink in May 2023. And last September the company announced it was opening enrollment in its first study to people with quadriplegia. Monday’s announcement did not take neuroscientists by surprise. Musk, the world’s richest man, “said he was going to do it,” says John Donoghue, an expert in brain-computer interfaces at Brown University. “He had done the preliminary work, built on the shoulders of others, including what we did starting in the early 2000s.” Neuralink’s original ambitions, which Musk outlined when he founded the company in 2016, included meshing human brains with artificial intelligence. Its more immediate aims seem in line with the neural keyboards and other devices that people with paralysis already use to operate computers. The methods and speed with which Neuralink pursued those goals, however, have resulted in federal investigations into dead study animals and the transportation of hazardous material. © 2024 SCIENTIFIC AMERICAN

Keyword: Robotics
Link ID: 29123 - Posted: 01.31.2024

James O’Brien for Quanta Magazine In recent decades, neuroscience has seen some stunning advances, and yet a critical part of the brain remains a mystery. I am referring to the cerebellum, so named for the Latin for “little brain,” which is situated like a bun at the back of the brain. This is no small oversight: The cerebellum contains three-quarters of all the brain’s neurons, which are organized in an almost crystalline arrangement, in contrast to the tangled thicket of neurons found elsewhere. Encyclopedia articles and textbooks underscore the fact that the cerebellum’s function is to control body movement. There is no question that the cerebellum has this function. But scientists now suspect that this long-standing view is myopic. Or so I learned in November in Washington, D.C., while attending the Society for Neuroscience annual meeting, the largest meeting of neuroscientists in the world. There, a pair of neuroscientists organized a symposium on newly discovered functions of the cerebellum unrelated to motor control. New experimental techniques are showing that in addition to controlling movement, the cerebellum regulates complex behaviors, social interactions, aggression, working memory, learning, emotion and more. The connection between the cerebellum and movement has been known since the 19th century. Patients suffering trauma to the brain region had obvious difficulties with balance and movement, leaving no doubt that it was critical for coordinating motion. Over the decades, neuroscientists developed a detailed understanding of how the cerebellum’s unique neural circuitry controls motor function. The explanation of how the cerebellum worked seemed watertight. Then, in 1998, in the journal Brain, neurologists reported on wide-ranging emotional and cognitive disabilities in patients with damage to the cerebellum. For example, in 1991, a 22-year-old female college student had fallen while ice skating; a CT scan revealed a tumor in her cerebellum. After it was removed surgically, she was a completely different person. The bright college student had lost her ability to write with proficiency, do mental arithmetic, name common objects or copy a simple diagram. Her mood flattened. She hid under covers and behaved inappropriately, undressing in the corridors and speaking in baby talk. Her social interactions, including recognizing familiar faces, were also impaired.

Keyword: Emotions; Movement Disorders
Link ID: 29118 - Posted: 01.27.2024

By Holly Barker Sensory issues associated with autism may be caused by fluctuating neuronal noise — the background hum of electrical activity in the brain — according to a new mouse study. Up to 90 percent of autistic people report sensory problems, including heightened sensitivity to sounds or an aversion to certain smells. Yet others barely register sensory cues and may seek out sensations by making loud noises or rocking back and forth. But thinking in terms of hyper- or hyposensitivity may be an oversimplification, says Andreas Frick, lead investigator and research director at INSERM. “It’s becoming clear now that things are a lot more nuanced.” For instance, the brain’s response to visual patterns — measured using electroencephalography (EEG) recordings — varies more between viewings in autistic people than in those without the condition, one study found. And functional MRI has detected similar variability among autistic people, suggesting sensory problems may arise from inconsistent brain responses. In the new study, Frick and his colleagues found variability in the activity of individual neurons in a mouse model of fragile X syndrome, one of the leading causes of autism. That variability in neuronal response maps to fluctuations in the levels of noise in the brain, the study found. Noise within the brain isn’t necessarily a bad thing. In fact, an optimum amount is ideal: a little can give neurons the ‘push’ they might need to fire an action potential, while too much can make it difficult for the brain to distinguish between different stimuli. But in animals modeling fragile X syndrome, noise fluctuates such that they process sensory information less reliably, Frick says. © 2023 Simons Foundation.

Keyword: Autism
Link ID: 29105 - Posted: 01.18.2024

By David Levin It can start small: a peculiar numbness; a subtle facial tic; an inexplicably stiff muscle. But then time goes by — and eventually, the tremors set in. Roughly a million people in the United States (and roughly 10 million people worldwide) live with Parkinson’s disease, a potent neurological disorder that progressively kills neurons in the brain. As it does so, it can trigger a host of crippling symptoms, from violent tremors to excruciating muscle cramps, terrifying nightmares and constant brain fog. While medical treatments can alleviate some of these effects, researchers still don’t know exactly what causes the disease to occur in the first place. A growing number of studies, however, are suggesting that it may be tied to an unlikely culprit: bacteria living inside our guts. Every one of us has hundreds or thousands of microbial species in our stomach, small intestine and colon. These bacteria, collectively called our gut microbiome, are usually considerate guests: Although they survive largely on food that passes through our insides, they also give back, cranking out essential nutrients like niacin (which helps our body convert food into energy) and breaking down otherwise indigestible plant fiber into substances our bodies can use. As Parkinson’s advances in the brain, researchers have reported that the species of bacteria present in the gut also shift dramatically, hinting at a possible cause for the disease. A 2022 paper published in the journal Nature Communications recorded those differences in detail. After sequencing the mixed-together genomes of fecal bacteria from 724 people — a group with Parkinson’s and another without — the authors saw a number of distinct changes in the guts of people who suffered from the disease. The Parkinson’s group had dramatically lower amounts of certain species of Prevotella, a type of bacterium that helps the body break down plant-based fiber (changes like this in gut flora could explain why people with Parkinson’s disease often experience constipation). At the same time, the study found, two harmful species of Enterobacteriaceae, a family of microbes that includes Salmonella, E. coli and other bugs, proliferated. Those bacteria may be involved in a chain of biochemical events that eventually kill brain cells in Parkinson’s patients, says Tim Sampson, a biologist at Emory University School of Medicine and coauthor of the study.

Keyword: Parkinsons
Link ID: 29098 - Posted: 01.13.2024

By Henkjan Honing In 2009, my research group found that newborns possess the ability to discern a regular pulse— the beat—in music. It’s a skill that might seem trivial to most of us but that’s fundamental to the creation and appreciation of music. The discovery sparked a profound curiosity in me, leading to an exploration of the biological underpinnings of our innate capacity for music, commonly referred to as “musicality.” In a nutshell, the experiment involved playing drum rhythms, occasionally omitting a beat, and observing the newborns’ responses. Astonishingly, these tiny participants displayed an anticipation of the missing beat, as their brains exhibited a distinct spike, signaling a violation of their expectations when a note was omitted. Yet, as with any discovery, skepticism emerged (as it should). Some colleagues challenged our interpretation of the results, suggesting alternate explanations rooted in the acoustic nature of the stimuli we employed. Others argued that the observed reactions were a result of statistical learning, questioning the validity of beat perception being a separate mechanism essential to our musical capacity. Infants actively engage in statistical learning as they acquire a new language, enabling them to grasp elements such as word order and common accent structures in their native language. Why would music perception be any different? To address these challenges, in 2015, our group decided to revisit and overhaul our earlier beat perception study, expanding its scope, method and scale, and, once more, decided to include, next to newborns, adults (musicians and non-musicians) and macaque monkeys. The results, recently published in Cognition, confirm that beat perception is a distinct mechanism, separate from statistical learning. The study provides converging evidence on newborns’ beat perception capabilities. In other words, the study was not simply a replication but utilized an alternative paradigm leading to the same conclusion. © 2023 NautilusNext Inc., All rights reserved.

Keyword: Hearing; Language
Link ID: 29067 - Posted: 12.27.2023

By Mark MacNamara The notion of boxing as the “sweet science” is often thought to have been coined in 1956 by the great New Yorker writer A.J. Liebling. He used the term as the title of his definitive book on the sport, but he took it—with much appreciation—from a British sportswriter, Pierce Egan. In 1813, Egan wrote about the “sweet science of bruising” in his master work, Boxiana. The book is a collection of magazine pieces set in a bloody, bare-knuckled world opposite Jane Austen’s. As for the “sweet science,” no one ever really defines it. A carefully thrown knockout punch to a sweet spot on the chin is one possible derivation. There’s also the play on a science with so little apparent sweetness. But that’s not it. The sweet science Liebling and Egan describe had more to do with British principles of “stoic virtues,” “generosity,” and “true courage”—altogether, life in a contradictory place. It’s a square ring, after all, where sometimes hope transcends the specter of an awful inevitability. Or so I’ve come to think, on a journey I’ve begun in the past year, exploring how the sweet science can be used as a treatment for Parkinson’s disease—that increasingly common degenerative disorder of the nervous system, tied to a loss of the brain chemical dopamine, which is involved in movement, memory, motivation, and cognition. Someone told her she moved like a wavy wind sock outside a used car lot. “Exactly how I feel,” she said. In October 2022, a longtime tennis partner noticed something “strange” in my stride, along with a noisy shuffle. “Fatigue,” I replied with pique. The truth is I’m 75 and had known something might not be right for years, particularly the ominous hand tremors, as well as the night-of-the-living-dead gait and a facial expression to match. Add severe anxiety in public places and bizarre nightmares, some quite disturbing. © 2023 NautilusNext Inc.,

Keyword: Parkinsons
Link ID: 29055 - Posted: 12.19.2023

By Sandra G. Boodman His plane was coming in for a landing at Philadelphia International Airport when Allen M. Weiss, a marketing professor at the University of Southern California, felt a spasm of pain pierce his left cheek near his nose. “It was really weird,” recalled Weiss, then director of Mindful USC, a group of meditation-based programs at the Los Angeles university. “My face froze up.” Within minutes the pain disappeared and the final leg of Weiss’s December 2015 trip home to California was uneventful. But over the next few months the sensation recurred in the same spot. At first the unpredictable pain was fairly mild and merely bothersome; later it became an excruciating daily torment. Several years after the pain first occurred Weiss, who had consulted dentists, oral pain experts and an otolaryngologist, was given a diagnosis that ended up being correct. But his complicated medical history, a radiology report that failed to describe an important finding and a cryptic warning by one of his doctors delayed effective treatment for three more years. “It was completely confusing,” Weiss said. In June 2023 he underwent surgery that has significantly reduced his pain and improved the quality of his life. N. Nicole Moayeri, the Santa Barbara, Calif., neurosurgeon who operated on Weiss, said a protracted search for a diagnosis and treatment is not unusual for those suffering from Weiss’s uncommon malady. “I commonly see people who’ve had multiple dental procedures for years” when the problem was not in their mouths, Moayeri said. “It’s really shocking to me that so many people suffer” with this for so long. After three months of intermittent pain following the flight, Weiss consulted his internist. For reasons that are unclear, the doctor told Weiss the cause was probably psychological, not physical, and that it wasn’t serious. He sent Weiss to an ear, nose and throat specialist whom he saw in March 2016. She performed an exam and ordered a CT scan that revealed a deviated septum, a typically painless condition estimated to affect up to 80 percent of the population in which the bone or cartilage that divides the nostrils is off-center. A moderate or severe deviation can contribute to the development of sinus infections, headaches and breathing problems. But Weiss had none of these. And a deviated septum didn’t explain the spasms of pain.

Keyword: Pain & Touch
Link ID: 29054 - Posted: 12.19.2023

By Carolyn Wilke Newborn bottlenose dolphins sport a row of hairs along the tops of their jaws. But once the animals are weaned, the whiskers fall out. “Everybody thought these structures are vestigial — so without any function,” said Guido Dehnhardt, a marine mammal zoologist at the University of Rostock in Germany. But Dr. Dehnhardt and his colleagues have discovered that the pits left by those hairs can perceive electricity with enough sensitivity that they may help the dolphins snag fish or navigate the ocean. The team reported its findings Thursday in The Journal of Experimental Biology. Dr. Dehnhardt first studied the whisker pits of a different species, the Guiana dolphin. He expected to find the typical structures of hair follicles, but those were missing. Yet the pits were loaded with nerve endings. He and his colleagues realized that the hairless follicles looked like the electricity-sensing structures on sharks and found that one Guiana dolphin responded to electrical signals. They wondered whether other toothed cetaceans, including bottlenose dolphins, could also sense electricity. For the new study, the researchers trained two bottlenose dolphins to rest their jaws, or rostrums, on a platform and swim away anytime they experienced a sensory cue like a sound or a flash of light. If they didn’t detect one of these signals, the dolphins were to stay put. “It’s basically the same as when we go to the doctor’s and do a hearing test — we have to press a button as soon as we hear a sound,” said Tim Hüttner, a biologist at the Nuremberg Zoo in Germany and a study co-author. Once trained, the dolphins also received electrical signals. “The dolphins responded correctly on the first trial,” Dr. Hüttner said. The animals were able to transfer what they had learned, revealing that they could also detect electric fields. Further study showed that the dolphins’ sensitivity to electricity was similar to that of the platypus, which is thought to use its electrical sense for foraging. © 2023 The New York Times Company

Keyword: Hearing
Link ID: 29037 - Posted: 12.09.2023

By Esther Landhuis Dropping an ice crystal into a bottle of near-frozen water produces a dramatic effect: very quickly, the liquid crystallizes into a block of ice. At the molecular level, an ice crystal has a distinct shape—a lattice structure. As incoming water molecules reshape to join the lattice, the crystal grows. Some researchers think an analogous process underlies Alzheimer’s disease, Parkinson’s disease and other neurodegenerative illnesses. According to this theory, these diseases begin when a particular protein misfolds, or fails to assume the proper shape for its intended role. That misshapen molecule ensnares normal versions of the protein, causing them to similarly misfold, and over time, these rogue proteins clump into toxic clusters that spread through the brain. In mad cow disease—a brain disorder in cattle that can spread to people who eat meat from ill animals —the toxic proteins, called prions, ravage the mind quickly, leading to dementia and death within months. Prion diseases are rare. About 350 cases of the most common type, Creutzfeldt-Jakob disease, are reported each year in the U.S. By comparison, each year, nearly 500,000 people in the U.S. are diagnosed with Alzheimer’s, which develops more gradually. Plaques made up of abnormal beta-amyloid proteins can accumulate in the brain for years or even decades before a person notices signs of mental decline. While the time lines for toxicity differ, “the mechanism of misfolding is the same,” says Mathias Jucker, a neuroscientist at the Hertie Institute for Clinical Brain Research at the University of Tübingen in Germany. Just as all of the water in a bottle freezes after a “‘misfolded’ water molecule” slips into the vessel, if “you have one misfolded protein, all the other ones will take the same shape.” The idea that many diseases could arise from a common prionlike process raises an intriguing and troubling question: Under certain circumstances, could neurodegenerative disorders be transmitted from person to person? © 2023 SCIENTIFIC AMERICAN,

Keyword: Alzheimers; Prions
Link ID: 29032 - Posted: 12.06.2023

Nell Greenfieldboyce If you've got itchy skin, it could be that a microbe making its home on your body has produced a little chemical that's directly acting on your skin's nerve cells and triggering the urge to scratch. That's the implication of some new research that shows how a certain bacteria, Staphylococcus aureus, can release an enzyme that generates an itchy feeling. What's more, a drug that interferes with this effect can stop the itch in laboratory mice, according to a new report in the journal Cell. "That's exciting because it's a drug that's already approved for another condition, but maybe it could be useful for treating itchy skin diseases like eczema," says Isaac Chiu, a scientist at Harvard Medical School who studies interactions between microbes and nerve cells. He notes that eczema or atopic dermatitis is actually pretty common, affecting about 20% of children and 10% of adults. In the past, says Chiu, research on itchy skin conditions has focused on the role of the immune response and inflammation in generating the itch sensation. People with eczema often take medications aimed at immune system molecules. But scientists have also long known that people with eczema frequently have skin that's colonized by Staphylococcus aureus, says Chiu, even though it's never been clear what role the bacteria might play in this condition. Chiu's previous lab work had made him realize that bacteria can directly act on nerve cells to cause pain. "So this made us ask: Could certain microbes like Staphylococcus aureus also particularly be in some way linked to itch?" says Chiu. "Is there a role for microbes in talking to itch neurons?" He and his colleagues first found that putting this bacteria on the skin of mice resulted in vigorous scratching by these animals, leading to damaged skin that spread beyond the original exposure site. © 2023 npr

Keyword: Pain & Touch
Link ID: 29022 - Posted: 11.26.2023

By Sandra G. Boodman The first sign of trouble was difficulty reading. In late 2014 Cathy A. Haft, a New York real estate broker who divides her time between Brooklyn and Long Island, thought she needed new glasses. But an eye exam found that her prescription was largely unchanged. Bladder problems came next, followed by impaired balance, intermittent dizziness and unexplained falls. By 2018 Haft, unable to show properties because she was too unsteady on her feet, was forced to retire. For the next four years specialists evaluated her for neuromuscular and balance-related ear problems in an attempt to explain her worsening condition, which came to include cognitive changes her husband feared was Alzheimer’s disease. In August 2022 Haft, by then dependent on a walker, consulted a Manhattan neurosurgeon. After observing her gait and reviewing images from a recent brain scan, he sent her to a colleague. Less than eight weeks later Haft underwent brain surgery for a condition that is frequently unrecognized or misdiagnosed. The operation succeeded in restoring skills that had gradually slipped away, stunting Haft’s life. “It’s pretty astonishing that this disorder is not that uncommon and no one put the pieces together,” she said. In her case a confluence of confounding symptoms, a complex medical history and the possible failure to take a holistic approach may have led doctors to overlook a condition that can sometimes be reversed — with dramatic results.

Keyword: Movement Disorders; Alzheimers
Link ID: 29020 - Posted: 11.26.2023

By Tina Hesman Saey WASHINGTON — Scientists have uncovered a clue about why it takes so long for Huntington’s disease to develop. And they may have a lead on how to stop the fatal brain disease. Huntington’s is caused by a mistakenly repeated bit of a gene called HTT. Until recently, researchers thought the number of repeats a person is born with doesn’t change, though repeats may expand when passed to future generations. But in some brain cells, the repeats can grow over time to hundreds of copies, geneticist Bob Handsaker reported November 2 at the annual meeting of the American Society of Human Genetics. Once the number of repeats passes a certain point, the activity of thousands of other genes in the brain cells changes drastically, leading the cells to die. These findings suggest that adding repeats to the HTT gene in vulnerable brain cells is what is driving Huntington’s disease, says Handsaker, of the Broad Institute of MIT and Harvard in Cambridge, Mass. The research also suggests that preventing the repeats from growing may stop the development of the disease. The new work gives “serious insight into the disease mechanism,” says Russell Snell, a geneticist at the University of Auckland in New Zealand who was not involved in the work. About 41,000 people in the United States have symptomatic Huntington’s disease, and another 200,000 are at risk of developing it. Inheriting just one copy of a repeat-riddled HTT gene produces symptoms. Even though individuals are born with the disease-causing gene, symptoms don’t usually appear until people are in their 30s to 50s. Those symptoms include depression, mood swings, forgetfulness, balance problems, involuntary movements and slurred speech. Eventually, a person with the disease may be paralyzed and can die from complications such as pneumonia or heart failure. © Society for Science & the Public 2000–2023.

Keyword: Huntingtons
Link ID: 29008 - Posted: 11.15.2023

By Veronique Greenwood When someone brushes a hand across your skin, it’s like a breeze blowing through a forest of countless small hairs. Nerves that surround your hair follicles detect that contact, and very far away in your brain, other cells fire. Some of the neurons responding to light contact might make you shiver and give you goose bumps. Some might tell you to move away. Or they might tell you to move closer. Scientists who study the sense of touch have explored which cells bear these messages, and they have made an intriguing discovery: Follicle cells triggered by hair movements release the neurotransmitters histamine and serotonin, chemical messengers linked to biological phenomena as varied as inflammation, muscle contraction and mood changes. The observation, reported in October in the journal Science Advances, lays the groundwork for tracing how gentle touch makes us feel the way it does. Studying hair follicles is challenging, because they begin to decay soon after being removed from the body, said Claire Higgins, a bioengineering professor at Imperial College London and an author of the study. So she and her colleagues went to a hair transplant clinic. There, they were able to look at freshly harvested follicles, which they gently prodded with a very small rod to simulate touch. The scientists knew from work done by other groups that the neurons in the skin surrounding hair follicles are capable of sensing movement. “When you brush your hair, you feel it because the sensory neurons are directly being stimulated,” Dr. Higgins said. But they were curious whether the cells of the follicle itself — the tube from which a hair sprouts — could be contributing to some of the feelings associated with more gentle touch. Not all of the follicle cells had movement sensors, but some did. The researchers identified these and watched them carefully as the rod touched them. “We found that when we stimulated our hair follicle cells, they actually released mood-regulating neurotransmitters serotonin and histamine,” Dr. Higgins said. © 2023 The New York Times Company

Keyword: Pain & Touch; Emotions
Link ID: 28999 - Posted: 11.11.2023

Liam Drew In a laboratory in San Francisco, California, a woman named Ann sits in front of a huge screen. On it is an avatar created to look like her. Thanks to a brain–computer interface (BCI), when Ann thinks of talking, the avatar speaks for her — and in her own voice, too. In 2005, a brainstem stroke left Ann almost completely paralysed and unable to speak. Last year, neurosurgeon Edward Chang, at the University of California, San Francisco, placed a grid of more than 250 electrodes on the surface of Ann’s brain, on top of the regions that once controlled her body, face and larynx. As Ann imagined speaking certain words, researchers recorded her neural activity. Then, using machine learning, they established the activity patterns corresponding to each word and to the facial movements Ann would, if she could, use to vocalize them. The system can convert speech to text at 78 words per minute: a huge improvement on previous BCI efforts and now approaching the 150 words per minute considered average for regular speech1. Compared with two years ago, Chang says, “it’s like night and day”. In an added feat, the team programmed the avatar to speak aloud in Ann’s voice, basing the output on a recording of a speech she made at her wedding. “It was extremely emotional for Ann because it was the first time that she really felt that she was speaking for almost 20 years,” says Chang. This work was one of several studies in 2023 that boosted excitement about implantable BCIs. Another study2 also translated neural activity into text at unprecedented speed. And in May, scientists reported that they had created a digital bridge between the brain and spinal cord of a man paralysed in a cycling accident3. A BCI decoded his intentions to move and directed a spinal implant to stimulate the nerves of his legs, allowing him to walk. © 2023 Springer Nature Limited

Keyword: Brain imaging; Language
Link ID: 28997 - Posted: 11.11.2023

Emily Waltz A highly experimental implant that delivers electrical stimulation to the spinal cord has substantially improved mobility for one man with advanced Parkinson’s disease, according to a report published today in Nature Medicine1. Stimulating spinal cord helps paralysed people to walk again The technology, developed by researchers at the Swiss Federal Institute of Technology in Lausanne (EPFL), enables the man to walk fluidly and to navigate terrain without falling — something he couldn’t do before the treatment. Parkinson’s causes uncontrollable movements and difficulty with coordination that worsens over time. The effects of the treatment have lasted for two years. “There are no therapies to address the severe gait problems that occur at a later stage of Parkinson’s, so it’s impressive to see him walking,” says Jocelyne Bloch, a neurosurgeon at the EPFL and a lead author of the paper. But with only one individual tested, it remains unclear whether the approach will work for other people with the disease. The next step “would be to do a randomized, controlled trial”, says Susan Harkema, a neuroscientist at the University of Louisville in Kentucky who works on stimulation therapy in people with spinal cord injuries. Spinal cord stimulation involves surgically implanting a neuroprosthetic device that delivers pulses of electricity to specific regions of the spinal cord in an effort to activate dysfunctional neural circuits. The technique has been used experimentally to enable people paralysed by spinal cord injury to stand on their own, and even to walk short distances. © 2023 Springer Nature Limited

Keyword: Parkinsons; Robotics
Link ID: 28994 - Posted: 11.08.2023