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

By Laura Sanders Like tiny, hairy Yodas raising X-wings from a swamp, rats can lift digital cubes and drop them near a target. But these rats aren’t using the Force. Instead, they are using their imagination. This telekinetic trick, described in the Nov. 3 Science, provides hints about how brains imagine new scenarios and remember past ones. “This is fantastic research,” says Mayank Mehta, a neurophysicist at UCLA. “It opens up a lot of exciting possibilities.” A deeper scientific understanding of the brain area involved in the feat could, for instance, help researchers diagnose and treat memory disorders, he says. Neuroscientist Albert Lee and his colleagues study how brains can go back in time by revisiting memories and jump ahead to imagine future scenarios. Those processes, sometimes called “mental time travel,” are “part of what makes our inner mental lives quite rich and interesting,” says Lee, who did the new study while at Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Va. To dip into these complex questions, the researchers began with a simpler one: “Can you be in one place and think about another place?” says Lee, who is now an HHMI investigator at Beth Israel Deaconess Medical Center in Boston. “The rat isn’t doing anything fancier than that. We’re not asking them to recall their summer vacation.” Neuroscientist and engineer Chongxi Lai, also now at Beth Israel Deaconess, Lee and colleagues trained rats to move on a spherical treadmill in the midst of a 3-D virtual world projected onto a surrounding screen. While the rats poked around their virtual world, electrodes recorded signals from nerve cells in the rats’ hippocampi, brain structures known to hold complex spatial information, among other things (SN: 10/6/14). In this way, researchers matched patterns of brain activity with spots in the virtual world. © Society for Science & the Public 2000–2023.

Keyword: Attention
Link ID: 28988 - Posted: 11.04.2023

By Matt Richtel An Oxford University researcher and her team showed that digital wearable devices can track the progression of Parkinson’s disease in an individual more effectively than human clinical observation can, according to a newly published paper. By tracking more than 100 metrics picked up by the devices, researchers were able to discern subtle changes in the movements of subjects with Parkinson’s, a neurodegenerative disease that afflicts 10 million people worldwide. The lead researcher emphasized that the latest findings were not a treatment for Parkinson’s. Rather, they are a means of helping scientists gauge whether novel drugs and other therapies for Parkinson’s are slowing the progression of the disease. Quotable Quotes The sensors — six per subject, worn on the chest, at the base of the spine and one on each wrist and foot — tracked 122 physiological metrics. Several dozen metrics stood out as closely indicating the disease’s progression, including the direction a toe moved during a step and the length and regularity of strides. “We have the biomarker,” said Chrystalina Antoniades, a neuroscientist at the University of Oxford and the lead researcher on the paper, which was published earlier this month in the journal npj Parkinson’s Disease. “It’s super exciting. Now we hope to be able to tell you: Is a drug working?” Until now, Dr. Antoniades said, drug trials for Parkinson’s had relied on clinical assessment of whether a treatment was slowing the progression of the disease. But clinical observation can miss changes that happen day to day or that might not show up clearly in periodic visits to a doctor, she added. In the paper, the study’s authors concluded that the sensors proved more effective at tracking the disease progression “than the conventionally used clinical rating scales.” © 2023 The New York Times Company

Keyword: Parkinsons
Link ID: 28965 - Posted: 10.17.2023

Marlys Fassett Itching can be uncomfortable, but it’s a normal part of your skin’s immune response to external threats. When you’re itching from an encounter with poison ivy or mosquitoes, consider that your urge to scratch may have evolved to get you to swat away disease-carrying pests. However, for many people who suffer from chronic skin diseases like eczema, the sensation of itch can fuel a vicious cycle of scratching that interrupts sleep, reduces productivity and prevents them from enjoying daily life. This cycle is caused by sensory neurons and skin immune cells working together to promote itching and skin inflammation. But, paradoxically, some of the mechanisms behind this feedback loop also stop inflammation from getting worse. In our newly published research, my team of immunologists and neuroscientists and I discovered that a specific type of itch-sensing neuron can push back on the itch-scratch-inflammation cycle in the presence of a small protein. This protein, called interleukin-31, or IL-31, is typically involved in triggering itching. This negative feedback loop – like the vicious cycle – is only possible because the itch-sensing nerve endings in your skin are closely intertwined with the millions of cells that make up your skin’s immune system. The protein IL-31 is key to the connection between the nervous and immune systems. This molecule is produced by some immune cells, and like other members of this molecule family, it specializes in helping immune cells communicate with each other. © 2010–2023, The Conversation US, Inc.

Keyword: Pain & Touch; Neuroimmunology
Link ID: 28961 - Posted: 10.14.2023

Linda Geddes Science correspondent The former Premier League goalkeeper Brad Friedel once said that to be able to work well in the box, you have to be able to think outside the box. Now scientific data supports the idea that goalies’ brains really do perceive the world differently – their brains appear able to merge signals from the different senses more quickly, possibly underpinning their unique abilities on the football pitch. Goalkeeping is the most specialised position in football, with the primary objective of stopping the opposition from scoring. But while previous studies have highlighted differences in physiological and performance profiles between goalkeepers and other players, far less was known about whether they have different perceptual or cognitive abilities. “Unlike other football players, goalkeepers are required to make thousands of very fast decisions based on limited or incomplete sensory information,” said Michael Quinn, a former goalkeeper in the Irish Premiership, who is now studying for a master’s degree in behavioural neuroscience at University College Dublin. Suspecting that this ability might hinge on an enhanced capacity to combine information from different senses, Quinn and researchers at Dublin City University and University College Dublin recruited 60 professional goalkeepers, outfield players and age-matched non-players to do a series of tests, looking for differences in their ability to distinguish sounds and flashes as separate from one another. Doing so enabled them to estimate volunteers’ temporal binding windows – the timeframe in which different sensory signals are fused together in the brain. The study, published in Current Biology, found that goalkeepers had a narrower temporal binding window relative to outfielders and non-soccer players. © 2023 Guardian News & Media Limited

Keyword: Attention; Vision
Link ID: 28954 - Posted: 10.10.2023

Regina G. Barber Ever had an itch you can't scratch? Maybe it's out of reach, or your hands are full, or you don't want to damage your skin. It can be deeply frustrating. And even though the itch response, or what scientists refer to simply as "itch," has a purpose — it's one of our bodies' alert systems — it can also go very wrong. The importance of a regular itch Itch is evolution's way of drawing our attention to something on our skin that needs removing. This could be a stinging bug, a nesting parasite or an irritating plant (poison ivy, anyone?!). All these things urge us to scratch, which generally removes the threat and soothes the itch. "We know that itch can activate sensory neurons and the signal will be transmitted to the brain. When we scratch the skin, somehow other neural circuits will be activated. And these neural circuits will suppress the itch circuits and alleviate the itch sensation," says Qin Liu, a neuroscientist at the Washington University School of Medicine in St. Louis. Because the itch sensation has separate neural circuitry from temperature, pressure and pain, applying pressure or ice or scratching can relieve an itch. They're effective neural distractions. Oftentimes, when someone experiences hives or an insect bite, histamine is involved, a chemical released by our immune system that can contribute to itchiness. So relieving that itch only requires antihistamine medication. "But most other forms of itch, like atopic dermatitis, eczema, other conditions, they don't actually have a pathway for histamine as the itch mediator," says Kwatra. © 2023 npr

Keyword: Pain & Touch
Link ID: 28929 - Posted: 09.27.2023

By Jocelyn Kaiser Parkinson’s disease, a brain disorder that gradually leads to difficulty moving, tremors, and usually dementia by the end, is often difficult to diagnose early in its yearslong progression. That makes testing experimental treatments challenging and slows people from getting existing drugs, which can’t stop the ongoing death of brain cells but temporarily improve many of the resulting symptoms. Now, a study using rodents and tissue from diagnosed Parkinson’s patients suggests DNA damage spotted in blood samples offers a simple way to diagnose the disease early. Although the potential test needs to be validated in clinical studies, the detected DNA damage joins a “flurry” of other biomarkers recently identified for Parkinson’s and “adds to our ability to state confidently that an individual has Parkinson’s disease or not,” says neurodegeneration researcher Mark Cookson of the National Institute on Aging, whose grantmaking arm helped fund the new work, published today in Science Translational Medicine. A blood test based on the findings could also help patients go on existing treatments earlier and boost clinical trials evaluating new therapies, the study’s authors say. “It’s really exciting because it’s something [physicians] could use to detect [Parkinson’s] before the clinical symptoms emerge,” says neuroscientist Malú Tansey of the University of Florida, who also was not involved with the research. Parkinson’s occurs when the death of certain neurons in the brain causes levels of the neurotransmitter dopamine to drop, leading to muscle stiffness, balance problems, speech and cognitive problems, and other symptoms over time. The disorder, tied to both environmental and genetic factors, afflicts up to 1 million people in the United States.

Keyword: Parkinsons
Link ID: 28897 - Posted: 09.07.2023