Chloe Tenn On October 4, physiologist David Julius and neurobiologist Arden Patapoutian were awarded the Nobel Prize in Physiology or Medicine for their work on temperature, pain, and touch perception. Julius researched the burning sensation people experience from chilies, and identified an ion channel, TRPV1 that is activated by heat. Julius and Patapoutian then separately reported on the TRPM8 ion channel that senses menthol’s cold in 2002. Patapoutian’s group went on to discover the PIEZO1 and PIEZO2 ion channels that are involved in sensing mechanical pressure. The Nobel Committee wrote that the pair’s work inspired further research into understanding how the nervous system senses temperature and mechanical stimuli and that the laureates “identified critical missing links in our understanding of the complex interplay between our senses and the environment.” This year saw innovations in augmenting the brain’s capabilities by plugging it in to advanced computing technology. For example, a biology teacher who lost her vision 16 years ago was able to distinguish shapes and letters with the help of special glasses that interfaced with electrodes implanted in her brain. Along a similar vein, a computer connected to a brain-implant system discerned brain signals for handwriting in a paralyzed man, enabling him to type up to 90 characters per minute with an accuracy above 90 percent. Such studies are a step forward for technologies that marry cutting-edge neuroscience and computational innovation in an attempt to improve people’s lives. © 1986–2021 The Scientist.

Keyword: Pain & Touch; Language
Link ID: 28134 - Posted: 12.31.2021

By Nicholas Bakalar Need more incentive to get a flu shot, or to keep taking extra precautions this flu season? A new study suggests there may be a link between influenza infection and an increased risk for Parkinson’s disease. For decades, neurologists have suspected there may be a link between the flu and Parkinson’s disease, a chronic and progressive disorder of the nervous system marked by problems with movement, cognitive changes and a range of other symptoms. Several earlier studies, for example, reported a sharp increase in Parkinson’s cases following the 1918 influenza pandemic. Some cases of Parkinson’s have been linked to environmental exposures to pesticides and other toxic chemicals, and genetics may also play a role, but most cases of Parkinson’s have no known cause. Treatments for Parkinson’s can help delay its progression, but there is no known cure. The new study, using Danish health care databases, included 10,231 men and women who had been diagnosed with Parkinson’s between 2000 and 2016. Researchers compared them with 51,196 controls who were matched for age and sex. The researchers tracked influenza infections beginning in 1977 using hospital and outpatient discharge records. The report appeared in JAMA Neurology. Parkinson’s takes years, if not decades, to develop, and initially may produce only subtle symptoms like a hand tremor. It may take years for doctors to diagnose the condition, so any connection between a flu infection and the disease would be evident only many years later. The researchers found that compared with people who had not had a flu infection, those who had the flu had a 70 percent higher risk of Parkinson’s 10 years later, and a 90 percent higher risk 15 years after. © 2021 The New York Times Company

Keyword: Parkinsons
Link ID: 28127 - Posted: 12.29.2021

By Gretchen Reynolds People who work out regularly and are aerobically fit tend to guzzle a surprising amount of alcohol, according to a new study, well timed for the holidays, of the interplay between fitness, exercise and imbibing. The study, which involved more than 40,000 American adults, finds that active, physically fit men and women are more than twice as likely to be moderate or heavy drinkers as people who are out of shape. The results add to mounting evidence from previous studies — and many of our bar tabs — that exercise and alcohol frequently go hand in hand, with implications for the health effects of each. Many people, and some researchers, might be surprised to learn how much physically active people tend to drink. In general, people who take up one healthy habit, such as working out, tend to practice other salubrious habits, a phenomenon known as habit clustering. Fit, active people seldom smoke, for instance, and tend to eat healthful diets. So, it might seem logical that people who often exercise would drink alcohol sparingly. But multiple studies in recent years have found close ties between working out and tippling. In one of the earliest, from 2001, researchers used survey answers from American men and women to conclude that moderate drinkers, defined in that study as people who finished off about a drink a day, were twice as likely as those who didn’t drink at all to exercise regularly. Later studies found similar patterns among college athletes, who drank substantially more than other collegians, a population not famous for its temperance. © 2021 The New York Times Company

Keyword: Drug Abuse; Obesity
Link ID: 28121 - Posted: 12.22.2021

By Cara Giaimo Sign up for Science Times Get stories that capture the wonders of nature, the cosmos and the human body. Get it sent to your inbox. It’s tough out there for a mouse. Outdoors, its enemies lurk on all sides: owls above, snakes below, weasels around the bend. Indoors, a mouse may find itself targeted by broom-wielding humans or bored cats. Mice compensate with sharp senses of sight, hearing and smell. But they may have another set of tools we’ve overlooked. A paper published last week in Royal Society Open Science details striking similarities between the internal structures of certain small mammal and marsupial hairs and those of man-made optical instruments. In this paper as well as other unpublished experiments, the author, Ian Baker, a physicist who works in private industry, posits that these hairs may act as heat-sensing “infrared antennae” — further cluing the animals into the presence of warm-blooded predators. Although much more work is necessary to connect the structure of these hairs to this potential function, the study paints an “intriguing picture,” said Tim Caro, a professor of evolutionary ecology at the University of Bristol in England who was not involved. Dr. Baker has spent decades working with thermal imaging cameras, which visualize infrared radiation produced by heat. For his employer, the British defense company Leonardo UK Ltd., he researches and designs infrared sensors. But in his spare time he often takes the cameras to fields and forests near his home in Southampton, England, to film wildlife. Over the years, he has developed an appreciation for “how comfortable animals are in complete darkness,” he said. That led him to wonder about the extent of their sensory powers. © 2021 The New York Times Company

Keyword: Pain & Touch; Evolution
Link ID: 28120 - Posted: 12.18.2021

Jon Hamilton Scientists may have learned why opioids depress breathing while relieving pain. The finding could lead to pain drugs that don't cause respiratory failure, the usual cause of death in opioid overdoses. When people feel pain, they tend to breathe faster. When they take an opioid to kill that pain, their breathing slows down. Now scientists think they know how pain and respiration are connected in the brain. NPR's Jon Hamilton reports that the discovery could eventually lead to safer pain drugs. JON HAMILTON, BYLINE: Sung Han has been studying the link between pain and breathing in his lab at the Salk Institute in San Diego. But he got a real-world demonstration recently while taking a shower. SUNG HAN: I forgot to change the temperature, and the cold water just suddenly came out and covered my entire body. And then I just - I was breathing really fast. HAMILTON: A typical reaction to what Han calls aversive sensory information - and he thinks he knows the cause. Han's lab has identified a brain circuit in mice that appears to link the emotional experience of pain to breathing rhythm. Han says the circuit involves two populations of brain cells both found in the same small area of the brain stem. HAN: One population regulate pain and the other population regulate breathing, and that's the reason why pain and breathing are interacting each other. HAMILTON: They're linked together. If that's also true in people, it would help explain the mysterious connection between breathing and emotion, which has puzzled scientists for centuries. And the finding, which appears in the journal Neuron, could also have practical applications. That's because both groups of brain cells - the ones for breathing and the ones for pain - respond to opioids. Han says this is why an overdose can be fatal. © 2021 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 28117 - Posted: 12.18.2021

By Lisa Sanders, M.D. The 66-year-old man had just started his third lap at the community swimming pool outside Poughkeepsie, N.Y., when it struck. As he was turning his head to take a breath, an octopus of pain wrapped around the right side of his skull, starting at the joint where the jaw connects and slamming across his face and head with tentacles of squeezing agony. For a moment he was paralyzed — first with pain, then with fear. He couldn’t breathe; he could barely move. He struggled to the side of the pool and hung on, his breath ragged through involuntarily clenched teeth. His wife hurried over. He was a good swimmer; what was wrong? She saw his lips move and leaned closer. His jaw was clenched. “I can’t speak,” he mumbled. She helped him out of the pool. “We’re going to go to urgent care,” she said as she handed him a towel. These strange pains had been tormenting the man for nearly three weeks. It started as a headache that woke him from a dead sleep, a squeezing pressure deep inside his brain. He got up and took some acetaminophen. When he awoke the next morning, the headache was gone, but the regions around his head and face where the pressure had been strongest felt strangely tender. He couldn’t even brush his hair on the right side of his head. Bizarre as this was, he most likely would have soon forgotten about it except that it happened again the next night — and just about every night since. The pain in his jaw started a couple of days later. Opening and closing his mouth, and especially chewing, made his jaw throb. Eating anything more solid than mashed potatoes triggered excruciating pain. He went to his dentist, who poked and prodded. The only tenderness was in the joint where the jaw attached to the skull. It’s most likely TMJ, the dentist concluded — temporomandibular joint pain. That joint and the many attached muscles make speech and facial expressions possible. Lots of people have pain there, the dentist added. Bad habits like jaw-clenching and tooth-grinding aggravate the joint. The treatment is behavior modification to unlearn these habits, and sometimes a bite block, a custom-made piece of acrylic worn at night to protect teeth from injury. © 2021 The New York Times Company

Keyword: Pain & Touch; Neuroimmunology
Link ID: 28113 - Posted: 12.15.2021

By Gretchen Reynolds Staying physically active as we age substantially drops our risk of developing dementia during our lifetimes, and it doesn’t require prolonged exercise. Walking or moving about, rather than sitting, may be all it takes to help bolster the brain, and a new study of octogenarians from Chicago may help to explain why. The study, which tracked how often older people moved or sat and then looked deep inside their brains after they passed away, found that certain vital immune cells worked differently in the brains of older people who were active compared to their more sedentary peers. Physical activity seemed to influence their brain’s health, their thinking abilities and whether they experienced the memory loss of Alzheimer’s disease. The findings add to growing evidence that when we move our bodies, we change our minds, no matter how advanced our age. Already, plenty of scientific evidence indicates that physical activity bulks up our brains. Older, sedentary people who begin walking for about an hour most days, for instance, typically add volume to their hippocampus, the brain’s memory center, reducing or reversing the shrinkage that otherwise commonly occurs there over the years. Active people who are middle-aged or older also tend to perform better on tests of memory and thinking skills than people of the same age who rarely exercise, and are nearly half as likely eventually to be diagnosed with Alzheimer’s disease. Almost as heartening, active people who do develop dementia usually show their first symptoms years later than inactive people do. But precisely how movement remodels our brains is still mostly mysterious, although scientists have hints from animal experiments. When adult lab mice and rats run on wheels, for example, they goose production of hormones and neurochemicals that prompt the creation of new neurons, as well as synapses, blood vessels and other tissues that connect and nurture those young brain cells. © 2021 The New York Times Company

Keyword: Alzheimers
Link ID: 28094 - Posted: 12.01.2021

Riluzole, a drug approved to treat amyotrophic lateral sclerosis (ALS), a disease affecting nerve cells controlling movement, could slow the gradual loss of a particular brain cell that occurs in Niemann-Pick disease type C1 (NPC1), a rare genetic disorder affecting children and adolescents, suggests a study in mice by scientists at the National Institutes of Health. The study was conducted by Forbes D. Porter, M.D., Ph.D., of NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), and colleagues in the National Human Genome Research Institute and National Institute of Arthritis and Musculoskeletal and Skin Disease. It appears in Molecular Genetics and Metabolism. The study was supported in part by a grant from the Ara Parseghian Medical Research Foundation. NPC1 results from an impaired ability to move cholesterol through cells, leading to difficulty controlling movements, liver and lung disease, impaired swallowing, intellectual decline and death. Much of the movement difficulties in NPC1 result from gradual loss of brain cells known as Purkinje neurons. The researchers found that mice with a form of NPC1 have a diminished ability to lower levels of glutamate — a brain chemical that stimulates neurons — after it has bound to a neuron’s surface. High levels of glutamate can be toxic to cells. The researchers believe the buildup of glutamate contributes to the brain cell loss seen in the disease. Riluzole blocks the release of glutamate and hence delays the progression of ALS in people.

Keyword: Movement Disorders
Link ID: 28083 - Posted: 11.20.2021

By David Dobbs Chronic pain is both one of the world’s most costly medical problems, affecting one in every five people, and one of the most mysterious. In the past two decades, however, discoveries about the crucial role played by glia — a set of nervous system cells once thought to be mere supports for neurons — have rewritten chronic pain science. These findings have given patients and doctors a hard-science explanation that chronic pain previously lacked. By doing so, this emerging science of chronic pain is beginning to influence care — not by creating new treatments, but by legitimizing chronic pain so that doctors take it more seriously. Although glia are scattered throughout the nervous system and take up almost half its space, they long received far less scientific attention than neurons, which do the majority of signaling in the brain and body. Some types of glia resemble neurons, with roughly starfish-like bodies, while others look like structures built with Erector sets, their long, straight structural parts joined at nodes. When first discovered in the mid-1800s, glia — from the Greek word for glue — were thought to be just connective tissue holding neurons together. Later they were rebranded as the nervous system’s janitorial staff, as they were found to feed neurons, clean up their waste and take out their dead. In the 1990s they were likened to secretarial staff when it was discovered they also help neurons communicate. Research over the past 20 years, however, has shown that glia don’t just support and respond to neuronal activity like pain signals — they often direct it, with enormous consequences for chronic pain. If you’re hearing this for the first time and you’re one of the billion-plus people on Earth who suffer from chronic pain (meaning pain lasting beyond three to six months that has no apparent cause or has become independent of the injury or illness that caused it), you might be tempted to say that your glia are botching their pain-management job. © 2021 The New York Times Company

Keyword: Pain & Touch; Glia
Link ID: 28075 - Posted: 11.13.2021

By Gina Kolata CAMBRIDGE, Mass. — When Sharif Tabebordbar was born in 1986, his father, Jafar, was 32 and already had symptoms of a muscle wasting disease. The mysterious illness would come to define Sharif’s life. Jafar Tabebordbar could walk when he was in his 30s but stumbled and often lost his balance. Then he lost his ability to drive. When he was 50, he could use his hands. Now he has to support one hand with another. No one could answer the question plaguing Sharif and his younger brother, Shayan: What was this disease? And would they develop it the way their father had? As he grew up and watched his father gradually decline, Sharif vowed to solve the mystery and find a cure. His quest led him to a doctorate in developmental and regenerative biology, the most competitive ranks of academic medical research, and a discovery, published in September in the journal Cell, that could transform gene therapy — medicine that corrects genetic defects — for nearly all muscle wasting diseases. That includes muscular dystrophies that affect about 100,000 people in the United States, according to the Muscular Dystrophy Association. Scientists often use a disabled virus called an adeno-associated virus, or AAV, to deliver gene therapy to cells. But damaged muscle cells like the ones that afflict Dr. Tabebordbar’s father are difficult to treat. Forty percent of the body is made of muscle. To get the virus to those muscle cells, researchers must deliver enormous doses of medication. Most of the viruses end up in the liver, damaging it and sometimes killing patients. Trials have been halted, researchers stymied. Dr. Tabebordbar managed to develop viruses that go directly to muscles — very few end up in the liver. His discovery could allow treatment with a fraction of the dosage, and without the disabling side effects. Dr. Jeffrey Chamberlain, who studies therapies for muscular diseases at the University of Washington and is not involved in Dr. Tabebordbar’s research, said the new method, “could take it to the next level,” adding that the same method also could allow researchers to accurately target almost any tissue, including brain cells, which are only beginning to be considered as gene therapy targets. © 2021 The New York Times Company

Keyword: Movement Disorders; Genes & Behavior
Link ID: 28066 - Posted: 11.06.2021

By James Gallagher An innovative type of medicine - called gene silencing - is set to be used on the NHS for people who live in crippling pain. The drug treats acute intermittent porphyria, which runs in families and can leave people unable to work or have a normal life. Clinical trials have shown severe symptoms were cut by 74% with the drug. While porphyria is rare, experts say the field of gene silencing has the potential to revolutionise medicine. Sisters Liz Gill and Sue Burrell have both had their lives turned around by gene silencing. Before treatment, Liz, from County Durham, remembers the trauma of living in "total pain" and, at its worst, she spent two years paralysed in hospital. Younger sister Sue says she "lost it all overnight" when she was suddenly in and out of hospital, made redundant and did know whether her partner would stick with her (he did). "It was scary," she tells me. Both became used to taking potent opioid painkillers on a daily basis. But even morphine could not block the pain during a severe attack that needed hospital treatment. Gene silencing gets to the root-cause of the sisters' disease rather than just managing their symptoms. Their porphyria leads to a build-up of toxic proteins in the body, that cause the physical pain. Gene silencing "mutes" a set of genetic instructions to block that protein production. Both had been taking the therapy as part of a clinical trial and are still getting monthly injections. © 2021 BBC.

Keyword: Pain & Touch
Link ID: 28046 - Posted: 10.23.2021

Brenda Patoine Science likes to package its successes in neat stories that show a clear progression from this to that. The “bench-to-bedside” story—when biological insights yield targeted treatments—is a long-time favorite. Reality, however, doesn’t always cooperate, and history is littered with basic-science discoveries that seemed important but failed to yield viable treatments. When they do succeed, it’s cause for celebration—and awards. Migraine research is an example. Although it is the second most disabling condition in the world, affecting one billion people, migraine had long been relegated to the backwaters of scientific research. Only recently has research bloomed—scientific papers sharply increased from the 1990s onward, with discoveries in basic science driving a new class of drugs that some in the field are calling game changers. This year, the recognition of four migraine researchers with a major neuroscience award has pushed the field into the limelight of science. The 2021 Brain Prize recognizes science that embodies the so-called bench-to-bedside research described above. That’s a jargony term scientists seem to love that denotes the rare and wonderful occurrence when laboratory research aimed at illuminating fundamental mechanisms (the “bench”) yields insights that lead to drugs that ultimately help millions of sick people (the “bedside”). In the case of migraine research, the leading character is a neuropeptide called calcitonin gene-related peptide (CGRP). © 2021 The Dana Foundation.

Keyword: Pain & Touch
Link ID: 28040 - Posted: 10.16.2021

Jordana Cepelewicz We often appreciate the world around us in terms of its glorious sights, stirring sounds and evocative smells, all of which mark important stimuli and changes in our environment. But senses that are no less crucial to our survival are often taken for granted, including our abilities to register heat, cold and touch, a form of perception called somatosensation. Because of them, we can feel the warmth of the sun or the gentle caress of a breeze against our skin, as well as the positions and movement of our own bodies. In fact, the somatosensory neurons that make all these sensations possible constitute the largest sensory system in mammals. Scientists knew that for somatosensation to occur, there must be molecular receptors on some cells that could detect temperature and touch, and could convert those stimuli into electrical and chemical signals for the nervous system to process. For the discovery of some of those receptors David Julius, a physiologist at the University of California, San Francisco, and Ardem Patapoutian, a molecular biologist and neuroscientist at Scripps Research in La Jolla, have now been awarded the 2021 Nobel Prize in Physiology or Medicine. Julius and his colleagues started with questions about receptors for heat and pain. To find answers, they turned to capsaicin, the compound that causes us to experience a burning and sometimes painful sensation when we eat chili peppers or other spicy food. Based on our physiological response to the chemical, which includes sweating, capsaicin seemed to be inducing the nervous system to register a change in body temperature. To figure out how, Julius and his team screened millions of DNA fragments for a gene that could induce a response to the compound in cells that typically don’t react to it at all. After an arduous search, and what the Nobel Prize committee called “a high-risk project,” the researchers identified a gene that allowed cells to sense capsaicin. It encoded a novel ion channel protein, later called TRPV1, that Julius and his team discovered could be activated by hot temperatures perceived as painful. All Rights Reserved © 2021

Keyword: Pain & Touch
Link ID: 28025 - Posted: 10.06.2021

Amanda Heidt Qin Liu studies sneezing for a personal reason: her entire family suffers from seasonal allergies. “Until you experience something chronically, it is really hard to appreciate how disruptive it can be,” says Liu, a neuroscientist at Washington University in St. Louis. And given the role of sneezing in pathogen transmission, a better understanding of the molecular underpinnings of the phenomenon could one day help scientists mitigate or treat infectious diseases. When Liu first started looking into the mechanisms governing sneezing, she found that scientists know surprisingly little about how this process works. While prior research had identified a region in the brains of cats and humans that is active during sneezing, the exact pathways involved in turning a stimulus like pollen or spicy food into a sneeze remained unknown. To study sneezing in more detail, Liu and her team developed a new model by exposing mice to irritants such as histamine and capsaicin—a chemical in spicy peppers—and characterizing the physical properties of their resulting sneezes. Then, focusing on that previously discovered sneeze center, located in the brain’s ventromedial spinal trigeminal nucleus (SpV), Liu attempted to map the neural pathway. SNEEZE TRIGGER: When exposed to allergens such as histamine or chemical irritants such as capsaicin (1), sensory neurons in the noses of mice produce a peptide called neuromedin B (NMB). This signaling molecule binds to neurons in a region of the brainstem known as the ventromedial spinal trigeminal nucleus (SpV), which is known to be active during sneezing (2). These neurons send electrical signals (3) to neurons in another brainstem region called the caudal ventral respiratory group (cVRG), which controls exhalation, thus driving the initiation and propagation of sneezing (4). Ablating the nasal neurons or disrupting NMB signaling led to a significantly reduced sneezing reflex in the mice. WEB | PDF © 1986–2021 The Scientist.

Keyword: Brain imaging; Pain & Touch
Link ID: 28014 - Posted: 10.02.2021

Abby Olena Delivering anything therapeutic to the brain has long been a challenge, largely due to the blood-brain barrier, a layer of cells that separates the vessels that supply the brain with blood from the brain itself. Now, in a study published August 12 in Nature Biotechnology, researchers have found that double-stranded RNA-DNA duplexes with attached cholesterol can enter the brains of both mice and rats and change the levels of targeted proteins. The results suggest a possible route to developing drugs that could target the genes implicated in disorders such as muscular dystrophy and amyotrophic lateral sclerosis (ALS). “It’s really exciting to have a study that’s focused on delivery to the central nervous system” with antisense oligonucleotides given systemically, says Michelle Hastings, who investigates genetic disease at the Rosalind Franklin University of Medicine and Science in Chicago and was not involved in the study. The authors “showed that it works for multiple targets, some clinically relevant.” In 2015, Takanori Yokota of Tokyo Medical and Dental University and colleagues published a study showing that a so-called heteroduplex oligonucleotide (HDO)—consisting of a short chain of both DNA and an oligonucleotide with modified bases paired with complementary RNA bound to a lipid on one end—was successful at decreasing target mRNA expression in the liver. Yokota’s team later joined forces with researchers at Ionis Pharmaceuticals to determine whether HDOs could cross the blood-brain barrier and target mRNA in the central nervous system. © 1986–2021 The Scientist.

Keyword: Genes & Behavior; ALS-Lou Gehrig's Disease
Link ID: 27998 - Posted: 09.18.2021

By Baland Jalal Obsessive-compulsive disorder (OCD) has puzzled artists and scientists for centuries. Afflicting one in 50 people, OCD can take several forms, such as compulsively putting things in just the right order or checking if the stove is turned off 10 times in a row. One type of OCD that affects nearly half of those with the condition entails irresistible washing urges. People with this type can spend hours scrubbing their hands in agitation after touching something as trivial as a doorknob even though they know this makes no sense. There is currently a shortage of effective therapies for OCD: 40 percent of patients do not benefit from existing treatments. A major issue is that today’s treatments are often too stressful. First-line “nonpharmacological therapies” involve telling patients to repeatedly touch things such as toilet seats and then refrain from washing their hands. But recent work by my colleagues and me has found something surprising: people diagnosed with OCD appear to have a more malleable “sense of self,” or brain-based “self-representation” or “body image”—the feeling of being anchored here and now in one’s body—than those without the disorder. This finding suggests new ways to treat OCD and perhaps unexpected insights into how our brain creates a distinction between “self” and “other.” In our recent experiments, for example, we showed that people with and without OCD responded differently to a well-known illusion. In our first study, a person without OCD watched as an experimenter used a paintbrush to stroke a rubber hand and the subject’s hidden real hand in precise synchrony. This induces the so-called rubber hand illusion: the feeling that a fake hand is your hand. When the experimenter stroked the rubber hand and the real one out of sync, the effect was not induced (or was greatly diminished). This compelling illusion illustrates how your brain creates your body image based on statistical correlations. It’s extremely unlikely for such stroking to be seen on a rubber hand and simultaneously felt on a hidden real one by chance. So your brain concludes, however illogically, that the rubber hand is part of your body. © 2021 Scientific American

Keyword: OCD - Obsessive Compulsive Disorder; Pain & Touch
Link ID: 27980 - Posted: 09.08.2021

Allison Whitten Our mushy brains seem a far cry from the solid silicon chips in computer processors, but scientists have a long history of comparing the two. As Alan Turing put it in 1952: “We are not interested in the fact that the brain has the consistency of cold porridge.” In other words, the medium doesn’t matter, only the computational ability. Today, the most powerful artificial intelligence systems employ a type of machine learning called deep learning. Their algorithms learn by processing massive amounts of data through hidden layers of interconnected nodes, referred to as deep neural networks. As their name suggests, deep neural networks were inspired by the real neural networks in the brain, with the nodes modeled after real neurons — or, at least, after what neuroscientists knew about neurons back in the 1950s, when an influential neuron model called the perceptron was born. Since then, our understanding of the computational complexity of single neurons has dramatically expanded, so biological neurons are known to be more complex than artificial ones. But by how much? To find out, David Beniaguev, Idan Segev and Michael London, all at the Hebrew University of Jerusalem, trained an artificial deep neural network to mimic the computations of a simulated biological neuron. They showed that a deep neural network requires between five and eight layers of interconnected “neurons” to represent the complexity of one single biological neuron. All Rights Reserved © 2021

Keyword: Brain imaging; Vision
Link ID: 27978 - Posted: 09.04.2021

Nicola Davis Premature babies appear to feel less pain during medical procedures when they are spoken to by their mothers, researchers have found. Babies that are born very early often have to spend time in neonatal intensive care units, and may need several painful clinical procedures. The situation can also mean lengthy separation from parents. Now researchers say they have found the sound of a mother’s voice seems to decrease the pain experienced by their baby during medical procedures. Dr Manuela Filippa, of the University of Geneva and first author of the study, said the research might not only help parents, by highlighting that they can play an important role while their baby is in intensive care, but also benefit the infants. Advertisement Last man out: the haunting image of America’s final moments in Afghanistan “We are trying to find non-pharmacological ways to lower the pain in these babies,” she said, adding that there was a growing body of evidence that parental contact with preterm babies could be important for a number of reasons, including attachment. Filippa said the team focused on voice because it was not always possible for parents to hold their babies in intensive care, while voice could be a powerful tool to share emotion. Mothers’ voices were studied in particular because infants would already have heard it in the womb. But Filippa said that did not mean a father’s voice could not become as familiar over time. “We are [also] running studies on fathers’ vocal contacts,” she said. Writing in the journal Scientific Reports, Filippa and colleagues at the University of Geneva, Parini hospital in Italy and the University of Valle d’Aosta, report how they examined the pain responses of 20 premature babies in neonatal intensive care to a routine procedure in which the foot is pricked and a few drops of blood collected. © 2021 Guardian News & Media Limited

Keyword: Pain & Touch; Development of the Brain
Link ID: 27973 - Posted: 09.01.2021

By Christiane Gelitz, Maddie Bender | To a chef, the sounds of lip smacking, slurping and swallowing are the highest form of flattery. But to someone with a certain type of misophonia, these same sounds can be torturous. Brain scans are now helping scientists start to understand why. People with misophonia experience strong discomfort, annoyance or disgust when they hear particular triggers. These can include chewing, swallowing, slurping, throat clearing, coughing and even audible breathing. Researchers previously thought this reaction might be caused by the brain overactively processing certain sounds. Now, however, a new study published in the Journal of Neuroscience has linked some forms of misophonia to heightened “mirroring” behavior in the brain: those affected feel distress while their brains act as if they are mimicking the triggering mouth movements. “This is the first breakthrough in misophonia research in 25 years,” says psychologist Jennifer J. Brout, who directs the International Misophonia Research Network and was not involved in the new study. The research team, led by Newcastle University neuroscientist Sukhbinder Kumar, analyzed brain activity in people with and without misophonia when they were at rest and while they listened to sounds. These included misophonia triggers (such as chewing), generally unpleasant sounds (like a crying baby), and neutral sounds. The brain's auditory cortex, which processes sound, reacted similarly in subjects with and without misophonia. But in both the resting state and listening trials, people with misophonia showed stronger connections between the auditory cortex and brain regions that control movements of the face, mouth and throat. Kumar found this connection became most active in participants with misophonia when they heard triggers specific to the condition. © 2021 Scientific American,

Keyword: Hearing; Attention
Link ID: 27955 - Posted: 08.21.2021

By Sabrina Imbler In a way, nausea is our trusty personal bodyguard. Feeling nauseated is widely accepted to be an evolutionary defense measure that protects people from pathogens and parasites. The urge to gag or vomit is “well-suited” to defend ourselves against things we swallow that might contain pathogens, according to Tom Kupfer, a psychological scientist at Nottingham Trent University in England. But vomiting is somewhat futile against a tick, an ectoparasite that latches on to skin, not stomachs. In an experiment that produced both stomach churning and skin crawling sensations — I can confirm these and some other physiological responses firsthand — Dr. Kupfer and Daniel Fessler, an evolutionary anthropologist from the University of California, Los Angeles, argue in a paper published on Wednesday in the journal Proceedings of the Royal Society B that humans have evolved to defend themselves against ectoparasites through a skin response that elicits scratching. Although some outside experts say more research is needed, the findings align with some understandings of the evolution of disgust. “It makes sense to have developed adaptive defensive strategies against the ‘nasty’ ones,” Cécile Sarabian, a cognitive ecologist studying animal disgust at the Kyoto University Primate Research Institute in Japan, wrote in an email. The disgusting investigation began in 2017 on the grounds of Chicheley Hall in Buckinghamshire, England. Here, Dr. Kupfer was presenting findings to colleagues on trypophobia, the aversion to clustered holes experienced by some people. His data showed that participants with trypophobia often reacted to holey images with the urge to itch or scratch, sometimes to the point of bleeding. Dr. Kupfer suggested that trypophobia might not represent fear, but rather a disgust reaction to signs of parasites or infectious diseases, which can both result in clusters of lesions or pustules.

Keyword: Pain & Touch
Link ID: 27926 - Posted: 07.28.2021