By Priyanka Runwal Researchers have for the first time recorded the brain’s firing patterns while a person is feeling chronic pain, paving the way for implanted devices to one day predict pain signals or even short-circuit them. Using a pacemaker-like device surgically placed inside the brain, scientists recorded from four patients who had felt unremitting nerve pain for more than a year. The devices recorded several times a day for up to six months, offering clues for where chronic pain resides in the brain. The study, published on Monday in the journal Nature Neuroscience, reported that the pain was associated with electrical fluctuations in the orbitofrontal cortex, an area involved in emotion regulation, self-evaluation and decision making. The research suggests that such patterns of brain activity could serve as biomarkers to guide diagnosis and treatment for millions of people with shooting or burning chronic pain linked to a damaged nervous system. “The study really advances a whole generation of research that has shown that the functioning of the brain is really important to processing and perceiving pain,” said Dr. Ajay Wasan, a pain medicine specialist at the University of Pittsburgh School of Medicine, who wasn’t involved in the study. About one in five American adults experience chronic pain, which is persistent or recurrent pain that lasts longer than three months. To measure pain, doctors typically rely on patients to rate their pain, using either a numerical scale or a visual one based on emojis. But self-reported pain measures are subjective and can vary throughout the day. And some patients, like children or people with disabilities, may struggle to accurately communicate or score their pain. “There’s a big movement in the pain field to develop more objective markers of pain that can be used alongside self-reports,” said Kenneth Weber, a neuroscientist at Stanford University, who was not involved in the study. In addition to advancing our understanding of what neural mechanisms underlie the pain, Dr. Weber added, such markers can help validate the pain experienced by some patients that is not fully appreciated — or is even outright ignored — by their doctors. © 2023 The New York Times Company

Keyword: Pain & Touch; Brain imaging
Link ID: 28794 - Posted: 05.23.2023

Katharine Sanderson Researchers have developed an electronic skin that can mimic the same process that causes a finger, toe or limb to move when poked or scalded. The technology could lead to the development of a covering for prosthetic limbs that would give their wearers a sense of touch, or help to restore sensation in people whose skin has been damaged. The ‘e-skin’ was developed in the laboratory of chemical engineer Zhenan Bao at Stanford University in California. Her team has long been trying to make a prosthetic skin that is soft and flexible, but that can also transmit electrical signals to the brain to allow the wearer to ‘feel’ pressure, strain or changes in temperature. The latest work, published on 18 May in Science1, describes a thin, flexible sensor that can transmit a signal to part of the motor cortex in a rat’s brain that causes the animal’s leg to twitch when the e-skin is pressed or squeezed. “This current e-skin really has all the attributes that we have been dreaming about,” says Bao. “We have been talking about it for a long time.” In healthy living skin, mechanical receptors sense information and convert it into electrical pulses that are transmitted through the nervous system to the brain. To replicate this, an electronic skin needs sensors and integrated circuits, which are usually made from rigid semiconductors. Flexible electronic systems are already available, but they typically work only at high voltages that would be unsafe for wearable devices. To make a fully soft e-skin, Bao’s team developed a flexible polymer for use as a dielectric — a thin layer in a semiconductor device that determines the strength of the signal and the voltage needed to run the device. The researchers then used the dielectric to make stretchy, flexible arrays of transistors, combined into a sensor that was thin and soft like skin. © 2023 Springer Nature Limited

Keyword: Pain & Touch; Robotics
Link ID: 28790 - Posted: 05.21.2023

By Meredith Wadman A groundbreaking epidemiological study has produced the most compelling evidence yet that exposure to the chemical solvent trichloroethylene (TCE)—common in soil and groundwater—increases the risk of developing Parkinson’s disease. The movement disorder afflicts about 1 million Americans, and is likely the fastest growing neurodegenerative disease in the world; its global prevalence has doubled in the past 25 years. The report, published today in JAMA Neurology, involved examining the medical records of tens of thousands of Marine Corps and Navy veterans who trained at Marine Corps Base Camp Lejeune in North Carolina from 1975 to 1985. Those exposed there to water heavily contaminated with TCE had a 70% higher risk of developing Parkinson’s disease decades later compared with similar veterans who trained elsewhere. The Camp Lejeune contingent also had higher rates of symptoms such as erectile dysfunction and loss of smell that are early harbingers of Parkinson’s, which causes tremors; problems with moving, speaking, and balance; and in many cases dementia. Swallowing difficulties often lead to death from pneumonia. About 90% of Parkinson’s cases can’t be explained by genetics, but there have been hints that exposure to TCE may trigger it. The new study, led by researchers at the University of California, San Francisco (UCSF), represents by far the strongest environmental link between TCE and the disease. Until now, the entire epidemiological literature included fewer than 20 people who developed Parkinson’s after TCE exposure. The Camp Lejeune analysis “is exceptionally important,” says Briana De Miranda, a neurotoxicologist at the University of Alabama at Birmingham who studies TCE’s pathological impacts in the brains of rats. “It gives us an extremely large population to assess a risk factor in a very carefully designed epidemiological study.”

Keyword: Parkinsons; Neurotoxins
Link ID: 28785 - Posted: 05.18.2023

Scott Hensley In a split vote, advisers to the Food and Drug Administration recommended that the agency approve the first gene therapy for Duchenne muscular dystrophy, the most common form of the genetic illness. The vote, 8 to 6, came after a day of testimony from speakers for Sarepta Therapeutics, the maker of the gene therapy called SRP-9001, FDA scientists and families whose children have Duchenne muscular dystrophy. The question before the panel was whether the benefits for the treatment outweigh the risks. While the FDA is not bound by the recommendations of its outside advisers, it usually follows them. The agency is expected to decide by the end of May. Gene therapy for muscular dystrophy stirs hopes and controversy Duchenne muscular dystrophy is the most common inherited neuromuscular disorder among children. It affects an estimated 10,000 to 12,000 children in the U.S. The genetic condition mainly afflicts boys and leads to progressive muscle damage, loss of ability to movement and eventually death. Sarepta's treatment involves a single infusion of viruses that has been genetically modified to carry a gene to patients' muscles to produce a miniature version of a protein called dystrophin. Patients with Duchenne muscular dystrophy are missing the muscle-protecting protein or don't make enough of it. While not a cure, Sarepta argues that its "micro-dystrophin" treatment can help slow the progression of the disease. The company's request for approval rested mainly on how much micro-dystrophin the treatment produces in patients' muscles instead of waiting for clear, real-world evidence that it's actually helping patients. © 2023 npr

Keyword: Muscles; Movement Disorders
Link ID: 28780 - Posted: 05.13.2023

By Rebecca Robbins The Food and Drug Administration on Tuesday authorized the first drug for a rare genetic form of the neurological disorder A.L.S., despite uncertainty about the treatment’s effectiveness. The decision reflects the agency’s push toward greater flexibility in approving treatments for patients with devastating illnesses and few, if any, options. Biogen, the pharmaceutical company bringing the drug to market, said it would price the drug “within a range comparable to other recently launched A.L.S. treatments.” An A.L.S. therapy approved last year was priced at $158,000 annually. The drug, which is known scientifically as tofersen and will be sold under the brand name Qalsody, targets a mutation in a gene known as SOD1 that is present in about 2 percent of the roughly 6,000 cases of A.L.S. diagnosed in the United States each year. Fewer than 500 people in the United States at any given time are expected to be eligible. The agency authorized the treatment via a policy that allows a drug to be fast-tracked onto the market under certain circumstances before there is conclusive proof that it works. Biogen will be required to provide confirmatory evidence, from ongoing clinical research, to keep the drug on the market. The decision is the first conditional approval granted for a medication for A.L.S., or amyotrophic lateral sclerosis, which generally causes paralysis and death within a few years. Fewer than half the patients eligible for Qalsody survive more than three years after their diagnosis. The approval is based on evidence that the drug can significantly reduce levels of a protein that has been linked to damage to nerve cells. Biogen has argued that these results are reasonably likely to help patients, even though the drug, in a clinical trial, did not significantly slow the progression of the disease, as measured by patients’ ability to speak, swallow and perform other activities of daily living. © 2023 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28753 - Posted: 04.26.2023

By Nora Bradford The classical view of how the human brain controls voluntary movement might not tell the whole story. That map of the primary motor cortex — the motor homunculus — shows how this brain region is divided into sections assigned to each body part that can be controlled voluntarily (SN: 6/16/15). It puts your toes next to your ankle, and your neck next to your thumb. The space each part takes up on the cortex is also proportional to how much control one has over that part. Each finger, for example, takes up more space than a whole thigh. A new map reveals that in addition to having regions devoted to specific body parts, three newfound areas control integrative, whole-body actions. And representations of where specific body parts fall on this map are organized differently than previously thought, researchers report April 19 in Nature. Research in monkeys had hinted at this. “There is a whole cohort of people who have known for 50 years that the homunculus isn’t quite right,” says Evan Gordon, a neuroscientist at Washington University School of Medicine in St. Louis. But ever since pioneering brain-mapping work by neurosurgeon Wilder Penfield starting in the 1930s, the homunculus has reigned supreme in neuroscience. Gordon and his colleagues study synchronized activity and communication between different brain regions. They noticed some spots in the primary motor cortex were linked to unexpected areas involved in action control and pain perception. Because that didn’t fit with the homunculus map, they wrote it off as a result of imperfect data. “But we kept seeing it, and it kept bugging us,” Gordon says. So the team gathered functional MRI data on volunteers as they performed various tasks. Two participants completed simple movements like moving just their eyebrows or toes, as well as complex tasks like simultaneously rotating their wrist and moving their foot from side to side. The fMRI data revealed which parts of the brain activated at the same time as each task was done, allowing the researchers to trace which regions were functionally connected to one another. Seven more participants were recorded while not doing any particular task in order to look at how brain areas communicate during rest. © Society for Science & the Public 2000–2023.

Keyword: Brain imaging
Link ID: 28748 - Posted: 04.22.2023

Max Kozlov The bizarre-looking ‘homunculus’ is one of neuroscience’s most fundamental diagrams. Found in countless textbooks, it depicts a deformed constellation of body parts mapped onto a narrow strip of the brain, showing the corresponding brain regions that control each part. But a study published in Nature1 on 19 April reveals that this brain strip, called the primary motor cortex, is much more complex than the famous diagram suggests. It might coordinate complex movements involving multiple muscles through connections to brain regions responsible for critical thinking, maintaining the body’s physiology and planning actions. The new results could help scientists better understand and treat brain injuries. “This study is very interesting and very important,” says Michael Graziano, a neuroscientist at Princeton University in New Jersey. It’s becoming clear that the primary motor cortex isn’t “just a simple roster of muscles down the brain that control the toes to the tongue”, he says. Little man in the brain The idea of the homunculus dates to the late nineteenth century, when researchers noticed that electrically stimulating the primary motor cortex corresponded to specific body parts twitching. Later work found that some body parts, such as the hands, feet and mouth, took up a disproportionate amount of space in the primary motor cortex compared with the rest of the body. In 1937, these findings culminated with the first publication of the motor homunculus, which translates to ‘little man’ in Latin. Neurosurgeon Wilder Penfield’s 1948 diagram of the motor homunculus (left) shows the areas of the primary motor cortex that control each body part. A new study redraws the diagram (right), adding regions connected to brain areas responsible for coordinating complex movements.Credit: E. Gordon et al./Nature © 2023 Springer Nature Limited

Keyword: Brain imaging
Link ID: 28747 - Posted: 04.22.2023

Asher Mullard The US Food and Drug Administration (FDA) is set to rule soon on the approval of a new drug for a rare form of amyotrophic lateral sclerosis (ALS). The hotly anticipated decision is expected to signpost the agency’s vision for neurological drugs — and its willingness to be flexible in the regulation of these therapeutics. People with the disease desperately need new treatments, because they face a degenerative condition that causes neuronal death and typically leads to fatal respiratory failure within three years of symptoms appearing1. Tofersen, developed by the biotechnology firms Biogen in Cambridge, Massachusetts, and Ionis Pharmaceuticals in Carlsbad, California, did not slow patients’ decline in a phase III trial2. However, some say the trial was too short, and point out that there were signs of possible benefit, such as a reduction in a biomarker of neuronal damage and death called neurofilament light chain (NFL). Because of this, Biogen has asked the FDA to approve the drug on an ‘accelerated’ basis, to fast-track it to patients with a guarantee that future trial data will determine whether it works. If approved, tofersen will become the latest example of the agency’s evolving approach to neurological drug development, which could boost industry investment in brain diseases. A vote of confidence for the drug would also supercharge interest in using NFL as a tool to measure brain health and to test drugs in future. “This could be the start of a new era,” says Valentina Bonetto, a neuroscientist at the Mario Negri Institute for Pharmacological Research in Milan, Italy. In March, the FDA convened a panel to discuss the tofersen data set. Its nine independent advisers rallied behind accelerated approval for the drug, voting unanimously that the available evidence supports a “reasonably likely” chance that tofersen will help people with SOD1 ALS. This rare disease is caused by genetic mutations that affect the protein SOD1, leading it to form toxic clumps in motor neurons in the brain, brainstem and spinal cord. The agency usually follows the recommendations of its advisory committee. © 2023 Springer Nature Limited

Keyword: ALS-Lou Gehrig's Disease ; Neuroimmunology
Link ID: 28744 - Posted: 04.18.2023

By Oliver Whang What is the relationship between mind and body? Maybe the mind is like a video game controller, moving the body around the world, taking it on joy rides. Or maybe the body manipulates the mind with hunger, sleepiness and anxiety, something like a river steering a canoe. Is the mind like electromagnetic waves, flickering in and out of our light-bulb bodies? Or is the mind a car on the road? A ghost in the machine? Maybe no metaphor will ever quite fit because there is no distinction between mind and body: There is just experience, or some kind of physical process, a gestalt. These questions, agonized over by philosophers for centuries, are gaining new urgency as sophisticated machines with artificial intelligence begin to infiltrate society. Chatbots like OpenAI’s GPT-4 and Google’s Bard have minds, in some sense: Trained on vast troves of human language, they have learned how to generate novel combinations of text, images and even videos. When primed in the right way, they can express desires, beliefs, hopes, intentions, love. They can speak of introspection and doubt, self-confidence and regret. But some A.I. researchers say that the technology won’t reach true intelligence, or true understanding of the world, until it is paired with a body that can perceive, react to and feel around its environment. For them, talk of disembodied intelligent minds is misguided — even dangerous. A.I. that is unable to explore the world and learn its limits, in the ways that children figure out what they can and can’t do, could make life-threatening mistakes and pursue its goals at the risk of human welfare. “The body, in a very simple way, is the foundation for intelligent and cautious action,” said Joshua Bongard, a roboticist at the University of Vermont. “As far as I can see, this is the only path to safe A.I.” At a lab in Pasadena, Calif., a small team of engineers has spent the past few years developing one of the first pairings of a large language model with a body: a turquoise robot named Moxie. About the size of a toddler, Moxie has a teardrop-shaped head, soft hands and alacritous green eyes. Inside its hard plastic body is a computer processor that runs the same kind of software as ChatGPT and GPT-4. Moxie’s makers, part of a start-up called Embodied, describe the device as “the world’s first A.I. robot friend.” © 2023 The New York Times Company

Keyword: Intelligence; Robotics
Link ID: 28735 - Posted: 04.12.2023

By Amber Dance Isabelle Lousada was in her early 30s when she collapsed at her Philadelphia wedding in 1995. A London architect, she had suffered a decade of mysterious symptoms: tingling fingers, swollen ankles, a belly distended by her enlarged liver. The doctors she first consulted suggested she had chronic fatigue syndrome or that she’d been partying and drinking too hard. But her new brother-in-law, a cardiologist, felt that something else must be going on. A fresh series of doctor’s visits led, finally, to the proper diagnosis: Malformed proteins had glommed together inside Lousada’s bloodstream and organs. Those giant protein globs are called amyloid, and the diagnosis was amyloidosis. Amyloid diseases that affect the brain, such as Alzheimer’s and Parkinson’s diseases, receive the lion’s share of attention from medical professionals and the press. In contrast, amyloid diseases that affect other body parts are less familiar and rarely diagnosed conditions, says Gareth Morgan, a biochemist at Boston University Chobanian & Avedisian School of Medicine. Physicians may struggle to recognize and distinguish them, especially in early stages. Treatment options have also been limited — Lousada, now CEO of the nonprofit Amyloidosis Research Consortium in Newton, Massachusetts, was fortunate to survive thanks to a stem cell transplant that is too grueling or unsuitable for many with amyloidosis. Several new medications have come out in the last five years — and these, Lousada says, “have been real game-changers.” But although these therapies can block the formation of new, damaging amyloid, they can’t dissolve the amyloid that’s already built up. The body has natural processes to do so, but these are often too slow to clear years’ worth of built-up amyloid, especially in older individuals. And so patients still deal with amyloid clogging their organs, and people still die of amyloidosis, even if they survive longer than they once did. © 2023 Annual Reviews

Keyword: Alzheimers; Parkinsons
Link ID: 28731 - Posted: 04.09.2023

By Lucy Odling-Smee Philip Kass spends 90% of his day lying on a twin bed in a sparsely decorated room that used to belong to his niece. He takes most meals with a plate balanced on his chest, and he usually watches television because reading is too stressful. “I’m barely living,” he told me on a warm night in June last year. Ever since a back injury 23 years ago, pain has been eating away at Kass’s life. It has cost him his career, his relationships, his mobility and his independence. Now 55, Kass lives with his sister and her family in San Francisco, California. He occasionally joins them for dinner, which means he’ll eat while standing. And once a day he tries to walk four or five blocks around the neighbourhood. But he worries that any activity, walking too briskly or sitting upright for more than a few minutes, will trigger a fresh round of torment that can take days or weeks to subside. Philip Kass has dealt with pain for more than two decades. Some of what Kass describes is familiar. I have been pinned to the floor by spinal pain several times in my life. In my twenties, I was immobilized for three months. In my thirties and forties, each episode of severe pain lasted more than a year. I spent at least another half decade standing or pacing through meetings, meals and movies — for fear that even a few minutes spent sitting would result in weeks of disabling pain. For years, I read anything I could find to better understand why my pain persisted.

Keyword: Pain & Touch
Link ID: 28723 - Posted: 03.29.2023

Miryam Naddaf It is thanks to proteins in the nose called odour receptors that we find the smell of roses pleasant and that of rotting food foul. But little is known about how these receptors detect molecules and translate them into scents. Now, for the first time, researchers have mapped the precise 3D structure of a human odour receptor, taking a step forwards in understanding the most enigmatic of our senses. The study, published in Nature on 15 March1, describes an olfactory receptor called OR51E2 and shows how it ‘recognizes’ the smell of cheese through specific molecular interactions that switch the receptor on. “It’s basically our first picture of any odour molecule interacting with one of our odour receptors,” says study co-author Aashish Manglik, a pharmaceutical chemist at the University of California, San Francisco. Smell mystery The human genome contains genes encoding 400 olfactory receptors that can detect many odours. Mammalian odour-receptor genes were first discovered in rats by molecular biologist Richard Axel and biologist Linda Buck in 19912. Researchers in the 1920s estimated that the human nose could discern around 10,000 smells3, but a 2014 study suggests that we can distinguish more than one trillion scents4. Each olfactory receptor can interact with only a subset of smelly molecules called odorants — and a single odorant can activate multiple receptors. It is “like hitting a chord on a piano”, says Manglik. “Instead of hitting a single note, it’s a combination of keys that are hit that gives rise to the perception of a distinct odour.” Beyond this, little is known about exactly how olfactory receptors recognize specific odorants and encode different smells in the brain. Technical challenges in producing mammalian olfactory-receptor proteins using standard laboratory methods have made it difficult to study how these receptors bind to odorants. © 2023 Springer Nature Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 28710 - Posted: 03.18.2023

ByClaudia Lopez Lloreda Peanuts have a dark side. In some people, they can cause a dangerous and sometimes deadly allergic reaction marked by a sharp drop in body temperature and blood pressure, as well as difficulty breathing. This anaphylactic shock has typically been blamed on the immune system going into overdrive. But a new study in mice pegs an additional culprit: the nervous system. The findings, reported today in Science Immunology, “are line with what people thought but no one was actually able to demonstrate,” says Sebastien Talbot, a neuroimmunologist at Queen’s University who was not involved in the study. The work, he says, could open up new targets to treat severe allergic reactions in people. Anaphylaxis strikes about one in 50 individuals in the United States every year. Besides peanuts, bee stings and some medicines are common triggers. These allergens cause the immune system’s mast cells to release a barrage of histamine and other molecules that spread throughout the body, dilating blood vessels and narrowing airways. Body temperature can also drop, making people feel cold and clammy, though why this happens has been less clear. Mice experience anaphylaxis, too. When exposed to an allergen, they lie on their bellies and stretch out. Such behaviors are controlled by the central nervous system, which made Soman Abraham, an immunologist at Duke University, suspect nerves may also play a role in severe allergic reactions. To find out, he and colleagues gave the mice ovalbumin—the main protein found in egg whites and a known trigger of anaphylaxis—and used electrodes and microscopy to record and measure neuron activity. As in humans, the rodents’ body temperature dropped—about 10°C. But the mice’s brains didn’t register this as a sudden freeze; instead, brain areas that typically respond to heat had higher levels of activity. This false feeling of warmth explains why the animals stretch out as if they’re overheating even as their body temperature drops.

Keyword: Neuroimmunology
Link ID: 28706 - Posted: 03.18.2023

By Christina Jewett The Food and Drug Administration has approved a Pfizer nasal spray for treatment of migraines that uses a different therapy from other nasal products on the market for severe headache pain, the company said on Friday. The fast-acting treatment, which is called zavegepant and will be sold as Zavzpret, performed better than a placebo in relieving pain and patients’ most bothersome symptoms, according to clinical trial results published in the journal Lancet Neurology. Participants in the trial who took the medication were more likely to report returning to normal function 30 minutes to two hours after taking it. The gains, though, were not significant for every patient. A study tracked the experience of 1,269 patients — half on the drug and half on a placebo — focusing on how they reported feeling two hours after using either substance. About 24 percent on the medication reported freedom from pain, compared to about 15 percent who took a placebo, according to the study. Dr. Timothy A. Collins, chief of the headache division at Duke University Medical Center’s neurology department, said the product gave doctors a new option in a nasal spray format that patients with migraines tended to appreciate. He said the condition often comes with nausea, so swallowing a pill can be unpleasant. He also said the drug presented few side effects, like drowsiness, that had been reported with other products. “We’ve been waiting for this medication to come out,” Dr. Collins said. “It’s a really helpful addition to migraine management.” One additional upside of the medication is that it’s safe for patients who have had a heart attack or a stroke, he added. Pfizer said the medication would be available in pharmacies in July, but did not disclose the estimated price of the new spray. The company estimated that nearly 40 million people in the United States suffered from migraines each year. © 2023 The New York Times Company

Keyword: Pain & Touch
Link ID: 28701 - Posted: 03.15.2023

By Darren Incorvaia Sitting in an exam room, surrounded by doctors and scientists, Heather Rendulic opened her left hand for the first time since suffering a series of strokes nine years earlier when she was in her early 20s. “It was an amazing feeling for me to be able to do that again,” Rendulic says. “It’s not something I ever thought was possible.” But immediately after a surgically implanted device sent electrical pulses into her spinal cord, Rendulic could not only open her hand but also showed other marked improvements in arm mobility, researchers report February 20 in Nature Medicine. “We all started crying,” Marco Capogrosso, a neuroscientist at the University of Pittsburgh, said in a February 15 news conference. “We didn’t really expect this could work as fast as that.” The approach is similar to that recently used for patients paralyzed by spinal cord injuries (SN: 08/03/22). It represents a promising new technique for restoring voluntary movement to those left with upper-body paralysis following strokes, the team says. A stroke occurs when blood supply to parts of the brain is cut off, often causing short-term or long-term issues with movement, speech and vision. Stroke is a leading, and often underappreciated, cause of paralysis; in the United States alone, 5 million people are living with some form of motor deficit due to stroke. While physical therapy can provide some improvements, no treatment exists to help these patients regain full control of their limbs — and their lives. Strokes cause paralysis because the connection between the brain and the spinal cord is damaged; the brain tries to tell the spinal cord to move certain muscles, but the message is muddled. © Society for Science & the Public 2000–2023.

Keyword: Stroke; Robotics
Link ID: 28678 - Posted: 02.22.2023

Max Kozlov A group of brain cells in mice becomes active both when the animals fight and when they watch other mice fight, a study1 shows. The work hints that such ‘mirror neurons’, which fire when an animal either observes or takes part in a particular activity, could shape complex social behaviours, such as aggression. The mirror neurons described in the study are the first to be found in the hypothalamus, an evolutionarily ancient brain region — suggesting that mirror neurons’ original purpose might have been to enhance defence and, ultimately, reproductive success, the authors speculate. The study was published in Cell on 15 February. “We’ve now shown that mirror neurons functionally participate in the behaviours they’re mirroring,” says Nirao Shah, a neuroscientist at Stanford University in California who co-authored the study. “That changes what we think about mirror neurons.” First identified in monkeys in the 1990s, mirror neurons generally fire when an animal takes a certain action, but they also fire when it sees another animal perform the same action. Previous work has linked mirror neurons’ activity to simple behaviours, such as reaching for an object, but not to complex social behaviours, such as fighting. But exactly how mirror-neuron activity contributes to cognitive functions has been controversial, says Pier Francesco Ferrari, a neuroethologist at the Institute of Cognitive Science Marc Jeannerod in Lyon, France. Some researchers have argued that the fact that mirror neurons fire both when an animal observes a behaviour and when it performs that behaviour itself shows that these neurons are involved in a higher-order awareness of others’ actions — and perhaps even contribute to empathy. But others say that there is little evidence to support this theory. © 2023 Springer Nature Limited

Keyword: Aggression; Attention
Link ID: 28674 - Posted: 02.18.2023

By Diana Kwon Alan Alda was running for his life. The actor, best known for his role on the television series M*A*S*H, wasn’t on a set. This threat was real—or at least it felt that way. So when he saw a bag of potatoes in front of him, he grabbed it and threw it at his attacker. Suddenly, the scene shifted. He was in his bedroom, having lurched out of sleep, and the sack of potatoes was a pillow he’d just chucked at his wife. Acting out dreams marks a disorder that occurs during the rapid eye movement (REM) phase of sleep. Called RBD, for REM sleep behavior disorder, it affects an estimated 0.5 to 1.25 percent of the general population and is more commonly reported in older adults, particularly men. Apart from being hazardous to dreamers and their partners, RBD may foreshadow neurodegenerative disease, primarily synucleinopathies—conditions in which the protein α-synuclein (or alpha-synuclein) forms toxic clumps in the brain. Not all nocturnal behaviors are RBD. Sleepwalking and sleep talking, which occur more often during childhood and adolescence, take place during non-REM sleep. This difference is clearly distinguishable in a sleep laboratory, where clinicians can monitor stages of sleep to see when a person moves. Nor is RBD always associated with a synucleinopathy: it can also be triggered by certain drugs such as antidepressants or caused by other underlying conditions such as narcolepsy or a brain stem tumor. When RBD occurs in the absence of these alternative explanations, the chance of future disease is high. Some epidemiological studies suggest that enacted dreaming predicts a more than 80 percent chance of developing a neurodegenerative disease within the patient’s lifetime. It may also be the first sign of neurodegenerative disease, which on average shows up within 10 to 15 years after onset of the dream disorder. One of the most common RBD-linked ailments is Parkinson’s disease, characterized mainly by progressive loss of motor control. Another is Lewy body dementia, in which small clusters of α-synuclein called Lewy bodies build up in the brain, disrupting movement and cognition. A third type of synucleinopathy, multiple system atrophy, interferes with both movement and involuntary functions such as digestion. RBD is one of the strongest harbingers of future synucleinopathy, more predictive than other early markers such as chronic constipation and a diminished sense of smell.

Keyword: Parkinsons; Sleep
Link ID: 28642 - Posted: 01.25.2023

ByMeredith Wadman A massive data mining study has found numerous associations between common viruses like the flu and devastating neurodegenerative disorders such as Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease). The findings expand on previous research linking individual viruses to neurological diseases. But experts caution that the study, which relied on electronic medical records rather than biological samples, merely describes correlations and doesn’t prove causation. Still, it’s “really exciting,” says Kristen Funk, a neuroimmunologist who studies Alzheimer’s at the University of North Carolina, Charlotte. Rather than homing in on, say, the relationship between herpes simplex infections and Alzheimer’s—a recent focus in her own field—“this research broadens that scope to look at different viruses and more neurodegenerative diseases.” Scientists have found connections between viruses and neurodegenerative diseases before. Previous studies uncovered ties between the influenza virus and Parkinson’s, for example, and between genital warts (caused by human papillomavirus) and dementia. A landmark project published in Science last year cemented another connection: Epidemiologists who analyzed 2 decades of data from the blood tests of 10 million U.S. soldiers reported that it’s nearly impossible to develop multiple sclerosis without first being infected with the Epstein-Barr virus—a ubiquitous pathogen long suspected of causing MS. Inspired by that paper, National Institutes of Health (NIH) researchers wondered whether they could mine other large databases to tease out more associations. They focused on viral links to six neurodegenerative diseases: Alzheimer’s, Parkinson’s, dementia, ALS, MS, and vascular dementia. (Some scientists dispute that MS and vascular dementia are neurodegenerative diseases.)

Keyword: Alzheimers; Parkinsons
Link ID: 28638 - Posted: 01.25.2023

By Tom Siegfried Survival of the fittest often means survival of the fastest. But fastest doesn’t necessarily mean the fastest moving. It might mean the fastest thinking. When faced with the approach of a powerful predator, for instance, a quick brain can be just as important as quick feet. After all, it is the brain that tells the feet what to do — when to move, in what direction, how fast and for how long. And various additional mental acrobatics are needed to evade an attacker and avoid being eaten. A would-be meal’s brain must decide whether to run or freeze, outrun or outwit, whether to keep going or find a place to hide. It also helps if the brain remembers where the best hiding spots are and recalls past encounters with similar predators. All in all, a complex network of brain circuitry must be engaged, and neural commands executed efficiently, to avert a predatory threat. And scientists have spent a lot of mental effort themselves trying to figure out how the brains of prey enact their successful escape strategies. Studies in animals as diverse as mice and crabs, fruit flies and cockroaches are discovering the complex neural activity — in both the primitive parts of the brain and in more cognitively advanced regions — that underlies the physical behavior guiding escape from danger and the search for safety. Lessons learned from such studies might not only illuminate the neurobiology of escape, but also provide insights into how evolution has shaped other brain-controlled behaviors. This research “highlights an aspect of neuroscience that is really gaining traction these days,” says Gina G. Turrigiano of Brandeis University, past president of the Society for Neuroscience. “And that is the idea of using ethological behaviors — behaviors that really matter for the biology of the animal that’s being studied — to unravel brain function.” © 2022 Annual Reviews

Keyword: Aggression; Attention
Link ID: 28609 - Posted: 12.24.2022

By Christina Jewett and Cade Metz A jumble of cords and two devices the size of soda cans protrude from Austin Beggin’s head when he undergoes testing with a team of researchers studying brain implants that are meant to restore function to those who are paralyzed. Despite the cumbersome equipment, it is also when Mr. Beggin feels the most free. He was paralyzed from the shoulders down after a diving accident eight years ago, and the brain device picks up the electrical surges that his brain generates as he envisions moving his arm. It converts those signals to cuffs on the major nerves in his arm. They allow him to do things he had not done on his own since the accident, like lift a pretzel to his mouth. “This is like the first time I’ve ever gotten the opportunity or I’ve ever been privileged and blessed enough to think, ‘When I want to open my hand, I open it,’” Mr. Beggin, 30, said. Days like that are always “a special day.” The work at the Cleveland Functional Electrical Stimulation Center represents some of the most cutting-age research in the brain-computer interface field, with the team connecting the brain to the arm to restore motion. It’s a field that Elon Musk wants to advance, announcing in a recent presentation that brain implants from his company Neuralink would someday help restore sight to the blind or return people like Mr. Beggin to “full-body functionality.” Mr. Musk also said the Neuralink device could allow anyone to use phones and other machines with new levels of speed and efficiency. Neuroscientists and Mr. Beggin alike see such giant advances as decades away, though. Scientists who have approval to test such devices in humans are inching toward restoring normal function in typing, speaking and limited movements. Researchers caution that the goal is much harder and more dangerous than it may seem. And they warn that Mr. Musk’s goals may never be possible — if it is even worth doing in the first place. © 2022 The New York Times Company

Keyword: Robotics
Link ID: 28591 - Posted: 12.13.2022