Chapter 11. Motor Control and Plasticity

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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 Barbara Casassus PARIS—Five public research institutions in France have imposed a 3-month moratorium on the study of prions—a class of misfolding, infectious proteins that cause fatal brain diseases—after a retired lab worker who handled prions in the past was diagnosed with Creutzfeldt-Jakob disease (CJD), the most common prion disease in humans. An investigation is underway to find out whether the patient, who worked at a lab run by the National Research Institute for Agriculture, Food and Environment (INRAE), contracted the disease on the job. If so, it would be the second such case in France in the past few years. In June 2019, an INRAE lab worker named Émilie Jaumain died at age 33, 10 years after pricking her thumb during an experiment with prion-infected mice. Her family is now suing INRAE for manslaughter and endangering life; her illness had already led to tightened safety measures at French prion labs. The aim of the moratorium, which affects nine labs, is to “study the possibility of a link with the [new patient’s] former professional activity and if necessary to adapt the preventative measures in force in research laboratories,” according to a joint press release issued by the five institutions yesterday. “This is the right way to go in the circumstances,” says Ronald Melki, a structural biologist at a prion lab jointly operated by the French national research agency CNRS and the French Alternative Energies and Atomic Energy Commission (CEA). “It is always wise to ask questions about the whole working process when something goes wrong.” "The occurrence of these harsh diseases in two of our scientific colleagues clearly affects the whole prion community, which is a small 'familial' community of less than 1000 people worldwide," Emmanuel Comoy, deputy director of CEA's Unit of Prion Disorders and Related Infectious Agents, writes in an email to Science. Although prion research already has strict safety protocols, "it necessarily reinforces the awareness of the risk linked to these infectious agents," he says. © 2021 American Association for the Advancement of Science.

Keyword: Prions
Link ID: 27925 - Posted: 07.28.2021

By Pam Belluck He has not been able to speak since 2003, when he was paralyzed at age 20 by a severe stroke after a terrible car crash. Now, in a scientific milestone, researchers have tapped into the speech areas of his brain — allowing him to produce comprehensible words and sentences simply by trying to say them. When the man, known by his nickname, Pancho, tries to speak, electrodes implanted in his brain transmit signals to a computer that displays his intended words on the screen. His first recognizable sentence, researchers said, was, “My family is outside.” The achievement, published on Wednesday in the New England Journal of Medicine, could eventually help many patients with conditions that steal their ability to talk. “This is farther than we’ve ever imagined we could go,” said Melanie Fried-Oken, a professor of neurology and pediatrics at Oregon Health & Science University, who was not involved in the project. Three years ago, when Pancho, now 38, agreed to work with neuroscience researchers, they were unsure if his brain had even retained the mechanisms for speech. “That part of his brain might have been dormant, and we just didn’t know if it would ever really wake up in order for him to speak again,” said Dr. Edward Chang, chairman of neurological surgery at University of California, San Francisco, who led the research. The team implanted a rectangular sheet of 128 electrodes, designed to detect signals from speech-related sensory and motor processes linked to the mouth, lips, jaw, tongue and larynx. In 50 sessions over 81 weeks, they connected the implant to a computer by a cable attached to a port in Pancho’s head, and asked him to try to say words from a list of 50 common ones he helped suggest, including “hungry,” “music” and “computer.” As he did, electrodes transmitted signals through a form of artificial intelligence that tried to recognize the intended words. © 2021 The New York Times Company

Keyword: Brain imaging; Language
Link ID: 27913 - Posted: 07.17.2021

By Emily Anthes Johnson & Johnson’s beleaguered Covid-19 vaccine may be associated with a small increased risk of Guillain–Barré syndrome, a rare but potentially serious neurological condition, federal officials said on Monday. The Food and Drug Administration has added a warning about the potential side effect to its fact sheets about the vaccine. The risk appears to be very small. So far, there have been 100 reports of the syndrome in people who had received the Johnson & Johnson vaccine. Nearly 13 million doses of the vaccine have been administered in the United States. Here are answers to some common questions about the syndrome and its connection to vaccination. What is Guillain-Barré syndrome? Guillain-Barré is a rare condition in which the body’s immune system attacks nerve cells. It can cause muscle weakness and paralysis. Although the symptoms often pass within weeks, in some cases, the condition can cause permanent nerve damage. In the United States, there are typically 3,000 to 6,000 cases of the syndrome per year, according to the Centers for Disease Control and Prevention. It is most common in adults over 50. The precise cause of the syndrome is unknown, but in many cases the condition follows another illness or infection, such as the flu. It has also been reported in people with Covid-19. This is not the first vaccine that has been linked to Guillain-Barré, although the risk appears to be tiny. A large swine flu vaccination campaign in 1976 led to a small uptick in the incidence of syndrome; the vaccine caused roughly one extra case of Guillain-Barré for every 100,000 people vaccinated. The seasonal flu shot is associated with roughly one to two additional cases for every million vaccines administered. © 2021 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27909 - Posted: 07.14.2021

By Lisa Sanders, M.D. The 22-year-old man struggled to get out of bed. The E.M.T.s were just outside his door, if he could only get there. The previous day he felt that he was coming down with something. Normally he never took naps, but that afternoon, he returned from class feeling completely wiped out and slept long and hard. Yet when he awoke, he felt even worse. Every muscle was sore. He felt feverish. This must be the flu, he told himself. He had the flu shot before starting school that year, but of course no vaccine is 100 percent effective. He spent the rest of that afternoon in bed, too tired and in too much pain to even get up to join his partner for dinner. When he awoke in the middle of the night to go to the bathroom, he was so weak and sore he could hardly sit up. He maneuvered to the edge of the bed and, using the headboard, pulled himself to his feet, but his partner had to help him get to the bathroom. Once he was there, the urine he produced was startlingly dark — the color of Coca-Cola. The next day he felt no better. His partner wanted to stay home with him, but he hurried her off to work. It’s just the flu, he assured her. But as the morning wore on, he started to worry. He called his parents, who were both nurses. They were worried too; influenza can be bad. When he got the same message from a doctor back home in New York, he started wondering if he should go to the hospital. He’d never been this sick before. © 2021 The New York Times Company

Keyword: Muscles; Genes & Behavior
Link ID: 27904 - Posted: 07.14.2021

By Marlene Cimons J. William Langston, who has been studying and treating Parkinson’s disease for nearly 40 years, always has found it striking that so many more men than women show up in his clinic. His observation is not anecdotal. It is grounded in science and shared by many physicians: Men are roughly 1.5 times more likely than women to develop Parkinson’s, a progressive disorder of the nervous system that impairs movement and can erode mental acuity. “It’s a big difference that is quite real,” says Langston, clinical professor of neurology, neuroscience and of pathology at the Stanford University School of Medicine and associate director of the Stanford Udall Center. “It’s pretty dramatic. I think anyone who sees a lot of Parkinson’s will tell you that.” While the disproportionate impact is clear, the reasons for it are not. “It’s a great mystery,” Langston says. Researchers still don’t know what it is that makes men more susceptible to Parkinson’s, or what it is about women that may protect them — or both. But they are trying to find out. “We in the research community have been working for decades to sort this out, but the answers are still elusive,” says Caroline Tanner, a neurology professor in the Weill Institute for Neurosciences at the University of California at San Francisco. “Nevertheless, it’s important to keep at it. We need to understand the mechanisms that underlie the specific differences between men and women so we can apply them to trying to prevent Parkinson’s.” Parkinson’s results from the death of key neurons in the substantia nigra region of the brain that produce the chemical messenger dopamine. Over time, the loss of these nerve cells disrupts movement, diminishes cognition, and can cause other symptoms, such as slurred speech and depression. © 1996-2021 The Washington Post

Keyword: Parkinsons; Sexual Behavior
Link ID: 27892 - Posted: 07.06.2021

Christopher McDermott, MBChB, FRCP, PhD Early in my clinical practice, my team and I subscribed to the traditional view of ALS: the disease was either familial or sporadic. People with “familial” ALS had some family history of ALS (and therefore a possible genetic component), while people with “sporadic” disease did not have a family history.1 But that view began to change with the discovery that mutations (or changes) in a gene called C9orf72 could play a role in both the sporadic and familial types of ALS. Over time, we learned that this one mutation accounted for approximately 40% of familial ALS cases. Even more surprising: it accounted for close to 10% of cases in people with no family history of ALS—people previously believed to have the sporadic form of the disease. As this story unfolded, we began to question our old assumptions about familial and sporadic ALS, and we realized that just asking our patients about their family history wasn’t enough. C9orf72 has been associated with other neurologic diseases as well, so now, I and other ALS specialists understood that someone with a family history of related conditions might also have a genetic cause for their ALS. At the same time, other genetic mutations were being found in people with no family history of the disease and whose ALS had seemingly appeared out of nowhere.1 It was becoming clear that some people with what we often referred to as sporadic ALS could actually have a genetic component to their disease.1 My own research supported this belief. The Sheffield Institute for Translational Neuroscience, where we help develop and study new therapies for neuromuscular diseases, had an extensive biobank of samples from people with ALS. As new genetic mutations were discovered, our researchers tested these samples and found that many people who we thought had sporadic ALS in fact had one or more genetic mutations. © 2013-2021 All rights reserved.

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 27885 - Posted: 07.03.2021

by Rachel Zamzow Most mornings, Huda Zoghbi, 67, climbs a glass-encased, curling staircase to reach her lab on the top and 13th floor of the Jan and Dan Duncan Neurological Research Institute in Houston, Texas. The twisting glass tower, which she designed with a team of architects, echoes the double helix of DNA — a structure that has been central to her career-long quest to uncover genes underlying neurological conditions. As the institute’s director — and as a scientist— she is known for going beyond the standard job description. Genetics researchers often cast a wide net and sequence thousands of genes at a time. But in her prolific career, Zoghbi has focused on a handful of genes, methodically building up an understanding of their function one careful step at a time. Thanks to that approach, Zoghbi has made a number of landmark discoveries, including identifying the genetic roots of Rett syndrome, an autism-related condition that primarily affects girls, as well as the genetic mutations that spur spinocerebellar ataxia, a degenerative motor condition. She has authored more than 350 journal articles. Her accomplishments have earned her almost every major biology and neuroscience research award, including the prestigious Breakthrough Prize in 2017 and the Brain Prize in 2020. “She’s clearly the international leader in the field,” said the late Stephen Warren, professor of human genetics at Emory University in Atlanta, Georgia. Zoghbi never set out to lead a large research center, she says — her heart is in the lab. That said, she has excelled at it: Since the institute’s inception in 2010, it has grown to host more than 200 scientists and fostered more than 70 new disease gene discoveries. © 2021 Simons Foundation

Keyword: Movement Disorders; Development of the Brain
Link ID: 27874 - Posted: 06.26.2021

By Nancy Clanton, Studies have shown COVID-19 can cause brain complications in some patients’ brains, from memory problems to strokes. A new study has found the brains of people who died from COVID-19 were remarkably similar to the brains of people who die from Alzheimer’s and Parkinson’s, showing inflammation and disrupted circuitry, researchers reported. “The brains of patients who died from severe COVID-19 showed profound molecular markers of inflammation, even though those patients didn’t have any reported clinical signs of neurological impairment,” study co-senior author Tony Wyss-Coray, a professor of neurology and neurological sciences at Stanford University, said in a press release. According to Wyss-Coray, about a third of hospitalized COVID-19 patients report neurological symptoms, such as fuzzy thinking, forgetfulness, difficulty concentrating and depression, and these problems continue for long haul patients even when they’ve recovered from COVID. For their study, his team analyzed brain tissue from eight people who died of COVID-19 and 14 who died of other causes. The researchers found significant inflammation in the brains of the deceased COVID-19 patients. However, their brain tissue showed no signs of SARS-CoV-2, the virus that causes COVID-19. Wyss-Coray added that scientists disagree about whether the virus is present in COVID-19 patients’ brains. © 2021 The Atlanta Journal-Constitution.

Keyword: Parkinsons; Alzheimers
Link ID: 27871 - Posted: 06.23.2021

Adrienne Matei Asked about the future of Parkinson’s disease in the US, Dr Ray Dorsey says, “We’re on the tip of a very, very large iceberg.” Dorsey, a neurologist at the University of Rochester Medical Center and author of Ending Parkinson’s Disease, believes a Parkinson’s epidemic is on the horizon. Parkinson’s is already the fastest-growing neurological disorder in the world; in the US, the number of people with Parkinson’s has increased 35% the last 10 years, says Dorsey, and “We think over the next 25 years it will double again.” Most cases of Parkinson’s disease are considered idiopathic – they lack a clear cause. Yet researchers increasingly believe that one factor is environmental exposure to trichloroethylene (TCE), a chemical compound used in industrial degreasing, dry-cleaning and household products such as some shoe polishes and carpet cleaners. Advertisement Employers think the pandemic was a time for earnest self-improvement. Screw that | Jessa Crispin To date, the clearest evidence around the risk of TCE to human health is derived from workers who are exposed to the chemical in the work-place. A 2008 peer-reviewed study in the Annals of Neurology, for example, found that TCE is “a risk factor for parkinsonism.” And a 2011 study echoed those results, finding “a six-fold increase in the risk of developing Parkinson’s in individuals exposed in the workplace to trichloroethylene (TCE).” Dr Samuel Goldman of The Parkinson’s Institute in Sunnyvale, California, who co-led the study, which appeared in the Annals of Neurology journal, wrote: “Our study confirms that common environmental contaminants may increase the risk of developing Parkinson’s, which has considerable public health implications.” It was off the back of studies like these that the US Department of Labor issued a guidance on TCE, saying: “The Board recommends [...] exposures to carbon disulfide (CS2) and trichloroethylene (TCE) be presumed to cause, contribute, or aggravate Parkinsonism.” © 2021 Guardian News & Media Limited

Keyword: Parkinsons
Link ID: 27856 - Posted: 06.16.2021

Ian Sample Science editor Regular strenuous exercise raises the risk of developing motor neurone disease (MND) in people who are genetically predisposed to the condition, researchers say. Scientists at the University of Sheffield found a causal relationship between high intensity physical activity and the disorder among those already susceptible to the disease. They believe the work marks a major step towards understanding the link between intense exercise, which may contribute to motor neurone injury in certain people, and the neurodegenerative disease, which affects about 5,000 individuals in the UK. “We have suspected for some time that exercise was a risk factor for MND, but until now this link was considered controversial,” said Dr Johnathan Cooper-Knoc, a neurologist at Sheffield. “This study confirms that in some people, frequent strenuous exercise leads to an increase in the risk of MND.” The life-time risk of developing MND is about 1 in 400, but previous studies have suggested it is six times greater in professional football players compared with the general population. A number of high-profile British sportsmen have shared their experience with MND in recent years, including rugby league’s Rob Burrow, rugby union’s Doddie Weir and the the footballer Stephen Darby. The Sheffield researchers emphasise that the vast majority of people who undertake vigorous exercise do not develop MND, and that their next step is to develop tests that identify people most at risk. © 2021 Guardian News & Media Limited

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27848 - Posted: 06.11.2021

By Nayef Al-Rodhan o In Chile, the National Commission for Scientific and Technological Research has begun to debate a “neurorights” bill to be written into the country’s constitution. The world, and most importantly the OECD, UNESCO and the United Nations, should be watching closely. The Chilean bill sets out to protect the right to personal identity, free will, mental privacy, equitable access to technologies that augment human capacities, and the right to protection against bias and discrimination. The landmark bill would be the first of its kind to pioneer a regulatory framework which protects human rights from the manipulation of brain activity. The relatively nascent concept of neurorights follows a number of recent medical innovations, most notably brain-computer interface technology (BCI), which has the potential to revolutionize the field of neuroscience. BCI-based therapy may be useful for poststroke motor rehabilitation and may be a potential method for the accurate detection and treatment of neurological diseases such as Alzheimer’s. Advocates claim there is therefore a moral imperative to use the technology, given the benefits it could bring; others worry about its ethical, moral and societal consequences. Many (mistakenly) see this process as being potentially undermined by premature governance restrictions, or accuse any mention of brake mechanisms as an exaggerated reaction to an unlikely science-fiction scenario. © 2021 Scientific American

Keyword: Robotics; Consciousness
Link ID: 27841 - Posted: 06.02.2021

By Richard Sima An elephant’s trunk is a marvel of biology. Devoid of any joints or bone, the trunk is an appendage made of pure muscle that is capable of both uprooting trees and gingerly plucking individual leaves and also boasts a sense of smell more powerful than a bomb-sniffing dog’s. Elephants use their trunks in a variety of ways. They use it to drink, store and spray water, and they also blow air through it to communicate — their 110-decibel bellows can be heard for miles. “It’s like a muscular multitool,” said Andrew Schulz, a mechanical engineering doctoral student at the Georgia Institute of Technology. In a study published Wednesday in The Journal of the Royal Society Interface, Mr. Schulz and his colleagues reported on how elephants can use their trunks for yet another function: applying suction to grab food, a behavior previously thought to be exclusive to fishes. Despite the ubiquity of elephants in children’s books and nature documentaries, there are numerous gaps in scientific knowledge about the biomechanics of their trunks that the new study helps fill. For example, the most recent detailed account of elephant trunk anatomy is a hand-drawn monograph that was published in 1908, Mr. Schulz said. Contrary to popular belief, the trunk does not act like a straw. “What they do is actually drink water into their trunk and they store it,” Mr. Schulz said. “So the elephant trunk is actually like a trunk.” Mr. Schulz completed his research in the lab of David Hu, which studies how animals move and function with an eye toward applying the discoveries toward human engineering problems. He said one reason elephants’ anatomy is poorly understood is because they are difficult to work with. © 2021 The New York Times Company

Keyword: Evolution; Learning & Memory
Link ID: 27840 - Posted: 06.02.2021

By Charles Q. Choi Precise control of the tongue is often vital in life, from the way frogs capture flies to human speech (SN: 1/31/17). But much remains unknown about how the brain controls the tongue, given how its quick motions are difficult to track. Now, experiments show that the brain circuits in mice that help the tongue lick water may be the same ones that help primates reach out to grasp objects, scientists report online May 19 in Nature. Using high-speed video, neuroscientist Tejapratap Bollu and colleagues recorded the sides and bottoms of mouse tongues as the rodents drank from a waterspout. With the help of artificial intelligence to develop 3-D simulations of the appendages, the researchers discovered that successful licks required previously unknown corrective movements, too fast to be seen in standard video. These adjustments came after the tongue missed unseen or distant droplets, or when the spout was unexpectedly retracted a millimeter or more. Inhibiting a brain region that controls the body’s voluntary motions impaired these corrections, suggesting this brain area was behind these movements. These newfound corrective motions are similar to ones that primates use when reaching out with their limbs for uncertain targets, the researchers say. Those primate adjustments are also controlled by similar brain circuits as those used by the mice. “This to me shows that mammalian brains use similar principles to control the tongue and the limb,” says Bollu, now at the Salk Institute for Biological Studies in La Jolla, Calif. “Everything we know about reaching in the primates can also be used to understand how the brain controls [tongue] movements.” © Society for Science & the Public 2000–2021.

Keyword: Movement Disorders
Link ID: 27828 - Posted: 05.27.2021

R. Douglas Fields The raging bull locked its legs mid-charge. Digging its hooves into the ground, the beast came to a halt just before it would have gored the man. Not a matador, the man in the bullring standing eye-to-eye with the panting toro was the Spanish neuroscientist José Manuel Rodriguez Delgado, in a death-defying public demonstration in 1963 of how violent behavior could be squelched by a radio-controlled brain implant. Delgado had pressed a switch on a hand-held radio transmitter to energize electrodes implanted in the bull’s brain. Remote-controlled brain implants, Delgado argued, could suppress deviant behavior to achieve a “psychocivilized society.” Unsurprisingly, the prospect of manipulating the human mind with brain implants and radio beams ignited public fears that curtailed this line of research for decades. But now there is a resurgence using even more advanced technology. Laser beams, ultrasound, electromagnetic pulses, mild alternating and direct current stimulation and other methods now allow access to, and manipulation of, electrical activity in the brain with far more sophistication than the needlelike electrodes Delgado stabbed into brains. Billionaires Elon Musk of Tesla and Mark Zuckerberg of Facebook are leading the charge, pouring millions of dollars into developing brain-computer interface (BCI) technology. Musk says he wants to provide a “superintelligence layer” in the human brain to help protect us from artificial intelligence, and Zuckerberg reportedly wants users to upload their thoughts and emotions over the internet without the bother of typing. But fact and fiction are easily blurred in these deliberations. How does this technology actually work, and what is it capable of? All Rights Reserved © 2021

Keyword: Robotics; Attention
Link ID: 27827 - Posted: 05.19.2021

By Lisa Sanders, M.D. “I can’t move my legs,” the 26-year-old man told his younger brother, who towered above him as he lay sprawled on the floor. He’d been on his computer for hours, he explained, and when he tried to stand up, he couldn’t. His legs looked normal, felt normal, yet they wouldn’t move. At first, he figured his legs must have fallen asleep. He pulled himself up, leaning on his desk, and slowly straightened until he was standing. He could feel the weight on his feet and knees. He let go of the desk and commanded his legs to move. Instead, they buckled, and he landed on the floor with a thud. His brother awkwardly pulled him onto the bed. Then they waited. Surely this weird paralysis would disappear just as suddenly as it came. An hour passed, then two. I’m calling an ambulance, the younger brother announced finally. Reluctantly, the elder agreed. He was embarrassed to be this helpless but worried enough to want help. When the E.M.T.s arrived, they were as confused as the brothers. The medics asked what the young man had been up to. Nothing bad, he assured them. For the past few weeks he had been getting back into shape. He changed his diet, cut out the junk and was drinking a protein concoction that was supposed to help him build muscle. And he was working out hard every day. He’d lost more than 20 pounds, he added proudly. © 2021 The New York Times Company

Keyword: Movement Disorders; Hormones & Behavior
Link ID: 27813 - Posted: 05.12.2021

Diana Kwon Two pharmaceutical companies have halted clinical trials of gene-targeting therapies for Huntington’s disease (HD), following the drugs’ disappointing performance. Researchers had hoped that the treatments — known as antisense oligonucleotides (ASOs) — would be a game changer for HD, an incurable genetic condition that affects cognition, behaviour and movement. But back-to-back announcements from Roche, headquartered in Basel, Switzerland, and Wave Life Sciences, in Cambridge, Massachusetts, have dealt a crushing blow to those affected by the disease. “I was really shocked, really tearful,” says Marion, a woman in London with HD, who was part of one of the trials. “We didn’t see it coming at all. I felt really frightened and worried about my future.” Marion requested that her last name be withheld to protect her privacy. In mid-March, Roche announced that it was halting a phase III study of its ASO drug, tominersen. A week later, Wave Life Sciences said that it would discontinue the development of two of its HD ASOs that were in phase I/II clinical trials. “The Roche trial in particular left the community quite devastated,” says Cath Stanley, chief executive of the Huntington’s Disease Association, a UK advocacy group supporting people with the disease. “There has been so much positive noise around it, both from researchers and clinicians and from the drug company themselves. I think the community was really swept up by that hope.” © 2021 Springer Nature Limited

Keyword: Huntingtons
Link ID: 27811 - Posted: 05.08.2021

By Christine Kenneally The first thing that Rita Leggett saw when she regained consciousness was a pair of piercing blue eyes peering curiously into hers. “I know you, don’t I?” she said. The man with the blue eyes replied, “Yes, you do.” But he didn’t say anything else, and for a while Leggett just wondered and stared. Then it came to her: “You’re my surgeon!” It was November, 2010, and Leggett had just undergone neurosurgery at the Royal Melbourne Hospital. She recalled a surge of loneliness as she waited alone in a hotel room the night before the operation and the fear she felt when she entered the operating room. She’d worried about the surgeon cutting off her waist-length hair. What am I doing in here? she’d thought. But just before the anesthetic took hold, she recalled, she had said to herself, “I deserve this.” Leggett was forty-nine years old and had suffered from epilepsy since she was born. During the operation, her surgeon, Andrew Morokoff, had placed an experimental device inside her skull, part of a brain-computer interface that, it was hoped, would be able to predict when she was about to have a seizure. The device, developed by a Seattle company called NeuroVista, had entered a trial stage known in medical research as “first in human.” A research team drawn from three prominent epilepsy centers based in Melbourne had selected fifteen patients to test the device. Leggett was Patient 14. © 2021 Condé Nast.

Keyword: Robotics; Epilepsy
Link ID: 27791 - Posted: 04.28.2021

By Kathiann Kowalski On most mornings, Jeremy D. Brown eats an avocado. But first, he gives it a little squeeze. A ripe avocado will yield to that pressure, but not too much. Brown also gauges the fruit’s weight in his hand and feels the waxy skin, with its bumps and ridges. “I can’t imagine not having the sense of touch to be able to do something as simple as judging the ripeness of that avocado,” says Brown, a mechanical engineer who studies haptic feedback — how information is gained or transmitted through touch — at Johns Hopkins University. Many of us have thought about touch more than usual during the COVID-19 pandemic. Hugs and high fives rarely happen outside of the immediate household these days. A surge in online shopping has meant fewer chances to touch things before buying. And many people have skipped travel, such as visits to the beach where they might sift sand through their fingers. A lot goes into each of those actions. “Anytime we touch anything, our perceptual experience is the product of the activity of thousands of nerve fibers and millions of neurons in the brain,” says neuroscientist Sliman Bensmaia of the University of Chicago. The body’s natural sense of touch is remarkably complex. Nerve receptors detect cues about pressure, shape, motion, texture, temperature and more. Those cues cause patterns of neural activity, which the central nervous system interprets so we can tell if something is smooth or rough, wet or dry, moving or still. © Society for Science & the Public 2000–2021.

Keyword: Pain & Touch; Robotics
Link ID: 27787 - Posted: 04.24.2021

by Peter Hess Dysfunction in a brain circuit that regulates movement may contribute to some of the motor learning difficulties associated with autism, according to a new mouse study. The mice lack one copy of a chromosomal region called 16p11.2. Up to about one-third of people with this deletion have autism, and some have speech and motor problems. Most autistic people have motor difficulties and show delays in developmental milestones such as standing and walking. The 16p mice, too, are slow to learn new motor tasks, such as balancing on a spinning rod. The explanation seems to be a shortage of the neurotransmitter noradrenaline in the motor cortex, which helps coordinate and execute movements. The dearth originates in the locus coeruleus, a part of the brainstem that serves as the brain’s main source of the chemical. “Noradrenaline is known to be involved in modulating the excitability of neurons,” says lead researcher Simon Chen, assistant professor of cellular and molecular medicine at the University of Ottawa in Ontario, Canada. “When there’s low noradrenaline in the motor cortex and the mouse is learning a movement, it takes them longer for the neural circuits to consolidate neurons that are important to control movement.” The learning process is similar for people, Chen says. When learning how to walk, for instance, a child loses her footing and falls many times. But once in a while, she will take a few more steps than she did in the previous attempt, and the brain remembers the movement that made that possible. © 2021 Simons Foundation

Keyword: Autism; Learning & Memory
Link ID: 27769 - Posted: 04.14.2021