Chapter 5. The Sensorimotor System

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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 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

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 Tom Zeller Jr. I have headaches. Not the low-grade, annoying, “I’ve got a headache” sort of headaches. I get those, too. Most everyone does, and they are a drag. No, when I say that I get headaches, I mean that at intervals that are largely unpredictable, a knot of pain rises deep inside my head, invariably sensed behind my right eyeball. It then swiftly clicks up through the intensity scale, racing past that dull ache you might get from staring at the screen too long, leapfrogging over that doozy you had the morning after your brother’s wedding, skipping past the agonizing-but-fleeting stab of an ice-cream headache, and arriving, within a matter of minutes, at a pain so piercing and sustained that I can only grip something sturdy, rock back and forth, and grunt until it subsides. Mine are what doctors call one of the “primary headaches” — recurring and often excruciating disorders that are not byproducts of another condition (or self-inflicted by last night’s cocktails), but relentless, and in many ways still poorly understood disorders unto themselves. We know them by common names like migraine, which affects tens of millions of Americans, disproportionately women. I suffer from another flavor known as cluster headaches (technically “trigeminal autonomic cephalalgias”). And there are others, with myriad and imperfectly drawn lines distinguishing them. If you experience migraines or cluster headaches — and research suggests that more than a billion people worldwide do — you probably know something about shuttling from doctor to doctor looking for someone who “gets it.” You know what it’s like to gladly gobble up pills that don’t really work and that leave you miserable in other ways. And you might even know the same sort of incredulous exasperation that has driven me to wonder, from my fetal position on the bathroom floor: “How is it possible that science can’t fix a damn headache?” © 2021 The New York Times Company

Keyword: Pain & Touch
Link ID: 27924 - Posted: 07.24.2021

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

Elena Renken For decades, neuroscientists have treated the brain somewhat like a Geiger counter: The rate at which neurons fire is taken as a measure of activity, just as a Geiger counter’s click rate indicates the strength of radiation. But new research suggests the brain may be more like a musical instrument. When you play the piano, how often you hit the keys matters, but the precise timing of the notes is also essential to the melody. “It’s really important not just how many [neuron activations] occur, but when exactly they occur,” said Joshua Jacobs, a neuroscientist and biomedical engineer at Columbia University who reported new evidence for this claim last month in Cell. For the first time, Jacobs and two coauthors spied neurons in the human brain encoding spatial information through the timing, rather than rate, of their firing. This temporal firing phenomenon is well documented in certain brain areas of rats, but the new study and others suggest it might be far more widespread in mammalian brains. “The more we look for it, the more we see it,” Jacobs said. Abstractions navigates promising ideas in science and mathematics. Journey with us and join the conversation. Some researchers think the discovery might help solve a major mystery: how brains can learn so quickly. The phenomenon is called phase precession. It’s a relationship between the continuous rhythm of a brain wave — the overall ebb and flow of electrical signaling in an area of the brain — and the specific moments that neurons in that brain area activate. A theta brain wave, for instance, rises and falls in a consistent pattern over time, but neurons fire inconsistently, at different points on the wave’s trajectory. In this way, brain waves act like a clock, said one of the study’s coauthors, Salman Qasim, also of Columbia. They let neurons time their firings precisely so that they’ll land in range of other neurons’ firing — thereby forging connections between neurons. All Rights Reserved © 2021

Keyword: Brain imaging
Link ID: 27898 - Posted: 07.08.2021

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 Anil Ananthaswamy “Everything became imbued with a sense of vitality and life and vividness. If I picked up a pebble from the beach, it would move. It would glisten and gleam and sparkle and be absolutely captivating,” says neuroscientist Anil Seth. “Somebody looking at me would see me staring at a stone for hours.” Or what seemed like hours to Seth. A researcher at the UK’s University of Sussex, he studies how the brain helps us perceive the world within and without, and is intrigued by what psychedelics such as LSD can tell us about how the brain creates these perceptions. So a few years ago, he decided to try some, in controlled doses and with trusted people by his side. He had a notebook to keep track of his experiences. “I didn’t write very much in the notebook,” he says, laughing. Instead, while on LSD, he reveled in a sense of well-being and marveled at the “fluidity of time and space.” He found himself staring at clouds and seeing them change into faces of people he was thinking of. If his attention drifted, the clouds morphed into animals. Seth went on to try ayahuasca, a hallucinogenic brew made from a shrub and a vine native to South America and often used in shamanistic rituals there. This time, he had a more emotional trip that dredged up powerful memories. Both experiences strengthened Seth’s conviction that psychedelics have great potential for teaching us about the inner workings of the brain that give rise to our perceptions. He’s not alone. Armed with fMRI scans, EEG recordings, computational models of the brain and reports from volunteers tripping on psychedelics, a small but growing number of neuroscientists are trying to take advantage of these drugs and the hallucinations they induce to better understand how the brain produces perceptions. © 2021 Annual Reviews, Inc

Keyword: Drug Abuse; Vision
Link ID: 27883 - Posted: 06.29.2021

By Emily Conover Scientists could be a step closer to understanding how some birds might exploit quantum physics to navigate. Researchers suspect that some songbirds use a “quantum compass” that senses the Earth’s magnetic field, helping them tell north from south during their annual migrations (SN: 4/3/18). New measurements support the idea that a protein in birds’ eyes called cryptochrome 4, or CRY4, could serve as a magnetic sensor. That protein’s magnetic sensitivity is thought to rely on quantum mechanics, the math that describes physical processes on the scale of atoms and electrons (SN: 6/27/16). If the idea is shown to be correct, it would be a step forward for biophysicists who want to understand how and when quantum principles can become important in various biological processes. In laboratory experiments, the type of CRY4 in retinas of European robins (Erithacus rubecula) responded to magnetic fields, researchers report in the June 24 Nature. That’s a crucial property for it to serve as a compass. “This is the first paper that actually shows that birds’ cryptochrome 4 is magnetically sensitive,” says sensory biologist Rachel Muheim of Lund University in Sweden, who was not involved with the research. Scientists think that the magnetic sensing abilities of CRY4 are initiated when blue light hits the protein. That light sets off a series of reactions that shuttle around an electron, resulting in two unpaired electrons in different parts of the protein. Those lone electrons behave like tiny magnets, thanks to a quantum property of the electrons called spin. © Society for Science & the Public 2000–2021.

Keyword: Animal Migration; Vision
Link ID: 27882 - Posted: 06.29.2021

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

Ed Yong Carl Schoonover and Andrew Fink are confused. As neuroscientists, they know that the brain must be flexible but not too flexible. It must rewire itself in the face of new experiences, but must also consistently represent the features of the external world. How? The relatively simple explanation found in neuroscience textbooks is that specific groups of neurons reliably fire when their owner smells a rose, sees a sunset, or hears a bell. These representations—these patterns of neural firing—presumably stay the same from one moment to the next. But as Schoonover, Fink, and others have found, they sometimes don’t. They change—and to a confusing and unexpected extent. Schoonover, Fink, and their colleagues from Columbia University allowed mice to sniff the same odors over several days and weeks, and recorded the activity of neurons in the rodents’ piriform cortex—a brain region involved in identifying smells. At a given moment, each odor caused a distinctive group of neurons in this region to fire. But as time went on, the makeup of these groups slowly changed. Some neurons stopped responding to the smells; others started. After a month, each group was almost completely different. Put it this way: The neurons that represented the smell of an apple in May and those that represented the same smell in June were as different from each other as those that represent the smells of apples and grass at any one time. This is, of course, just one study, of one brain region, in mice. But other scientists have shown that the same phenomenon, called representational drift, occurs in a variety of brain regions besides the piriform cortex. Its existence is clear; everything else is a mystery. Schoonover and Fink told me that they don’t know why it happens, what it means, how the brain copes, or how much of the brain behaves in this way. How can animals possibly make any lasting sense of the world if their neural responses to that world are constantly in flux? (c) 2021 by The Atlantic Monthly Group

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27852 - Posted: 06.11.2021