Chapter 5. The Sensorimotor System

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By Gunjan Sinha Light therapy can help lift moods, heal wounds, and boost the immune system. Can it improve symptoms of Parkinson’s disease, too? A first-of-its-kind trial scheduled to launch this fall in France aims to find out. In seven patients, a fiber optic cable implanted in their brain will deliver pulses of near-infrared (NIR) light directly to the substantia nigra, a region deep in the brain that degenerates in Parkinson’s disease. The team, led by neurosurgeon Alim- Louis Benabid of the Clinatec Institute—a partnership between several government-funded research institutes and industry—hopes the light will protect cells there from dying. The study is one of several set to explore how Parkinson’s patients might benefit from light. “I am so excited,” says neuropsychologist Dawn Bowers of the University of Florida College of Medicine, who is recruiting patients for a trial in which NIR will be beamed into the skull instead of delivered with an implant. Small tests in people with Parkinson’s and animal models of the disease have already suggested benefits, but some mainstream Parkinson’s researchers are skeptical. No one has shown exactly how light might protect the key neurons—or why it should have any effect at all on cells buried deep in the brain that never see the light of day. Much or all of the encouraging hints seen so far in people may be the result of the placebo effect, skeptics say. Because there are no biomarkers that correlate well with changes in Parkinson’s symptoms, “we are reliant on observing behavior,” says neurobiologist David Sulzer of Columbia University Irving Medical Center, an editor of the journal npj Parkinson’s Disease. “It’s not easy to guard against placebo effects.” © 2020 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 27482 - Posted: 09.19.2020

By Laura J. Snyder I’m an inveterate storyteller,” confesses the celebrated neurologist and writer Oliver Sacks at the start of Oliver Sacks: His Own Life. “I tell many stories, some comic, some tragic.” Tales of both types abound in this elegiac yet lighthearted film based on director Ric Burns’s interviews with Sacks and his friends, colleagues, family members, and patients in the months before and after the physician’s death in 2015 at the age of 82. The result is a vivid portrait of an ebullient, provocative, brilliant man who transformed the practice of medicine and spearheaded the neurodiversity movement. Born into an upper-middle-class Jewish family in northwest London in 1933, Sacks was the youngest of four sons. He was an outsider: one of only three Jews at his elite prep school; a gay adolescent at a time when gay sex was illegal; an introverted, dreamy, chemistry-obsessed boy in a family of accomplished physicians. His father was a general practitioner who made house calls, and his mother was one of the first female surgeons in England. His two eldest brothers were already studying medicine when he was in high school. Sacks dutifully followed his expected career path and was drawn to neurology when his third brother, Michael, developed schizophrenia. But after completing medical training, Sacks fled the homophobic confines of his nation and family—his mother had called him “an abomination.” Paul Theroux tells Burns that Sacks’s “great luck” was ending up in Los Angeles in 1960, where he found ample “guys, weights, drugs, and hospitals.” © 2020 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 27477 - Posted: 09.19.2020

By Lisa Sanders, M.D. The pain woke the 52-year-old physician from a dead sleep. It was as if all the muscles in his right leg, from those in the buttock down his thigh to the very bottom of his calf, were on fire. He shifted slightly to see if he could find a more comfortable position. There was a jag of pain, and he almost cried out. He glanced at the clock: 4 a.m. In just three hours he would have to get up. He had a full day of patients to see. Massage didn’t help. He couldn’t get comfortable lying flat, so finally he moved to the living room, to a recliner. Only then, and only by lying completely still, did he manage to get the pain to abate. He drifted off, but never for long. The searing pain in his leg and buttock slowly eased, and by the time his alarm went off, he could stand and walk — though his muscles still ached and he had to baby his right leg, causing a limp. Between patients, he arranged to see his own doctor. He’d had pain off and on in his buttocks, one side or the other, for more than a year. The pain was in the middle of each cheek and was worse when he was sitting and at the end of the day. Walking to and from his car on the way home was brutal. And then, as mysteriously as it came, it would disappear — only to come back a week or two later. When he first told his doctor about his pain, the exam didn’t show much. He was a little tender at the bottom of the bones you sit on, called the ischia. His doctor thought it was ischial bursitis. Between the tips of the ischia and the largest muscles of the buttocks, there are little pads called bursae. Sometimes these pads become inflamed. The man’s doctor recommended stretching exercises for the muscles around the bursae. He did them regularly, though he wasn’t sure they helped. The pain he had that night, though, was different, and a whole lot worse. Again, his doctor couldn’t find much. Maybe it was a kind of nerve pain, like sciatica, the patient suggested. The doctor agreed and ordered an M.R.I. to look for a pinched nerve. The result was normal. © 2020 The New York Times Company

Keyword: Pain & Touch; Neuroimmunology
Link ID: 27474 - Posted: 09.16.2020

By Gretchen Reynolds Exercise makes it easier to bounce back from too much stress, according to a fascinating new study with mice. It finds that regular exercise increases the levels of a chemical in the animals’ brains that helps them remain psychologically resilient and plucky, even when their lives seem suddenly strange, intimidating and filled with threats. The study involved mice, but it is likely to have implications for our species, too, as we face the stress and discombobulation of the ongoing pandemic and today’s political and social disruptions. Stress can, of course, be our ally. Emergencies and perils require immediate responses, and stress results in a fast, helpful flood of hormones and other chemicals that prime our bodies to act. “If a tiger jumps out at you, you should run,” says David Weinshenker, a professor of human genetics at Emory University School of Medicine in Atlanta and the senior author of the new study. The stress response, in that situation, is appropriate and valuable. But if, afterward, we “jump at every little noise” and shrink from shadows, we are overreacting to the original stress, Dr. Weinshenker continues. Our response has become maladaptive, because we no longer react with appropriate dread to dreadful things but with twitchy anxiety to the quotidian. We lack stress resilience. In interesting past research, scientists have shown that exercise seems to build and amplify stress resilience. Rats that run on wheels for several weeks, for instance, and then experience stress through light shocks to their paws, respond later to unfamiliar — but safe — terrain with less trepidation than sedentary rats that also experience shocks. But the physiological underpinnings of the animals’ relative buoyancy after exercise remain somewhat mysterious. And, rats are just one species. Finding similar relationships between physical activity and resilience in other animals would bolster the possibility that a similar link exists in people. © 2020 The New York Times Company

Keyword: Stress; Hormones & Behavior
Link ID: 27461 - Posted: 09.09.2020

By Amanda Loudin Last summer while out on a bike ride, 35-year-old Andrew Bernstein of Boulder, Colo., was hit by a van that knocked him off the road and kept on going. A passing driver spotted Bernstein lying, unmoving, in a ditch and called 911. Bernstein’s injuries were life threatening. After multiple surgeries, 10 weeks recovering in the hospital and more than three weeks in inpatient rehab, Bernstein has spent the better part of every week since then working with a number of practitioners to help him progress to where he is today — in a wheelchair and walking with the assistance of a full-length leg brace and crutches. But almost all of that effort came to a complete halt when the coronavirus pandemic hit in March and all of his physical therapy facilities either closed or dramatically reduced their patient contact. “I typically worked with a variety of therapists nine or 10 times a week at four different facilities,” Andrew Bernstein says. He was given a home-based plan but “the disruptions to my therapies was challenging. It was frustrating to do without supervision, because my condition changes from one week to the next, something my therapists might notice even if I don’t.”“I typically worked with a variety of therapists nine or 10 times a week at four different facilities,” Andrew Bernstein says. He was given a home-based plan but “the disruptions to my therapies was challenging. It was frustrating to do without supervision, because my condition changes from one week to the next, something my therapists might notice even if I don’t.”

Keyword: Pain & Touch
Link ID: 27460 - Posted: 09.09.2020

By Tanya Lewis During Musk’s demonstration, he strolled near a pen containing several pigs, some of which had Neuralink implants. One animal, named Gertrude, had hers for two months. The device’s electrodes were situated in a part of Gertrude’s cortex that connected to neurons in her snout. And for the purposes of the demo, her brain signals were converted to audible bleeps that became more frequent as she sniffed around the pen and enjoyed some tasty treats. Musk also showed off a pig whose implant had been successfully removed to show that the surgery was reversible. Some of the other displayed pigs had multiple implants. Neuralink implantable device Neuralink implantable device, v0.9. Credit: Neuralink Neuralink, which was founded by Musk and a team of engineers and scientists in 2016, unveiled an earlier, wired version of its implant technology in 2019. It had several modules: the electrodes were connected to a USB port in the skull, which was intended to be wired to an external battery and a radio transmitter that were located behind the ear. The latest version consists of a single integrated implant that fits in a hole in the skull and relays data through the skin via a Bluetooth radio. The wireless design makes it seem much more practical for human use but limits the bandwidth of data that can be sent, compared with state-of-the-art brain-computer interfaces. The company’s goal, Musk said in the demo, is to “solve important spine and brain problems with a seamlessly implanted device”—a far cry from his previously stated, much more fantastic aim of allowing humans to merge with artificial intelligence. This time Musk seemed more circumspect about the device’s applications. As before, he insisted the demonstration was purely intended as a recruiting event to attract potential staff. Neuralink’s efforts build on decades of work from researchers in the field of brain-computer interfaces. Although technically impressive, this wireless brain implant is not the first to be tested in pigs or other large mammals.] © 2020 Scientific American,

Keyword: Robotics; Movement Disorders
Link ID: 27457 - Posted: 09.07.2020

By Pam Belluck Seven years ago, Joshua Cohen, then a junior at Brown University majoring in biomedical engineering, was captivated by the question of why people develop brain disorders. “How does a neuron die?” he wondered. After poring over scientific studies, he sketched out his ideas for a way to treat them. “I was sitting in my dorm room and I had kind of written out the research on these crazy-looking diagrams,” he recalled. A study published on Wednesday in the New England Journal of Medicine reported that the experimental treatment he and another Brown student, Justin Klee, conceived might hold promise for slowing progression of amyotrophic lateral sclerosis, the ruthless disease that robs people of their ability to move, speak, eat and ultimately breathe. More than 50 clinical trials over 25 years have failed to find effective treatments for A.L.S., also called Lou Gehrig’s disease, which often causes death within two to five years. But now, scientific advances and an influx of funding are driving clinical trials for many potential therapies, generating hope and intense discussion among patients, doctors and researchers. The new study reported that a two-drug combination slowed progression of A.L.S. paralysis by about six weeks over about six months, approximately 25 percent more than a placebo. On average, patients on a placebo declined in 18 weeks to a level that patients receiving the treatment didn’t reach until 24 weeks, said the principal investigator, Dr. Sabrina Paganoni, a neuromuscular medicine specialist at Massachusetts General Hospital’s Healey & AMG Center for A.L.S. “It’s such a terrible disease and as you can imagine, for the folks who have it or the family members, it’s just desperation that something’s going to work,” said Dr. Walter Koroshetz, director of the National Institute of Neurological Disorders and Stroke, who wasn’t involved in the new study. “Any kind of slowing of progression for a patient with A.L.S. might be valuable even though it’s not a big effect.” © 2020 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27455 - Posted: 09.05.2020

Ian Sample Science editor Brain scans of cosmonauts have revealed the first clear evidence of how the organ adapts to the weird and often sickness-inducing challenge of moving around in space. Analysis of scans taken from 11 cosmonauts, who spent about six months each in orbit, found increases in white and grey matter in three brain regions that are intimately involved in physical movement. The changes reflect the “neuroplasticity” of the brain whereby neural tissue, in this case the cells that govern movement or motor activity, reconfigures itself to cope with the fresh demands of life in orbit. “With the techniques we used, we can clearly see there are microstructural changes in three major areas of the brain that are involved in motor processing,” said Steven Jillings, a neuroscientist at the University of Antwerp in Belgium. Visitors to the International Space Station face a dramatic shock to the system for a whole host of reasons, but one of the most striking is weightlessness. While the space station and its occupants are firmly in the grip of gravity – they are constantly falling around the planet – the body must recalibrate its senses to cope with the extreme environment. Images of the cosmonauts’ brains, taken before and after missions lasting on average 171 days, and again seven months later, confirmed that the cerebrospinal fluid that bathes the brain redistributes itself in orbit, pushing the brain up towards the top of the skull. This also expands fluid-filled cavities called ventricles, which may be linked to a loss of sharpness in the cosmonauts’ vision, a condition called spaceflight-associated neuro-ocular syndrome or Sans. © 2020 Guardian News & Media Limited

Keyword: Learning & Memory
Link ID: 27453 - Posted: 09.05.2020

By Gillian R. Brassil and Jeré Longman A restrictive Idaho law — temporarily blocked by a federal judge Monday night — has amplified a charged debate about who should be allowed to compete in women’s sports, as transgender athletes have become increasingly accepted on the playing field while still facing strong resistance from some competitors and lawmakers. While scientific and societal views of sex and gender identity have changed significantly in recent decades, a vexing question persists regarding athletes who transition from male to female: how to balance inclusivity, competitive fairness and safety. There are no uniform guidelines — in fact the existing rules that govern sports often conflict — to determine the eligibility of transgender women and girls (policy battles have so far primarily centered on regulating women’s sports). And there is scant research on elite transgender athletes to guide sports officials as they attempt to provide equitable access to sports while reconciling any residual physiological advantages that may carry on from puberty. Dr. Eric Vilain, a geneticist specializing in sexual development who has advised the N.C.A.A. and the International Olympic Committee on policies for transgender athletes, said that sports leaders were confronted with “two almost irreconcilable positions” in setting eligibility standards — one relying on an athlete’s declared gender and the other on biological litmus tests. Politics, too, have entered the debate in a divided United States. While transgender people have broadly been more accepted across the country, the Trump administration and some states have sought to roll back protections for transgender people in health care, the military and other areas of civil rights, fueling a rise in hate crimes, according to the Human Rights Campaign. In March, Idaho became the first state to bar transgender girls and women from participating in women’s sports. © 2020 The New York Times Company

Keyword: Sexual Behavior
Link ID: 27426 - Posted: 08.20.2020

Abby Carney Shortly after relocating to Texas from California three years ago, Cheryl Webster started hosting a game night at her home as a way of meeting new people. They stopped meeting due to Covid-19, and Webster has only heard from one person in the group in the months since they were able to play. Eventually, she decided to pick up the phone herself – but nobody called back. “I think that’s the hardest part about loneliness,” she said. “Is it my fault? Am I not a very nice person? Or is there something wrong with me?” End of the office: the quiet, grinding loneliness of working from home Read more Webster, 65, is a proactive doer who volunteers regularly and has even helped finance the education of several friends’ children. She sits on the board of the Austin housing authority and the chamber of commerce, and is sure the Christian business leaders’ group she meets with monthly would say flattering things about her. Though divorced and childless, Webster is not a Havisham spinster – putting herself “out there” comes naturally. And so she supposes many people in her life would be surprised to learn that she’s lonely. Despite following the advice of experts to ward off the feeling, her heart still aches. Advertisement Webster is not alone. A growing number of people share her affliction – so much so that some governments are incorporating loneliness into their health public policy. To help people like her, a number of scientists are researching medical solutions, such as pills and nasal sprays. But will treating loneliness like a disease, rather than an existential question, work to ease their pain? © 2020 Guardian News & Media Limited

Keyword: Pain & Touch; Hormones & Behavior
Link ID: 27405 - Posted: 08.06.2020

Lenny Bernstein The Centers for Disease Control and Prevention warned parents and caregivers Tuesday to watch out for an uncommon, polio-like condition that mostly strikes children, usually between August and November. Acute flaccid myelitis, which may be caused by any of several viruses, is marked by a sudden weakness or paralysis of the limbs. Since surveillance began in 2014, prevalence of the ­syndrome has spiked in even-numbered years, often afflicting children about 5 years old. The disease is very rare, but a quick response is critical once the weakness sets in; the disease can progress over hours or days and lead to permanent paralysis or respiratory failure, according to a report issued Tuesday by the CDC. Among 238 cases in 2018 reviewed by the CDC, 98 percent of patients were hospitalized, 54 percent required intensive care, and 23 percent were placed on ventilators to help them breathe. Most patients were hospitalized within a day of experiencing weakness, but about 10 percent were not hospitalized until four or more days later, possibly because of failure to recognize the syndrome, the report said. Limb weakness, difficulty walking and limb pain are often preceded by fever or respiratory illness, usually by about six days, the CDC said. Hundreds of U.S. children have been affected, and many do not fully recover. A number of viruses — including West Nile virus, adenovirus and non-polio enteroviruses — are known to produce the symptoms in a small number of people who become infected by those pathogens. But enterovirus, particularly one dubbed EV-D68, appears to be the most common cause, the CDC said. The National Institute of Allergy and Infectious Diseases is working on a vaccine for EV-D68. © 1996-2020 The Washington Post

Keyword: Movement Disorders; Muscles
Link ID: 27403 - Posted: 08.06.2020

By Abdul-Kareem Ahmed “He doesn’t look like himself,” his wife said. It was midnight, and I was consulting on a patient in the emergency room. He was 48 years old and complaining of a headache. Ten years ago my attending had partially removed a benign tumor growing in his cerebellum, part of the hindbrain that controls movement, coordination and speech. Our team had also placed a shunt in his brain. The brain is buoyed and bathed by cerebrospinal fluid. This clear fluid is made in large cavities, called ventricles, and is eventually absorbed by veins. The tumor’s inoperable remnant had blocked the fluid’s natural escape, causing it to build up, a condition known as hydrocephalus. A shunt is a thin rubber tube that is placed in the ventricles of the brain and tunneled under the skin, into the abdomen. It can have a programmable pressure valve, a gauge that sits under the scalp. His shunt had been siphoning excess fluid to his abdomen for years where it was absorbed, preventing life-threatening high pressure in the brain. Today, however, something was wrong, and I thought it was revealed on his new head CT. His ventricles were very large, suggesting high pressure. “I get a bad headache when I sit up,” he mumbled. “Sometimes I vomit. I feel better when I lie flat.” His wife, a strong and kindhearted woman, corroborated his complaint. “He’s also having memory problems, and he’s losing his balance when he walks,” she added. His symptoms were the opposite of what I expected. He was describing a low-pressure headache. He was relieved by lying down but worsened when sitting up.

Keyword: Pain & Touch
Link ID: 27397 - Posted: 08.03.2020

Jon Hamilton This is the story of a fatal genetic disease, a tenacious scientist and a family that never lost hope. Conner Curran was 4 years old when he was diagnosed with Duchenne Muscular Dystrophy, a genetic disease that causes muscles to waste away. Conner's mother, Jessica Curran, remembers some advice she got from the doctor who made that 2015 diagnosis: "Take your son home, love him, take him on trips while he's walking, give him a good life and enjoy him because there are really not many options right now." Five years later, Conner is not just walking, but running faster than ever, thanks to an experimental gene therapy that took more than 30 years to develop. Conner was the first child to receive the treatment — a single infusion designed to fix the genetic mutation that was gradually causing his muscles cells to die. The treatment can't bring back the cells he's lost (he remains smaller and weaker than his twin brother, Kyle), but it has allowed the muscle cells he still has to function better. Since Conner's treatment, eight other boys with Duchenne have received two different doses of the gene therapy. Preliminary results on six of them, tested a year after treatment, showed they, too, had improved strength and endurance at an age when boys with Duchenne usually become weaker. © 2020 npr

Keyword: Muscles; Movement Disorders
Link ID: 27387 - Posted: 07.27.2020

Ewen Callaway Despite their rough and tumble existence, Neanderthals had a biological predisposition to a heightened sense of pain, finds a first-of-its kind genome study published in Current Biology on 23 July1. Evolutionary geneticists found that the ancient human relatives carried three mutations in a gene encoding the protein NaV1.7, which conveys painful sensations to the spinal cord and brain. They also showed that in a sample of British people, those who had inherited the Neanderthal version of NaV1.7 tend to experience more pain than others. “It’s a first example, to me, about how we begin to perhaps get an idea about Neanderthal physiology by using present-day people as transgenic models,” says Svante Pääbo at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, who led the work with Hugo Zeberg at the Karolinska Institute in Stockholm. Pain-sensing protein Researchers have access to only a few Neanderthal genomes, and most of those have been sequenced at a low resolution. This has made it hard to identify mutations that evolved after their lineage split from that of humans some 500,000–750,000 years ago. But in the past few years, Pääbo and his team have generated three high-quality Neanderthal genomes from DNA found in caves in Croatia and Russia. This allows them to confidently identify mutations that were probably common in Neanderthals, yet very rare in humans. Mutations in a gene called SCN9A — which encodes the NaV1.7 protein — stood out because all of the Neanderthals had three mutations that alter the shape of the protein. The mutated version of the gene was found on both sets of chromosomes in all three Neanderthals, hinting that it was common across their populations. © 2020 Springer Nature Limited

Keyword: Pain & Touch; Evolution
Link ID: 27382 - Posted: 07.25.2020

Laura P.W. Ranum An FDA-approved diabetes drug shows early signs of promise against the most common genetic form of amyotrophic lateral sclerosis, a devastating neurological condition that causes paralysis. ALS is a progressive disease that affects neurons in the brain and spinal cord. Motor neurons transmit signals from our brain to our muscles and allow us to move. ALS causes these motor neurons to die, resulting in the loss of a patient’s ability to speak, eat, move and breathe. Notable ALS patients include New York Yankees baseball star Lou Gehrig (the disease is often called Lou Gehrig’s disease), physicist Stephen Hawking and New Orleans Saints football star Steve Gleason. There are currently more than 30,000 cases of ALS in the United States, and life expectancy after diagnosis is typically 2 to 5 years. There is currently no cure for ALS. I am a scientist who studies neurological diseases that run in families, and I have been working hard to find a treatment to stop ALS. Our team has made a discovery, detailed in a scientific study, that paves the way for further research for improving disease in a genetic type of ALS caused by a mutation in a gene with the unwieldy name chromosome 9 open reading frame 72 (C9orf72), based on its location on chromosome 9. In addition to ALS, mutations in this gene can also cause frontotemporal dementia, which can cause apathy, loss of emotional control and cognitive decline. Some patients with the C9orf72 mutation develop ALS, others develop frontotemporal dementia and some develop both. Together, these diseases are referred to here as C9-ALS/FTD. I have been focusing on C9-ALS, which is the most common genetic type of ALS which is caused by a mutation in the C9orf72 gene. The mutation occurs when six letters of DNA that make up part of the gene’s genetic code – GGGGCC – are repeated hundreds of extra times. It is as if a single word is repeated hundreds of times in the same sentence. © 2010–2020, The Conversation US, Inc.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27379 - Posted: 07.21.2020

By Jane E. Brody Michael Richard Clifford, a 66-year-old retired astronaut living in Cary, N.C., learned before his third spaceflight that he had Parkinson’s disease. He was only 44 and in excellent health at the time, and had no family history of this disabling neurological disorder. What he did have was years of exposure to numerous toxic chemicals, several of which have since been shown in animal studies to cause the kind of brain damage and symptoms that afflict people with Parkinson’s. As a youngster, Mr. Clifford said, he worked in a gas station using degreasers to clean car engines. He also worked on a farm where he used pesticides and in fields where DDT was sprayed. Then, as an aviator, he cleaned engines readying them for test flights. But at none of these jobs was he protected from exposure to hazardous chemicals that are readily inhaled or absorbed through the skin. Now Mr. Clifford, a lifelong nonsmoker, believes that his close contact with these various substances explains why he developed Parkinson’s disease at such a young age. Several of the chemicals have strong links to Parkinson’s, and a growing body of evidence suggests that exposure to them may very well account for the dramatic rise in the diagnosis of Parkinson’s in recent decades. To be sure, the medical literature is replete with associations between people’s habits and exposures and their subsequent risk of developing various ailments, from allergies to heart disease and cancer. Such linkages do not — and cannot by themselves — prove cause and effect. Sometimes, though, the links are so strong and the evidence so compelling that there can be little doubt that one causes the other. The link of cigarette smoking to lung cancer is a classic example. Despite tobacco industry claims that there was no definitive proof, the accumulation of evidence, both experimental and epidemiological, eventually made it impossible to deny that years of smoking can cause cancer even long after a person has quit. © 2020 The New York Times Company

Keyword: Parkinsons; Neurotoxins
Link ID: 27378 - Posted: 07.21.2020

by Angie Voyles Askham The autism gene SHANK3 is crucial for the development and function of muscles and the motor neurons that control them, according to a new study1. This relationship may explain why some people with mutations in the gene have low muscle tone, says co-lead investigator Maria Demestre, senior researcher at the Institute for Bioengineering of Catalonia in Barcelona. “It opens an avenue for treatment.” Between 1 and 2 percent of people with autism have a mutation in SHANK3. Deletions of the chromosomal region containing SHANK3 lead to Phelan-McDermid syndrome, characterized by intellectual disability, speech delay and, often, autism. One of the earliest signs of the syndrome in infants is hypotonia, or low muscle tone, which can result in difficulty feeding and a delay in reaching developmental milestones such as crawling and walking. SHANK3 encodes a protein that helps neurons communicate throughout the brain. But studies have shown that the gene is also found in other parts of the body and that mutations or deletions of genes in peripheral cells can contribute to autism traits2. SHANK3 is heavily expressed throughout the motor system of both mice and people, the new work shows. Muscle cells derived from people with Phelan-McDermid syndrome fail to mature, and mice deficient in SHANK3 have poor muscle function. The results add to “the growing appreciation of the role of autism-associated genes — in this case, SHANK3 — outside of the brain,” says David Ginty, professor of neurobiology at Harvard Medical School, who was not involved in the study. © 2020 Simons Foundation

Keyword: Autism; Movement Disorders
Link ID: 27375 - Posted: 07.21.2020

By Erik Stokstad Dogs are renowned for their world-class noses, but a new study suggests they may have an additional—albeit hidden—sensory talent: a magnetic compass. The sense appears to allow them to use Earth’s magnetic field to calculate shortcuts in unfamiliar terrain. The finding is a first in dogs, says Catherine Lohmann, a biologist at the University of North Carolina, Chapel Hill, who studies “magnetoreception” and navigation in turtles. She notes that dogs’ navigational abilities have been studied much less compared with migratory animals such as birds. “It’s an insight into how [dogs] build up their picture of space,” adds Richard Holland, a biologist at Bangor University who studies bird navigation. There were already hints that dogs—like many animals, and maybe even humans—can perceive Earth’s magnetic field. In 2013, Hynek Burda, a sensory ecologist at the Czech University of Life Sciences Prague who has worked on magnetic reception for 3 decades, and colleagues showed dogs tend to orient themselves north-south while urinating or defecating. Because this behavior is involved in marking and recognizing territory, Burda reasoned the alignment helps dogs figure out the location relative to other spots. But stationary alignment isn’t the same thing as navigation. In the new study, Burda’s graduate student, Kateřina Benediktová, initially put video cameras and GPS trackers on four dogs and took them on trips into the forest. The dogs would scamper off to chase the scent of an animal for 400 meters on average. The GPS tracks showed two types of behavior during their return trips to their owner (see map, below). In one, dubbed tracking, a dog would retrace its original route, presumably following the same scent. In the other behavior, called scouting, the dog would return along a completely new route, bushwhacking without any backtracking. Benediktová et al., eLife (2020) 10.7554 (CC BY) © 2020 American Association for the Advancement of Science.

Keyword: Animal Migration
Link ID: 27374 - Posted: 07.18.2020

Kayt Sukel A 44-year-old male patient, with no history of cardiovascular disease, arrived at an emergency room in New York City after experiencing difficulty speaking and moving the right side of his body. The on-call physician quickly determined he had suffered a stroke—a condition that normally affects people who are decades older. In Italy, a 23-year-old man sought care for a complete facial palsy and feelings of “pins and needles” in his legs. Doctors discovered axonal sensory-motor damage suggesting Guillain Barré Syndrome, a rare autoimmune neurological disorder where the immune system, sometimes following an infection, mistakes some of the body’s own peripheral nerve cells as foreign invaders and attacks them. A 58-year-old woman in Detroit was rushed to the hospital with severe cognitive impairment, unable to remember anything beyond her own name. MRI scans showed widespread inflammation across the patient’s brain, leading doctors to diagnose a rare but dangerous neurological condition called acute necrotizing hemorrhagic encephalopathy. At first glance, it may seem that these patients have little in common. Yet all three were also suffering from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease, better known as Covid-19. While most individuals infected with this new virus exhibit fever, cough, and respiratory symptoms, doctors across the globe are also documenting patients presenting with a handful of neurological manifestations—leading clinicians and researchers to wonder if Covid-19 also has the ability to invade the human nervous system. “As more people are being tested and diagnosed with this virus, physicians are starting to see more uncommon symptoms and complications, including neurological ones,” says Diane Griffin, M.D., Ph.D., a researcher at Johns Hopkins University’s Bloomberg School of Public Health. “But as Covid-19 is a new virus, we aren’t yet sure why these things are happening. Is the virus getting into the brain directly? Is it affecting the brain through other means? These are important questions to answer.” © 2020 The Dana Foundation

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27370 - Posted: 07.16.2020

By Gretchen Reynolds Exercise may help change exercisers’ brains in surprising ways, according to a new study of physical activity and brain health. The study, which included both mice and people, found that exercise prompts the liver to pump out a little-known protein, and that chemically upping the levels of that protein in out-of-shape, elderly animals rejuvenates their brains and memories. The findings raise provocative questions about whether the brain benefits of exercise might someday be available in a capsule or syringe form — essentially “exercise in a pill.” We already have considerable evidence, of course, that physical activity protects brains and minds from some of the declines that otherwise accompany aging. In past rodent studies, animals that ran on wheels or treadmills produced more new neurons and learned and remembered better than sedentary mice or rats. Similarly, older people who took up walking for the sake of science added tissue volume in portions of their brains associated with memory. Even among younger people, those who were more fit than their peers tended to perform better on cognitive tests. But many questions remain unanswered about how, at a cellular level, exercise remodels the brain and alters its function. Most researchers suspect that the process involves the release of a cascade of substances inside the brain and elsewhere in the body during and after exercise. These substances interact and ignite other biochemical reactions that ultimately change how the brain looks and works. But what the substances are, where they originate and how they meet and mingle has remained unclear. So, for the new study, which was published this month in Science, researchers at the University of California, San Francisco, and other institutions decided to look inside the minds and bloodstreams of mice. In past research from the same lab, the scientists had infused blood from young mice into older ones and seen improvements in the aging animals’ thinking. It was like “transferring a memory of youth through blood,” says Saul Villeda, a professor at U.C.S.F., who conducted the study with his colleagues Alana Horowitz, Xuelai Fan and others. © 2020 The New York Times Company

Keyword: Hormones & Behavior
Link ID: 27368 - Posted: 07.16.2020