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

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

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

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

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

Amy Fleming Taking a stroll with Shane O’Mara is a risky endeavour. The neuroscientist is so passionate about walking, and our collective right to go for walks, that he is determined not to let the slightest unfortunate aspect of urban design break his stride. So much so, that he has a habit of darting across busy roads as the lights change. “One of life’s great horrors as you’re walking is waiting for permission to cross the street,” he tells me, when we are forced to stop for traffic – a rude interruption when, as he says, “the experience of synchrony when walking together is one of life’s great pleasures”. He knows this not only through personal experience, but from cold, hard data – walking makes us healthier, happier and brainier. We are wandering the streets of Dublin discussing O’Mara’s book, In Praise of Walking, a backstage tour of what happens in our brains while we perambulate. Our jaunt begins at the grand old gates of his workplace, Trinity College, and takes in the Irish famine memorial at St Stephen’s Green, the Georgian mile, the birthplace of Francis Bacon, the site of Facebook’s new European mega-HQ and the salubrious seaside dwellings of Sandymount. O’Mara, 53, is in his element striding through urban landscapes – from epic hikes across London’s sprawl to more sedate ambles in Oxford, where he received his DPhil – and waxing lyrical about science, nature, architecture and literature. He favours what he calls a “motor-centric” view of the brain – that it evolved to support movement and, therefore, if we stop moving about, it won’t work as well. © 2020 Read It Later, Inc.

Keyword: Depression
Link ID: 27364 - Posted: 07.15.2020

For every cell in the body there comes a time when it must decide what it wants to do for the rest of its life. In an article published in the journal PNAS, National Institutes of Health researchers report for the first time that ancient viral genes that were once considered “junk DNA” may play a role in this process. The article describes a series of preclinical experiments that showed how some human endogenous retrovirus (HERV-K) genes inscribed into chromosomes 12 and 19 may help control the differentiation, or maturation, of human stem cells into the trillions of neurons that are wired into our nervous systems. The experiments were performed by researchers in a lab led by Avindra Nath, M.D., clinical director, at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). Over the course of evolution, the human genome has absorbed thousands of human endogenous retrovirus genes. As a result, nearly eight percent of the DNA that lines our chromosomes includes remnants of these genes. Although once thought to be inactive, or “junk”, recent studies have shown that these genes may be involved in human embryonic development, the growth of some tumors, and nerve damage during multiple sclerosis. Previously, researchers in Dr. Nath’s lab showed that amyotrophic lateral sclerosis (ALS) may be linked to activation of the HERV-K gene. In this study, led by Tongguang (David) Wang, M.D., Ph.D., staff scientist at NINDS, the team showed that deactivation of the gene may free stem cells to become neurons. The researchers performed most of their experiments on blood cells, drawn from healthy volunteers at the NIH’s Clinical Center, that they genetically transformed into induced pluripotent stem cells, which can then turn into any cell type in the body. Surprisingly, they found that the surfaces of the stem cells were lined with high levels of HERV-K, subtype HML-2, an envelope protein, that viruses often use to latch onto and infect cells. These proteins progressively disappeared as the cells were served two rounds of “cocktails.” One round nudged the cells into an intermediate, neural stem cell state followed by a second round that pushed the cells into finally becoming neurons.

Keyword: ALS-Lou Gehrig's Disease ; Development of the Brain
Link ID: 27359 - Posted: 07.14.2020

By Laura Sanders Exercise’s power to boost the brain might require a little help from the liver. A chemical signal from the liver, triggered by exercise, helps elderly mice keep their brains sharp, suggests a study published in the July 10 Science. Understanding this liver-to-brain signal may help scientists develop a drug that benefits the brain the way exercise does. Lots of studies have shown that exercise helps the brain, buffering the memory declines that come with old age, for instance. Scientists have long sought an “exercise pill” that could be useful for elderly people too frail to work out or for whom exercise is otherwise risky. “Can we somehow get people who can’t exercise to have the same benefits?” asks Saul Villeda, a neuroscientist at the University of California, San Francisco. Villeda and colleagues took an approach similar to experiments that revealed the rejuvenating effects of blood from young mice (SN: 5/5/14). But instead of youthfulness, the researchers focused on fitness. The researchers injected sedentary elderly mice with plasma from elderly mice that had voluntarily run on wheels over the course of six weeks. After eight injections over 24 days, the sedentary elderly mice performed better on memory tasks, such as remembering where a hidden platform was in a pool of water, than elderly mice that received injections from sedentary mice. Comparing the plasma of exercised mice with that of sedentary mice showed an abundance of proteins produced by the liver in mice that ran on wheels. The researchers closely studied one of these liver proteins produced in response to exercise, called GPLD1. GPLD1 is an enzyme, a type of molecular scissors. It snips other proteins off the outsides of cells, releasing those proteins to go do other jobs. Targeting these biological jobs with a molecule that behaves like GPLD1 might be a way to mimic the brain benefits of exercise, the researchers suspect. © Society for Science & the Public 2000–2020.

Keyword: Learning & Memory; Development of the Brain
Link ID: 27358 - Posted: 07.11.2020

By Jocelyn Kaiser It’s well established that exercise can sharpen the mind: People and mice who work out do better on cognitive tests, and elderly people who are physically active reduce their risk of dementia. Now, in a surprising finding, researchers report that blood from a mouse that exercises regularly can perk up the brain of a “couch potato” mouse. This effect, traced to a specific liver protein in the blood, could point the way to a drug that confers the brain benefits of exercise to an old or feeble person who rarely leaves a chair or bed. “Can your brain think that you exercised, from just something in your blood?” asks aging researcher Saul Villeda of the University of California, San Francisco (UCSF), who led the rodent research. The study grew out of research in Villeda’s lab and others suggesting blood from a young mouse can rejuvenate the brain and muscles of an old mouse. Some teams have since claimed to find specific proteins that explain the benefits of this “young blood.” Graduate student Alana Horowitz and postdoc Xuelai Fan in Villeda’s group wondered whether exercise—not just youth—could confer similar benefits via the blood. It was easy to enough to test: Put a wheel in a cage full of mice, and the mostly inactive animals will run for miles at night. The researchers collected blood from elderly or middle-aged mice that had an exercise wheel in their cage for 6 weeks and then transfused this blood into old mice without a wheel in their cage. Couch potato mice receiving this blood eight times over 3 weeks did nearly as well on learning and memory tests, such as navigating through a maze, as the exercising mice. A control group of couch potatoes receiving blood from similarly old, nonexercising mice saw no boost. The rodents getting the blood from the active mice also grew roughly twice as many new neurons in the hippocampus, a brain region involved in learning and memory, Villeda’s team reports today in Science. That change is comparable to what’s seen in rodents that directly exercise. © 2020 American Association for the Advancement of Science.

Keyword: Alzheimers; Development of the Brain
Link ID: 27357 - Posted: 07.11.2020

Ian Sample Science editor Doctors may be missing signs of serious and potentially fatal brain disorders triggered by coronavirus, as they emerge in mildly affected or recovering patients, scientists have warned. Neurologists are on Wednesday publishing details of more than 40 UK Covid-19 patients whose complications ranged from brain inflammation and delirium to nerve damage and stroke. In some cases, the neurological problem was the patient’s first and main symptom. The cases, published in the journal Brain, revealed a rise in a life-threatening condition called acute disseminated encephalomyelitis (Adem), as the first wave of infections swept through Britain. At UCL’s Institute of Neurology, Adem cases rose from one a month before the pandemic to two or three per week in April and May. One woman, who was 59, died of the complication. A dozen patients had inflammation of the central nervous system, 10 had brain disease with delirium or psychosis, eight had strokes and a further eight had peripheral nerve problems, mostly diagnosed as Guillain-Barré syndrome, an immune reaction that attacks the nerves and causes paralysis. It is fatal in 5% of cases. “We’re seeing things in the way Covid-19 affects the brain that we haven’t seen before with other viruses,” said Michael Zandi, a senior author on the study and a consultant at the institute and University College London Hospitals NHS foundation trust. “What we’ve seen with some of these Adem patients, and in other patients, is you can have severe neurology, you can be quite sick, but actually have trivial lung disease,” he added. “Biologically, Adem has some similarities with multiple sclerosis, but it is more severe and usually happens as a one-off. Some patients are left with long-term disability, others can make a good recovery.” © 2020 Guardian News & Media Limited

Keyword: Stroke; Movement Disorders
Link ID: 27354 - Posted: 07.08.2020

Sherry H-Y. Chou Aarti Sarwal Neha S. Dangayach The patient in the case report (let’s call him Tom) was 54 and in good health. For two days in May, he felt unwell and was too weak to get out of bed. When his family finally brought him to the hospital, doctors found that he had a fever and signs of a severe infection, or sepsis. He tested positive for SARS-CoV-2, the virus that causes COVID-19 infection. In addition to symptoms of COVID-19, he was also too weak to move his legs. When a neurologist examined him, Tom was diagnosed with Guillain-Barre Syndrome, an autoimmune disease that causes abnormal sensation and weakness due to delays in sending signals through the nerves. Usually reversible, in severe cases it can cause prolonged paralysis involving breathing muscles, require ventilator support and sometimes leave permanent neurological deficits. Early recognition by expert neurologists is key to proper treatment. We are neurologists specializing in intensive care and leading studies related to neurological complications from COVID-19. Given the occurrence of Guillain-Barre Syndrome in prior pandemics with other corona viruses like SARS and MERS, we are investigating a possible link between Guillain-Barre Syndrome and COVID-19 and tracking published reports to see if there is any link between Guillain-Barre Syndrome and COVID-19. Some patients may not seek timely medical care for neurological symptoms like prolonged headache, vision loss and new muscle weakness due to fear of getting exposed to virus in the emergency setting. People need to know that medical facilities have taken full precautions to protect patients. Seeking timely medical evaluation for neurological symptoms can help treat many of these diseases. © 2010–2020, The Conversation US, Inc.

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27353 - Posted: 07.08.2020

Jon Hamilton The same process that causes dew drops to form on a blade of grass appears to play an important role in Alzheimer's disease and other brain diseases. The process, known as phase transition, is what allows water vapor to condense into liquid water, or even freeze into solid ice. That same sort of process allows brain cells to constantly reorganize their inner machinery. But in degenerative diseases that include amyotrophic lateral sclerosis, frontotemporal dementia and Alzheimer's, the phase transitions inside neurons seem to go awry, says Dr. J. Paul Taylor, a neurogeneticist at St. Jude Children's Research Hospital in Memphis, and an investigator with the Howard Hughes Medical Institute. This malfunctioning prompts the interior of the cell to become too viscous, Taylor says. "It's as if you took a jar of honey [and] left it in the refrigerator overnight." In this sticky environment, structures that previously could nimbly disassemble and move around become "irreversibly glommed together," says Clifford Brangwynne, a professor of chemical and biological engineering at Princeton University and an investigator with the Howard Hughes Medical Institute. "And when they're irreversibly stuck like that, they can no longer leave to perform functions elsewhere in the cell." That glitch seems to allow toxins to begin to build up in and around these dysfunctional cells, Taylor says — including the toxins associated with Alzheimer's and other neurodegenerative diseases. The science behind this view of brain diseases has emerged only in the past decade. In 2009, Brangwynne was part of a team that published a study showing that phase transitions are important inside cells — or at least inside the reproductive cells of worms. © 2020 npr

Keyword: ALS-Lou Gehrig's Disease ; Alzheimers
Link ID: 27351 - Posted: 07.08.2020

By Gretchen Reynolds When we start to lift weights, our muscles do not strengthen and change at first, but our nervous systems do, according to a fascinating new study in animals of the cellular effects of resistance training. The study, which involved monkeys performing the equivalent of multiple one-armed pull-ups, suggests that strength training is more physiologically intricate than most of us might have imagined and that our conception of what constitutes strength might be too narrow. Those of us who join a gym — or, because of the current pandemic restrictions and concerns, take up body-weight training at home — may feel some initial disappointment when our muscles do not rapidly bulge with added bulk. In fact, certain people, including some women and most preadolescent children, add little obvious muscle mass, no matter how long they lift. But almost everyone who starts weight training soon becomes able to generate more muscular force, meaning they can push, pull and raise more weight than before, even though their muscles may not look any larger and stronger. Scientists have known for some time that these early increases in strength must involve changes in the connections between the brain and muscles. The process appears to involve particular bundles of neurons and nerve fibers that carry commands from the brain’s motor cortex, which controls muscular contractions, to the spinal cord and, from there, to the muscles. If those commands become swifter and more forceful, the muscles on the receiving end should respond with mightier contractions. Functionally, they would be stronger. But the mechanics of these nervous system changes have been unclear. Understanding the mechanics better could also have clinical applications: If scientists and doctors were to better understand how the nervous system changes during resistance training, they might be better able to help people who lose strength or muscular control after a stroke, for example, or as a result of aging or for other reasons. © 2020 The New York Times Company

Keyword: Muscles
Link ID: 27350 - Posted: 07.08.2020

By Gretchen Reynolds When we start to lift weights, our muscles do not strengthen and change at first, but our nervous systems do, according to a fascinating new study in animals of the cellular effects of resistance training. The study, which involved monkeys performing the equivalent of multiple one-armed pull-ups, suggests that strength training is more physiologically intricate than most of us might have imagined and that our conception of what constitutes strength might be too narrow. Those of us who join a gym — or, because of the current pandemic restrictions and concerns, take up body-weight training at home — may feel some initial disappointment when our muscles do not rapidly bulge with added bulk. In fact, certain people, including some women and most preadolescent children, add little obvious muscle mass, no matter how long they lift. But almost everyone who starts weight training soon becomes able to generate more muscular force, meaning they can push, pull and raise more weight than before, even though their muscles may not look any larger and stronger. Scientists have known for some time that these early increases in strength must involve changes in the connections between the brain and muscles. The process appears to involve particular bundles of neurons and nerve fibers that carry commands from the brain’s motor cortex, which controls muscular contractions, to the spinal cord and, from there, to the muscles. If those commands become swifter and more forceful, the muscles on the receiving end should respond with mightier contractions. Functionally, they would be stronger. © 2020 The New York Times Company

Keyword: Movement Disorders; Learning & Memory
Link ID: 27343 - Posted: 07.02.2020