by Chloe Williams / A new flexible electrode array can detect the activity of neurons in a rat’s brain at high resolution for more than a year1. The device could be used to study how neuronal activity is altered in autism. Arrays usually have wires connected to each electrode to pick up its signal, but this design is bulky and works only in arrays consisting of 100 electrodes or fewer, limiting the array’s coverage and resolution. Devices with thousands of electrodes have integrated switches to consolidate signals into fewer wires. But these devices usually have a lifespan of only a few days. Their polymer-based coatings are often permeable to water or contain tiny defects that allow body fluids to seep into the device and current to leak out, damaging both the device and brain tissue. The new device combines electronic switches and a specialized protective coating so that scientists can record activity at the surface of the brain at high resolution over extended periods of time. The array, called Neural Matrix, consists of 1,008 surface electrodes laid out in 28 columns and 36 rows. Switches, or transistors, built into the array combine signals from all the electrodes in a column to a single output wire. The signals from each electrode in the column are recorded via the wire in a specific sequence, making it possible to separate them later. © 2020 Simons Foundation

Keyword: Brain imaging
Link ID: 27282 - Posted: 06.04.2020

By Robert Martone When a concert opens with a refrain from your favorite song, you are swept up in the music, happily tapping to the beat and swaying with the melody. All around you, people revel in the same familiar music. You can see that many of them are singing, the lights flashing to the rhythm, while other fans are clapping in time. Some wave their arms over their head, and others dance in place. The performers and audience seem to be moving as one, as synchronized to one another as the light show is to the beat. A new paper in the journal NeuroImage has shown that this synchrony can be seen in the brain activities of the audience and performer. And the greater the degree of synchrony, the study found, the more the audience enjoys the performance. This result offers insight into the nature of musical exchanges and demonstrates that the musical experience runs deep: we dance and feel the same emotions together, and our neurons fire together as well. In the study, a violinist performed brief excerpts from a dozen different compositions, which were videotaped and later played back to a listener. Researchers tracked changes in local brain activity by measuring levels of oxygenated blood. (More oxygen suggests greater activity, because the body works to keep active neurons supplied with it.) Musical performances caused increases in oxygenated blood flow to areas of the brain related to understanding patterns, interpersonal intentions and expression. Data for the musician, collected during a performance, was compared to those for the listener during playback. In all, there were 12 selections of familiar musical works, including “Edelweiss,” Franz Schubert’s “Ave Maria,” “Auld Lang Syne” and Ludwig van Beethoven’s “Ode to Joy.” The brain activities of 16 listeners were compared to that of a single violinist. © 2020 Scientific American,

Keyword: Hearing
Link ID: 27277 - Posted: 06.03.2020

Diana Kwon What if you could boost your brain’s processing capabilities simply by sticking electrodes onto your head and flipping a switch? Berkeley, California–based neurotechnology company Humm has developed a device that it claims serves that purpose. Their “bioelectric memory patch” is designed to enhance working memory—the type of short-term memory required to temporarily hold and process information—by noninvasively stimulating the brain. In recent years, neurotechnology companies have unveiled direct-to-consumer (DTC) brain stimulation devices that promise a range of benefits, including enhancing athletic performance, increasing concentration, and reducing depression. Humm’s memory patch, which resembles a large, rectangular Band-Aid, is one such product. Users can stick the device to their forehead and toggle a switch to activate it. Electrodes within the patch generate transcranial alternating current stimulation (tACS), a method of noninvasively zapping the brain with oscillating waves of electricity. The company recommends 15 minutes of stimulation to give users up to “90 minutes of boosted learning” immediately after using the device. The product is set for public release in 2021. Over the last year or so, Humm has generated much excitement among investors, consumers, and some members of the scientific community. In addition to raising several million dollars in venture capital funding, the company has drawn interest both from academic research labs and from the United States military. According to Humm cofounder and CEO Iain McIntyre, the US Air Force has ordered approximately 1,000 patches to use in a study at their training academy that is set to start later this year. © 1986–2020 The Scientist

Keyword: Learning & Memory
Link ID: 27269 - Posted: 05.29.2020

By Nicoletta Lanese, Scientists sent patterns of electricity coursing across people’s brains, coaxing their brains to see letters that weren’t there. The experiment worked in both sighted people and blind participants who had lost their sight in adulthood, according to the study, published today (May 14) in the journal Cell. Although this technology remains in its early days, implanted devices could potentially be used in the future to stimulate the brain and somewhat restore people’s vision. Known as visual prosthetics, the implants were placed on the visual cortex and then stimulated in a pattern to “trace” out shapes that the participants could then “see.” More advanced versions of these implants could work similarly to cochlear implants, which stimulate nerves of the inner ear with electrodes to help enhance the wearer’s hearing ability. “An early iteration [of such a device] could provide detection of the contours of shapes encountered,” study authors neuroscientist Michael Beauchamp and neurosurgeon Dr. Daniel Yoshor, both at the Baylor College of Medicine, told Live Science in an email. (Yoshor will start a new position at the Perelman School of Medicine at the University of Pennsylvania this summer.) “The ability to detect the form of a family member or to allow more independent navigation would be a wonderful advance for many blind patients.” The study authors crafted the letters by stimulating the brain with electrical currents, causing it to generate so-called phosphenes — tiny pinpricks of light that people sometimes perceive without any actual light entering their eyes. © 2020 Scientific American

Keyword: Vision; Robotics
Link ID: 27250 - Posted: 05.16.2020

Amber Dance A mouse finds itself in a box it’s never seen before. The walls are striped on one side, dotted on the other. The orange-like odor of acetophenone wafts from one end of the box, the spiced smell of carvone from the other. The mouse remembers that the orange smell is associated with something good. Although it may not recall the exact nature of the reward, the mouse heads toward the scent. Except this mouse has never smelled acetophenone in its life. Rather, the animal is responding to a false memory, implanted in its brain by neuroscientists at the Hospital for Sick Children in Toronto. Sheena Josselyn, a coauthor on a 2019 Nature Neuroscience study reporting the results of the project, says the goal was not to confuse the rodent, but for the scientists to confirm their understanding of mouse memory. “If we really understand memory, we should be able to trick the brain into remembering something that never happened at all,” she explains. By simultaneously activating the neurons that sense acetophenone and those associated with reward, the researchers created the “memory” that the orange-y scent heralded good things. Thanks to optogenetics, which uses a pulse of light to activate or deactivate neurons, Josselyn and other scientists are manipulating animal memories in all kinds of ways. Even before the Toronto team implanted false memories into mice, researchers were making rodents forget or recall an event with the flick of a molecular light switch. With every flash of light, they test their hypotheses about how these animals—and by extension, people—collect, store, and access past experiences. Scientists are also examining how memory formation and retrieval change with age, how those processes are altered in animal models of Alzheimer’s disease, and how accessing memories can influence an animal’s emotional state. © 1986–2020 The Scientist.

Keyword: Learning & Memory; Alzheimers
Link ID: 27228 - Posted: 05.02.2020

Ruth Williams Scientists have created a light-responsive opsin so sensitive that even when engineered into cells deep within tissue it can respond to an external light stimulus, according to a report in Neuron yesterday (April 30). Experiments in mice and macaques showed that shining blue light on the surface of the skull or brain was sufficient to activate opsin-expressing neurons six millimeters deep. “I was pretty blown away that this was even possible,” says Gregory Corder, who studies the neurological basis of pain and addiction at the University of Pennsylvania and who was not involved with the work. At that sort of depth, he continues, “essentially no part of the rodent brain is off-limits now for doing this non-invasive [technique]. . . . It’s pretty impressive.” “This development will help to extend the use of optogenetics in non-human primate models, and bring the techniques closer to clinical application in humans,” adds neurological disease expert Adriana Galvan of Yerkes National Primate Research Center in an email to The Scientist. Galvan was not a member of the research team. Optogenetics is a technique whereby excitable cells, such as neurons, can be controlled at will by light. To do this, cells are genetically engineered to produce ion channels called opsins that sit in the cells’ membranes and open in response to a certain wavelength of light. Switching on the light, then, floods the cells with ions, causing them to fire. Because light doesn’t penetrate tissue easily, to activate opsin-producing neurons deep in the brain of a living animal, researchers insert fiber optic cables. This is “highly invasive,” says Galvan, explaining that “the brain tissue can be damaged.” © 1986–2020 The Scientist.

Keyword: Brain imaging
Link ID: 27226 - Posted: 05.02.2020

By Lisa Sanders, M.D. “Honey” — the woman could hear fear tightening her husband’s voice as he called out to her — “I think your mother just died.” She ran into the living room. Her 78-year-old mother sat rigid in a chair, her skin gray and lifeless. Her eyes were open but all white, as if she were trying to see the back of her own skull. Then her arms started to make little jerking movements; her lips parted as saliva seeped out the corner of her mouth onto her chin. Then her body slumped. She seemed awake but confused after this seizure-like episode. Should I call an ambulance? the husband asked. No, his wife responded. Her mother had a complicated medical history, including a kidney transplant 12 years before and an autoimmune disease. An ambulance would want to take her to the nearby Hartford Hospital. But her doctors were at Yale New Haven Hospital — some 30 miles from their home in Cromwell, Conn. They helped the woman into the car. It was only a half-hour drive to the hospital that March 10 evening, but it seemed to last forever. Would her mother make it? Her eyes were closed, and she looked very pale. Her other daughter worked at the hospital and was waiting with a wheelchair when they arrived. The daughters made sure that the doctors and nurses knew that their mother took two medications to keep her immune system from killing her transplanted kidney. Because of those immune-suppressing drugs, she’d had many infections over the years. Six months earlier, she nearly lost her kidney to a particularly aggressive bacterium. She’d been well since then, until a few days earlier when she came down with a cold. It was just a sore throat and a runny nose, but the couple were worried enough to move her into their home to keep an eye on her. She didn’t want to eat because of the pain in her throat, but otherwise she seemed to be doing well. © 2020 The New York Times Company

Keyword: Epilepsy
Link ID: 27224 - Posted: 04.30.2020

By Matthew Cobb We are living through one of the greatest of scientific endeavours – the attempt to understand the most complex object in the universe, the brain. Scientists are accumulating vast amounts of data about structure and function in a huge array of brains, from the tiniest to our own. Tens of thousands of researchers are devoting massive amounts of time and energy to thinking about what brains do, and astonishing new technology is enabling us to both describe and manipulate that activity. A neuroscientist explains: the need for ‘empathetic citizens’ - podcast We can now make a mouse remember something about a smell it has never encountered, turn a bad mouse memory into a good one, and even use a surge of electricity to change how people perceive faces. We are drawing up increasingly detailed and complex functional maps of the brain, human and otherwise. In some species, we can change the brain’s very structure at will, altering the animal’s behaviour as a result. Some of the most profound consequences of our growing mastery can be seen in our ability to enable a paralysed person to control a robotic arm with the power of their mind. Every day, we hear about new discoveries that shed light on how brains work, along with the promise – or threat – of new technology that will enable us to do such far-fetched things as read minds, or detect criminals, or even be uploaded into a computer. Books are repeatedly produced that each claim to explain the brain in different ways. And yet there is a growing conviction among some neuroscientists that our future path is not clear. It is hard to see where we should be going, apart from simply collecting more data or counting on the latest exciting experimental approach. As the German neuroscientist Olaf Sporns has put it: “Neuroscience still largely lacks organising principles or a theoretical framework for converting brain data into fundamental knowledge and understanding.” Despite the vast number of facts being accumulated, our understanding of the brain appears to be approaching an impasse. © 2020 Guardian News & Media Limited

Keyword: Robotics
Link ID: 27084 - Posted: 02.28.2020

Jordana Cepelewicz Decisions, decisions. All of us are constantly faced with conscious and unconscious choices. Not just about what to wear, what to eat or how to spend a weekend, but about which hand to use when picking up a pencil, or whether to shift our weight in a chair. To make even trivial decisions, our brains sift through a pile of “what ifs” and weigh the hypotheticals. Even for choices that seem automatic — jumping out of the way of a speeding car, for instance — the brain can very quickly extrapolate from past experiences to make predictions and guide behavior. In a paper published last month in Cell, a team of researchers in California peered into the brains of rats on the cusp of making a decision and watched their neurons rapidly play out the competing choices available to them. The mechanism they described might underlie not just decision-making, but also animals’ ability to envision more abstract possibilities — something akin to imagination. The group, led by the neuroscientist Loren Frank of the University of California, San Francisco, investigated the activity of cells in the hippocampus, the seahorse-shaped brain region known to play crucial roles both in navigation and in the storage and retrieval of memories. They gave extra attention to neurons called place cells, nicknamed “the brain’s GPS” because they mentally map an animal’s location as it moves through space. Place cells have been shown to fire very rapidly in particular sequences as an animal moves through its environment. The activity corresponds to a sweep in position from just behind the animal to just ahead of it. (Studies have demonstrated that these forward sweeps also contain information about the locations of goals or rewards.) These patterns of neural activity, called theta cycles, repeat roughly eight times per second in rats and represent a constantly updated virtual trajectory for the animals. All Rights Reserved © 2020

Keyword: Attention; Learning & Memory
Link ID: 27070 - Posted: 02.25.2020

Merrit Kennedy As doctors in London performed surgery on Dagmar Turner's brain, the sound of a violin filled the operating room. The music came from the patient on the operating table. In a video from the surgery, the violinist moves her bow up and down as surgeons behind a plastic sheet work to remove her brain tumor. The King's College Hospital surgeons woke her up in the middle of the operation in order to ensure they did not compromise parts of the brain necessary for playing the violin, such as parts that control precise hand movements and coordination. "We knew how important the violin is to Dagmar, so it was vital that we preserved function in the delicate areas of her brain that allowed her to play," Keyoumars Ashkan, a neurosurgeon at King's College Hospital, said in a press release. Turner, 53, learned that she had a slow-growing tumor in 2013. Late last year, doctors found that it had become more aggressive and the violinist decided to have surgery to remove it. In an interview with ITV News, Turner recalled doctors telling her, "Your tumor is on the right-hand side, so it will not affect your right-hand side, it will affect your left-hand side." "And I'm just like, 'Oh, hang on, this is my most important part. My job these days is playing the violin,' " she said, making a motion of pushing down violin strings with her left hand. Ashkan, an accomplished pianist, and his colleagues came up with a plan to keep the hand's functions intact. © 2020 npr

Keyword: Epilepsy; Movement Disorders
Link ID: 27054 - Posted: 02.20.2020

By Pallab Ghosh Science correspondent, BBC News, Seattle US researchers are developing a better understanding of the human brain by studying tissue left over from surgery. They say that their research is more likely to lead to new treatments than studies based on mouse and rat models. Dr Ed Lein, who leads the initiative at the Allen Institute has set up a scheme with local doctors to study left over tissue just hours after surgery. He gave details at the American Association for the Advancement of Science meeting in Seattle. "It is a little bit crazy that we have such a huge field where we are trying to solve brain diseases and there is very little understanding of the human brain itself," said Dr Lein. "The field as a whole is largely assuming that the human brain is similar to those of animal models without ever testing that view. "But the mouse brain is a thousand times smaller, and any time people look, they find significant differences." Dr Lein and his colleagues at the Allen Institute in Seattle set up the scheme with local neurosurgeons to study brain tissue just hours after surgery - with the consent of the patient. It functions as if it is still inside the brain for up to 48 hours after it has been removed. So Dr Lein and his colleagues have to drop everything and often have to work through the night once they hear that brain tissue has become available. © 2020 BBC

Keyword: Brain imaging; Epilepsy
Link ID: 27040 - Posted: 02.14.2020

Jon Hamilton Scientists have taken a small step toward personalizing treatment for depression. A study of more than 300 people with major depression found that brain wave patterns predicted which ones were most likely to respond to the drug sertraline (Zoloft), a team reported Monday in the journal Nature Biotechnology. If the approach pans out, it could offer better care for the millions of people in the U.S. with major depression. "This is definitely a step forward," says Michele Ferrante, who directs the computational psychiatry and computational neuroscience programs at the National Institute of Mental Health. He was not a part of the study. Right now, "one of our great frustrations is that when a patient comes in with depression we have very little idea what the right treatment for them is," says Dr. Amit Etkin, an author of the study and a professor of psychiatry at Stanford University. "Essentially, the medications are chosen by trial and error." Etkin is also the CEO of Alto Neuroscience, a Stanford-backed start-up developing computer-based approaches to diagnosing mental illness and selecting treatments. In the study, researchers used artificial intelligence to analyze the brainwave patterns in more than 300 patients who'd been diagnosed with major depression. Then they looked to see what happened when these same patients started treatment with sertraline. And one pattern of electrical activity seemed to predict how well a patient would do. "If the person scores particularly high on that, the recommendation would be to get sertraline," Etkin says. © 2020 npr

Keyword: Depression
Link ID: 27034 - Posted: 02.11.2020

Jon Hamilton Scientists have found a clue to how autism spectrum disorder disrupts the brain's information highways. The problem involves cells that help keep the traffic of signals moving smoothly through brain circuits, a team reported Monday in the journal Nature Neuroscience. The team found that in both mouse and human brains affected by autism, there's an abnormality in cells that produce a substance called myelin. That's a problem because myelin provides the "insulation" for brain circuits, allowing them to quickly and reliably carry electrical signals from one area to another. And having either too little or too much of this myelin coating can result in a wide range of neurological problems. For example, multiple sclerosis occurs when the myelin around nerve fibers is damaged. The results, which vary from person to person, can affect not only the signals that control muscles, but also the ones involved in learning and thinking. The finding could help explain why autism spectrum disorders include such a wide range of social and behavioral features, says Brady Maher, a lead investigator at the Lieber Institute for Brain Development and an associate professor in the psychiatry department at Johns Hopkins School of Medicine. "Myelination could be a problem that ties all of these autism spectrum disorders together," Maher says. And if that's true, he says, it might be possible to prevent or even reverse the symptoms using drugs that affect myelination. © 2020 npr

Keyword: Autism; Glia
Link ID: 27019 - Posted: 02.04.2020

Sydney Lupkin Sometimes, the approval of a new generic drug offers more hype than hope for patients' wallets, as people with multiple sclerosis know all too well. New research shows just how little the introduction of a generic version of Copaxone — one of the most popular MS drugs — did to lower their medicine costs. MS is an autoimmune disease that gradually damages the central nervous system, disrupting communication between the brain and the rest of the body. Its symptoms are different from patient to patient across a lifetime but can include weakness, numbness, vision problems, tremors and even paralysis. There's no cure for MS, though some patients experience long remissions of symptoms. Several prescription drugs can stave off multiple sclerosis attacks and slow down the disease, says Deborah Ewing-Wilson, a neurologist with University Hospitals Cleveland Medical Center. But the cost of some of the most effective medicines — which have undergone frequent price hikes over the years — can put added stress on her patients. "They are extremely expensive," says Ewing-Wilson. On average, the medicines cost $70,000 per year, according to a 2017 study. Some prices have increased fivefold from when the drugs were first approved by the Food and Drug Administration. Even with insurance, says Ewing-Wilson, patients can be left on the hook for anywhere from $3,000 to more than $50,000 a year. Some patients tell her they need to skip their medications altogether because they're unaffordable. So when a generic version of the injectable MS drug Copaxone — also known as glatiramer acetate — was launched in 2015, Dan Hartung, a drug policy researcher at Oregon Health & Science University, and his colleagues thought that might spur some price relief. After all, if a cheap multiple sclerosis drug were available, wouldn't patients flock to it, forcing other manufacturers to lower their prices to compete? © 2020 npr

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26980 - Posted: 01.22.2020

Katarina Zimmer As early as the 1990s, researchers proposed that a very common type of herpes virus—then known as human herpesvirus 6 (HHV6)—could be somehow involved in the development of multiple sclerosis, a neurodegenerative disease characterized by autoimmune reactions against the protective myelin coating of the central nervous system. However, the association between HHV6 and the disease soon became fraught with controversy as further studies produced discordant results. Complicating matters further, HHV6 turned out to be two related, but distinct variants—HHV6A and HHV6B. Because the two viruses are similar, for a while no method existed to tell whether a patient had been infected with one or the other, or both—making it difficult to draw a definitive association between either of the viruses and the disease. Now, a collaboration of European researchers has developed a technique capable of distinguishing antibodies against one variant from the other. Using that method in a Swedish cohort of more than 8,700 multiple sclerosis patients and more than 7,200 controls, they found that patients were much more likely to carry higher levels of anti-HHV6A antibodies than healthy people, while they were likelier to carry fewer antibodies against HHV6B. The findings, published last November in Frontiers in Immunology, hint that previous contradictory results may at least be partially explained by the fact that researchers couldn’t distinguish between the two viruses. “This article now makes a pretty convincing case that it is HHV6A that correlates with multiple sclerosis, and not HHV6B,” remarks Margot Mayer-Pröschel, a neuroscientist at the University of Rochester Medical Center who wasn’t involved in the study. “Researchers can now focus on one of these viruses rather than looking at [both] of them together.” © 1986–2020 The Scientist.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26956 - Posted: 01.14.2020

Ryan F. Mandelbaum Scientists have uncovered a new kind of electrical process in the human brain that could play a key role in the unique way our brains compute. Our brains are computers that work using a system of connected brain cells, called neurons, that exchange information using chemical and electric signals called action potentials. Researchers have discovered that certain cells in the human cortex, the outer layer of the brain, transmit signals in a way not seen in corresponding rodent cells. This process might be important to better understanding our unique brains and to improving programs that are based on a model of the human brain. “Human neurons may be more powerful computational devices than previously thought,” study corresponding author Matthew Larkum at Humboldt University of Berlin told Gizmodo in an email. Human brains have a thick cortex, especially the second and third layers (L2/3) from the surface. These layers contain brain cells with lots of branches, called dendrites, that connect them to and exchange information with other brain cells. The researchers acquired and analyzed slices of L2/3 tissue from patients with epilepsy and tumors, focusing specifically on these dendrites. Larkum explained via email that epilepsy surgeries provided a sufficient amount of available cortex tissue, while the tumor patient tissue was used to ensure that the observations weren’t unique to people with epilepsy. The team hooked the tissues to a patch clamp—essentially a system that constructs an electrical circuit from the cells and a measurement instrument—and used fluorescing microscope to observe the action of these L2/3 cells. The team noticed that inputted electrical currents ignited more action potentials than they would in rodent cells and that a chemical that should have blocked the dendrites’ activity did not completely do so. © 2020 G/O Media Inc.

Keyword: Learning & Memory
Link ID: 26934 - Posted: 01.04.2020

By Jennifer Couzin-Frankel Andrea VonMarkle arrived in Madison by helicopter ambulance 2 years ago, her life hanging in the balance. One month earlier she'd been a healthy 21-year-old juggling community college, waitressing, and weightlifting at a local gym. But after several weeks of feeling vaguely ill and forgetful, she was struck by a terrifying crisis. On New Year's Eve, VonMarkle's aunt had returned to the home they shared in northern Michigan to find her niece in trouble. "The door was open, and our dog was running down the street," VonMarkle says of the scene that greeted her aunt. "I just kept saying, ‘I don't know what's going on, and I don't know why I don't know.’" Then she started seizing. The seizures, which VonMarkle had never experienced before, didn't stop. Doctors at a local hospital were unable to quell her brain's electrical storm with powerful antiseizure medications. Because unremitting seizures can destroy brain tissue and damage other organs, the doctors put her into a medically induced coma. "They didn't know what to do with me," she says, "so they flew me to Madison," where the University of Wisconsin hospital had more resources and staff. VonMarkle, unconscious for weeks, wouldn't find out until much later what a stroke of luck that was. She became one of the first people whose sudden-onset, life-threatening epilepsy would be treated in a whole new way: not with standard antiseizure medications, but by disabling the deeper roots of the disease. For her, that meant a drug normally used for arthritis that seemed to soothe the inflammation powering her seizures. © 2019 American Association for the Advancement of Science.

Keyword: Epilepsy
Link ID: 26896 - Posted: 12.13.2019

There are three treatment options commonly used by doctors in the emergency room to treat patients with refractory status epilepticus, severe seizures that continue even after benzodiazepine medications, which are effective in controlling seizures in more than two-thirds of patients. New findings published in the New England Journal of Medicine reveal that the three drugs, levetiracetam, fosphenytoin, and valproate, are equally safe and effective in treating patients with this condition. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “Doctors can be confident that the particular treatment they choose for their patients with status epilepticus is safe and effective and may help them avoid the need to intubate the patient as well as stays in the intensive care unit,” said Robin Conwit, M.D., NINDS program director and an author of the study. “This was a truly collaborative, multidisciplinary study that involved pediatricians, emergency medicine doctors, neurologists, pharmacologists, and biostatisticians all contributing their expertise.” In the Established Status Epilepticus Treatment Trial (ESETT), led by Robert Silbergleit, M.D., professor at the University of Michigan, Ann Arbor; Jordan Elm, Ph.D., professor at Medical University of South Carolina; James Chamberlain, M.D., professor at George Washington University; and Jaideep Kapur, M.B., B.S., Ph.D., professor at the University of Virginia, more than 380 children and adults were randomized to receive levetiracetam, fosphenytoin, or valproate when they came to the emergency room experiencing a seizure. The researchers were trying to determine which of the anticonvulsant drugs was most effective in stopping seizures and improving a patient’s level of responsiveness within 60 minutes of administering treatment.

Keyword: Epilepsy
Link ID: 26870 - Posted: 12.04.2019

By Sofie Bates In multiple sclerosis, barriers that guard the brain become leaky, allowing some disease-causing immune cells to invade. Now scientists have identified a key molecule in the process that helps B cells breach the barriers. ALCAM, a protein produced by B cells, helps the immune cells sneak into the central nervous system, researchers report November 13 in Science Translational Medicine. Tests in mice and in artificial human brain barriers show that B cells without ALCAM, or activated leukocyte cell adhesion molecule, had trouble getting through the brain’s barriers. And in mice with a disease with some characteristics similar to MS, blocking ALCAM seemed to alleviate the disease’s severity. These early results indicate that the protein may be a good target for new treatments for multiple sclerosis in people, the researchers say. “This is a very important puzzle piece in how we understand multiple sclerosis,” says David Leppert, a neurologist at the University Hospital Basel in Switzerland who was not involved in the work. “How it translates into clinical applications is yet another question.” Worldwide, over 2.3 million people have multiple sclerosis, including nearly 1 million adults in the United States. Scientists think that rogue immune cells invade the brain and strip away the protective coating on nerve cells — leading to neurological issues and physical disability as the disease progresses. There’s no cure, and treatments don’t work for advanced stages of multiple sclerosis. Scientists have developed over a dozen medications to treat MS symptoms (SN: 11/29/17), one of which uses antibodies to destroy the body’s B cells. But that approach weakens patients’ immune systems, opening the door for future infections or cancer. In the new study, the researchers are instead focusing on preventing disease-causing B cells from entering the brain. © Society for Science & the Public 2000–2019

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26859 - Posted: 11.29.2019

Ashley P. Taylor Autoimmune diseases tend to ease up during pregnancy, and for women with multiple sclerosis, physicians have documented fewer relapses of the condition while women are pregnant compared to before and after having a baby. Anecdotally, many MS patients also feel better when they’re expecting. Researchers believe that this happens because during pregnancy, the body reins in its immune response so as to not reject the fetus—and in doing so counteracts autoimmune diseases. But as to how exactly this all works, scientists are uncertain. “Obviously, everybody would love to understand why it happens because if you could bottle that property of pregnancy, perhaps you could use it therapeutically,” Adrian Erlebacher, a reproductive immunologist at the University of California, San Francisco, tells The Scientist. To investigate why this happens in pregnant women with multiple sclerosis (MS), Stefan Gold, a neuroscientist at the Institute of Neuroimmunology and Multiple Sclerosis at the Universitätsklinikum Hamburg-Eppendorf, in Hamburg, Germany, and colleagues examined T cell populations in 11 MS patients before, during, and after pregnancy and in 12 women without MS during and after pregnancy. They categorized the T cells into different groups based on a genetic analysis of the cells’ receptors. In the first trimester, they found, MS patients’ T cells were dominated by just a few types, called clones, each with a different T cell receptor. Between the first and third trimesters, those dominant clones declined in abundance, and T cells became more evenly distributed across the different populations, Gold says. In women without MS, the pregnancy-associated changes in the T cell repertoire were not significant. Gold and his colleagues reported their results in Cell Reports on October 22. © 1986–2019 The Scientist.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26830 - Posted: 11.19.2019