Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals

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by Peter Hess / Infants with particular patterns of electrical activity in the brain go on to have high levels of autism traits as toddlers, a new study shows1. Specifically, babies who have unusually high or low synchrony between certain brain waves — as measured by electroencephalography (EEG) — at 3 months old tend to score high on a standardized scale of autism-linked behaviors when they are 18 months old. These levels of synchrony reflect underlying patterns of connectivity in the brain. The findings suggest that EEG could help clinicians identify autistic babies long before these children show behaviors flagged by standard diagnostic tests. The work “reinforces the concept and the truism that brain development is affected before autism diagnoses are made,” says lead researcher Shafali Spurling Jeste, associate professor of psychiatry and neurology at the University of California, Los Angeles. “We believe that we could work to start rewiring the brain if we intervene effectively and early enough. That message, quite simply, is a very important one.” The study involved ‘baby sibs,’ the younger siblings of autistic children. Baby sibs are 10 to 20 times more likely to have autism than the general population. Previous research showed similar patterns of altered connectivity in functional magnetic resonance imaging (MRI) data from infants who were later diagnosed with autism, but MRI is costly and prone to errors. EEG measurements, on the other hand, are relatively inexpensive and simple to perform, which makes them more practical for clinical use, says Charles Nelson, professor of pediatrics and neuroscience at Harvard University, who was not involved in the study. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27380 - Posted: 07.25.2020

Salvatore Domenic Morgera How the brain works remains a puzzle with only a few pieces in place. Of these, one big piece is actually a conjecture: that there’s a relationship between the physical structure of the brain and its functionality. The brain’s jobs include interpreting touch, visual and sound inputs, as well as speech, reasoning, emotions, learning, fine control of movement and many others. Neuroscientists presume that it’s the brain’s anatomy – with its hundreds of billions of nerve fibers – that make all of these functions possible. The brain’s “living wires” are connected in elaborate neurological networks that give rise to human beings’ amazing abilities. It would seem that if scientists can map the nerve fibers and their connections and record the timing of the impulses that flow through them for a higher function such as vision, they should be able to solve the question of how one sees, for instance. Researchers are getting better at mapping the brain using tractography – a technique that visually represents nerve fiber routes using 3D modeling. And they’re getting better at recording how information moves through the brain by using enhanced functional magnetic resonance imaging to measure blood flow. But in spite of these tools, no one seems much closer to figuring out how we really see. Neuroscience has only a rudimentary understanding of how it all fits together. To address this shortcoming, my team’s bioengineering research focuses on relationships between brain structure and function. The overall goal is to scientifically explain all the connections – both anatomical and wireless – that activate different brain regions during cognitive tasks. We’re working on complex models that better capture what scientists know of brain function. t © 2010–2020, The Conversation US, Inc.

Keyword: Brain imaging
Link ID: 27373 - Posted: 07.18.2020

By Lisa Sanders, M.D. The early-morning light wakened the middle-aged man early on a Saturday morning in 2003. He felt his 51-year-old wife move behind him and turned to see her whole body jerking erratically. He was a physician, a psychiatrist, and knew immediately that she was having a seizure. He grabbed his phone and dialed 911. His healthy, active wife had never had a seizure before. But this was only the most recent strange episode his wife had been through over the past 18 months. A year and a half earlier, the man returned to his suburban Pittsburgh home after a day of seeing patients and found his wife sitting in the kitchen, her hair soaking wet. He asked if she had just taken a shower. No, she answered vaguely, without offering anything more. Before he could ask her why she was so sweaty, their teenage son voiced his own observations. Earlier that day, the boy reported, “She wasn’t making any sense.” That wasn’t like her. Weeks later, his daughter reported that when she arrived home from school, she heard a banging sound in a room in the attic. She found her mother under a futon bed, trying to sit up and hitting her head on the wooden slats underneath. Her mother said she was looking for something, but she was obviously confused. The daughter helped her mother up and brought her some juice, which seemed to help. With both episodes, the children reported that their mother didn’t seem upset or distressed. The woman, who had trained as a psychiatrist before giving up her practice to stay with the kids, had no recollection of these odd events. The Problem Is Sugar Her husband persuaded her to see her primary-care doctor. Upon hearing about these strange spells, the physician said she suspected that her patient was having episodes of hypoglycemia. Very low blood sugar sends the body into a panicked mode of profuse sweating, shaking, weakness and, in severe cases, confusion. She referred her to a local endocrinologist. © 2020 The New York Times Company

Keyword: Epilepsy
Link ID: 27341 - Posted: 07.02.2020

by Peter Hess Early behavioral signs predict seizures in autistic children, according to a new study1. Previous work has shown that 5 to 46 percent of people with autism experience seizures. And autistic adults with epilepsy have, on average, less cognitive ability and weaker daily living skills than their autistic peers who do not have seizures2. The new study shows that people with autism who begin having seizures during childhood show small but significant behavioral differences before they ever experience a seizure, compared with those who do not develop epilepsy. They score lower than their peers on measures of quality of life and adaptive behaviors, which include communication, daily living skills, socialization and motor skills. They score higher on a measure of hyperactivity. The results suggest that seizures and certain behavioral issues in autism could have common origins, says co-lead investigator Jamie Capal, associate professor of pediatrics and neurology at the University of North Carolina at Chapel Hill. “I think it really does show us that in individuals with autism who eventually have epilepsy, there is some shared mechanism early on that we just haven’t been able to identify,” Capal says. Early signs: To investigate the relationship between childhood behaviors in autism and the development of seizures, the researchers analyzed data on 472 autistic children aged 2 to 15 from the Autism Treatment Network, a medical registry that includes 12 clinics in the United States and Canada. None of the children had experienced seizures before enrolling in the network, but 22 developed seizures two to six years after enrollment. © 2020 Simons Foundation

Keyword: Autism; Epilepsy
Link ID: 27294 - Posted: 06.09.2020

By Lisa Sanders, M.D. “I know what Danny has,” said the boy’s aunt to the boy’s mother, her sister-in-law. Her voice on the phone cracked with excitement. “I saw someone just like him on TV!” This was last fall, and Danny was 18. He had been a medical mystery since he was 7 months old. His mother recalled that she had just finished changing his diaper and picked him up when she heard him make a strange clicking noise, his mouth opening and closing oddly. And then his head flopped back as she held him. She hurried to the living room of their Queens home to show her husband, but by the time she got there, Danny was fine. Those sudden episodes of clicking and collapse happened again and again, eventually occurring more than 100 times a day. His first doctors thought these episodes could be tiny seizures. But none of the antiseizure medications they prescribed helped. Then, when Danny was 8, and almost too big for his mother to catch when he slow-motion slumped to the floor, his parents found a doctor who was willing to explore a different diagnosis and treatment. Could this be a rare disease known as cataplexy? In this disorder, patients have episodes of sudden weakness in the skeletal muscles of the body. In some, cataplexy may affect only the face or neck, causing the eyelids to droop or the head to fall forward. But in others, it can also affect the entire body. These episodes are often triggered by strong emotion, which was the case for Danny. Cataplexy is usually part of another rare disorder, narcolepsy, in which the normal control of sleep and wakefulness is somehow lost. Those with narcolepsy have sudden episodes of sleep that invade their waking hours and transient periods of wakefulness that disrupt their sleep. © 2020 The New York Times Company

Keyword: Sleep; Epilepsy
Link ID: 27290 - Posted: 06.08.2020

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