Jyoti Madhusoodanan Douglas Storace still has the dollar bill that he triumphantly taped above his laboratory bench seven years ago, a trophy from a successful wager. His postdoctoral mentor, Larry Cohen at Yale University in New Haven, Connecticut, bet that Storace couldn’t express a protein sensor of voltage changes in mice back in September 2012. Storace won. The bill is a handy reminder that the experiments he aims to try in his new lab can work. And it’s a testament to just how tricky it is to correctly express these sensors and track their signals. Storace, now an assistant professor at Florida State University in Tallahassee, plans to use these sensors, known as genetically encoded voltage indicators (GEVIs), to study how neurons in the olfactory bulb sense and react to smells. GEVIs are voltage-sensitive, fluorescent proteins that change colour when a neuron fires or receives a signal. Because GEVIs can be targeted to individual cells and directly indicate a cell’s electrical signals, researchers consider them to be the ideal probes for studying neurons. But they have proved frustratingly difficult to use. “Being able to visualize voltage changes in a cell has always been the dream,” says neuroscientist Bradley Baker at the Korea Institute of Science and Technology in Seoul. “But probes that looked great often didn’t behave in ways that were useful.” Early GEVIs disappointed on several levels. They were bright when a cell was resting and dimmed when the cell fired an action potential, producing signals that were tough to distinguish from the background. And they failed to concentrate in the nerve-cell membranes, where they function. But researchers are beginning to solve these issues. Some are turning to advanced fluorescent proteins or chemical dyes for better signals; others are using directed evolution and high-throughput screens to make GEVIs more sensitive to voltage changes. Meanwhile, biologists are putting these molecules through their paces. GEVIs, says neuroscientist Katalin Toth at Laval University in Quebec City, Canada, are not yet widely used, but they’re getting there. “They are becoming brighter and faster — and growing in popularity,” she says. “I think this is the dawn of GEVIs.” © 2019 Springer Nature Limited

Keyword: Brain imaging
Link ID: 26703 - Posted: 10.15.2019

By Gina Kolata A new drug, created to treat just one patient, has pushed the bounds of personalized medicine and has raised unexplored regulatory and ethical questions, scientists reported on Wednesday. The drug, described in the New England Journal of Medicine, is believed to be the first “custom” treatment for a genetic disease. It is called milasen, named after the only patient who will ever take it: Mila (mee-lah) Makovec, who lives with her mother, Julia Vitarello, in Longmont, Colo. Mila, 8, has a rapidly progressing neurological disorder that is fatal. Her symptoms started at age 3. Within a few years, she had gone from an agile, talkative child to one who was blind and unable to stand or hold up her head. She needed a feeding tube and experienced up to 30 seizures a day, each lasting one or two minutes. Ms. Vitarello learned in December 2016 that Mila had Batten’s disease. But the girl’s case was puzzling, doctors said. Batten’s disease is recessive — a patient must inherit two mutated versions of a gene, MFSD8, to develop the disease. Mila had one just mutated gene, and the other copy seemed normal. That should have been sufficient to prevent the disease. In March 2017, Dr. Timothy Yu and his colleagues at Boston Children’s Hospital discovered that the problem with the intact gene lay in an extraneous bit of DNA that had scrambled the manufacturing of an important protein. That gave Dr. Yu an idea: Why not make a custom piece of RNA to block the effects of the extraneous DNA? Developing such a drug would be expensive, but there were no other options. © 2019 The New York Times Company

Keyword: Epilepsy
Link ID: 26688 - Posted: 10.10.2019

Jessica Wright Delicate lines dance across a screen mounted on the wall of the operating room. Their peaks and valleys become pronounced, suddenly flatten into a straight line—and then return, stronger than before. These digital traces represent the buzz of neurons in 12-year-old Kevin Lightner, read by two thin electrodes that surgeons have inserted deep into his brain. Kevin, who has autism and has had seizures since he was 8 years old, lies uncharacteristically still in the center of the room, draped under a blue sheet, his tiger-print pajamas neatly folded on a nearby shelf. What’s happening in this room may be the last chance to bring Kevin’s seizures under control. An hour and a half ago, neurosurgeon Saadi Ghatan removed a roughly 2-inch by 1-inch piece of the top of Kevin’s skull. He replaced it with a rectangular metal device, carefully screwed into the newly exposed edges of bone. The implant, a “responsive neurostimulation device,” is now transmitting signals from the electrodes planted in Kevin’s thalamus. The surgeons’ hope is that the device will learn to recognize what kind of brain activity precedes Kevin’s seizures and discharge electrical pulses to prevent them—like a “defibrillator for the brain,” as Ghatan puts it. If it works, it could save Kevin’s life. Ghatan projects the device’s readout to the screen by gently placing a black wand over the exposed metal in Kevin’s skull. The signal on the screen is surprisingly strong, given that it stems from the thalamus, a brain region that reveals its activity only weakly, if at all—and so is rarely the choice for monitoring seizures. © 1986–2019 The Scientist.

Keyword: Autism; Epilepsy
Link ID: 26687 - Posted: 10.10.2019

By Caroline Wyatt BBC News "I don't like to think of the future. It's such a big question mark. I just keep living in the present." Karine Mather was diagnosed with MS when she was 27, although she noticed the first symptoms much earlier. It started off as a mental-health issue with anxiety and depression, she remembers. Later, she noticed she was starting to limp when she walked longer distances. Karine began using a walker to help with her balance and stamina, and then a scooter when she could no longer walk very far. "I got to the stage where the wheelchair became quite liberating, and gave me back a sense of freedom again. Now I rely on the power-chair full-time because I can't stand by myself any more." Now Karine and her wife, Sarah, have had to give up their full-time jobs. Karine was forced to stop working as a customer service adviser at a bank because she could no longer fulfil the physical demands of work and Sarah gave up working as a data analyst so she could take care of Karine. Now 34, Karine retains the use of just one hand, and suffers pain, stiffness and spasticity in her body that has got worse as the disease has progressed. "It feels like a fist clenching all the time. And I have days when my mind is cloudy and I miss out words and sentences." Both remain upbeat but the financial, as well as the emotional, impact of MS has been huge. Karine's MS is the type known as "primary progressive", or PPMS, which meant that for the first years after diagnosis, no disease-modifying treatment was available. One new drug - Ocrevus, or ocrelizumab - was recently licensed for early PPMS in the UK but came too late to help Karine. Now the MS Society is launching an ambitious "Stop MS" appeal, aiming to raise £100m to fund research over the next decade into treatments that can stop the progression of disability in MS. © 2019 BBC

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26682 - Posted: 10.09.2019

By Benedict Carey For more than a decade, doctors have been using brain-stimulating implants to treat severe depression in people who do not benefit from medication, talk therapy or electroshock sessions. The treatment is controversial — any psychosurgery is, given its checkered history — and the results have been mixed. Two major trials testing stimulating implant for depression were halted because of disappointing results, and the approach is not approved by federal health regulators. Now, a team of psychiatric researchers has published the first long-term results, reporting Friday on patients who had stimulating electrodes implanted as long ago as eight years. The individuals have generally fared well, maintaining their initial improvements. The study, appearing in the American Journal of Psychiatry, was small, with just 28 subjects. Even still, experts said the findings were likely to extend interest in a field that has struggled. “The most impressive thing here is the sustained response,” Dr. Darin Dougherty, director of neurotherapeutics at Massachusetts General Hospital, said. “You do not see that for anything in this severe depression. The fact that they had this many people doing well for that long, that’s a big deal.” The implant treatment is known as deep brain stimulation, or D.B.S., and doctors have performed it for decades to help people control the tremors of Parkinson’s disease. In treating depression, surgeons thread an electrode into an area of the brain that sits beneath the crown of the head and is known to be especially active in people with severe depression. Running electrical current into that region, known as Brodmann Area 25, effectively shuts down its activity, resulting in relief of depression symptoms in many patients. The electrode is connected to a battery that is embedded in the chest. The procedure involves a single surgery; the implant provides continuous current from then on. © 2019 The New York Times Company

Keyword: Consciousness
Link ID: 26673 - Posted: 10.04.2019

By Rahma Ibrahim University researchers have discovered a new subset of cells — “metronome cells” — that may act as timekeepers in the brain, a finding that contributes new information to one of the biggest debates in neuroscience. While scientists have long known about the existence of cells in the brain that tend to be more reactive to stimuli — called fast spiking cells — they have long debated the function of a specific frequency of rhythm produced by those cells, called gamma oscillations. Some neuroscientists believe that gamma oscillations are at the root of how the brain functions. Other equally qualified scientists believe that these rhythms are merely a byproduct of brain activity. “Scientists’ faces will either light up or grow very overcast when someone mentions gamma oscillation,” explained Christopher Moore, professor of neuroscience and supervisor of the study. These gamma oscillations produce structured ripples in the brain at an interval of 40 Hertz, or 40 cycles per second. This regular pattern has led scientists to believe that perhaps the gamma oscillations act as an organizing clock, helping to align and connect information coming from different areas of the brain. Moore compared this theory to an orchestra; just as a conductor of an orchestra connects the various parts, the gamma oscillations have been thought to have similar function. If the conductor stops, then the whole orchestra cannot make good music. But for years, scientists have acknowledged limitations with this theory. Fast spiking cells and gamma rhythms have been found to respond to stimulus from outside the body of the cell. This raises concern if researchers assume that these oscillations act as a timekeeper; if the conductor is distracted every time they hear a trumpet, then the orchestra cannot be conducted.

Keyword: Sleep
Link ID: 26649 - Posted: 09.27.2019

Katarina Zimmer Several recent studies in high-profile journals reported to have genetically engineered neurons to become responsive to magnetic fields. In doing so, the authors could remotely control the activity of particular neurons in the brain, and even animal behavior—promising huge advances in neuroscientific research and speculation for applications even in medicine. “We envision a new age of magnetogenetics is coming,” one 2015 study read. But now, two independent teams of scientists bring those results into question. In studies recently posted as preprints to bioRxiv, the researchers couldn’t replicate those earlier findings. “Both studies . . . appear quite meticulously executed from a biological standpoint—multiple tests were performed across multiple biological testbeds,” writes Polina Anikeeva, a materials and cognitive scientist at MIT, to The Scientist in an email. “I applaud the authors for investing their valuable time and resources into trying to reproduce the results of their colleagues.” The promise of magnetogenetics Being able to use small-scale magnetic fields to control cells or entire organisms would have enormous potential for research and medical therapies. It would be a less invasive method than optogenetics, which requires the insertion of optical fibers to transmit light pulses to specific groups of neurons, and would provide a more rapid means of inducing neural activity than chemogenetics, which sparks biochemical reactions that can take several seconds to stimulate neurons. © 1986–2019 The Scientist

Keyword: Pain & Touch; Brain imaging
Link ID: 26642 - Posted: 09.24.2019

Ian Sample Science editor Society must prepare for a technological revolution in which brain implants allow people to communicate by telepathy, download new skills, and brag about their holidays in “neural postcards”, leading scientists say. While such far-fetched applications remain fiction for now, research into brain implants and other neural devices is advancing so fast that the Royal Society has called for a “national investigation” into the technology. “In 10 years’ time this is probably going to touch millions of people,” said Tim Constandinou, director of the next generation neural interfaces lab at Imperial College London, and co-chair of a new Royal Society report called iHuman. “These technologies are not possible today, but we are heading in that direction.” A neuroscientist explains: the need for ‘empathetic citizens’ - podcast The report foresees a “neural revolution” driven by electronic implants that communicate directly with the brain and other parts of the nervous system. By 2040, the scientists anticipate that implants will help the paralysed to walk, with other devices alleviating the symptoms of neurodegenerative diseases and treatment-resistant depression. The new wave of devices will go beyond existing products such as cochlear implant hearing aids and deep brain stimulators for people with Parkinson’s disease, with gadgets that help the healthy. In research labs, scientists are working on ways for people to type with their brains, and share thoughts by connecting their minds. Other teams are developing helmets and headbands to speed up learning and improve memory. “People could become telepathic to some degree, able to converse not only without speaking but without words, through access to each other’s thoughts at a conceptual level. This could enable unprecedented collaboration with colleagues and deeper conversations with friends,” the report states. © 2019 Guardian News & Media Limited

Keyword: Brain imaging; Depression
Link ID: 26595 - Posted: 09.10.2019

By Joanna Broder It had been two agonizing years of not knowing what was wrong with their baby who, since birth, had frequent spells of eye flickering, uncontrollable muscle contractions, pain and temporary paralysis. Simon and Nina Frost had spared no expense, taking Annabel to all the best neurologists around the country. Finally a potential diagnosis emerged: alternating hemiplegia of childhood, an ultrarare genetic disorder. The Frosts’ initial excitement at having answers quickly waned, however. They learned that, for many of the 900 or so children in the world affected by AHC, mutations in one of the genes that code for a subunit of the body’s critical sodium potassium pump interferes with the body’s ability to repeatedly fire nerve cells. In addition to Annabel’s other symptoms, difficulty breathing, choking and falling are common. They also learned that there is no effective treatment or cure, that any one of Annabel’s episodes has the potential to lead to permanent brain damage or death, and that it is hard to get information about the disease. Foundations dedicated to AHC informally recommend only four physicians in the United States as knowledgeable enough about the disorder to see patients. Of those who are closest to the Frosts, who live in Northwest D.C., one was too busy to see Annabel. There was a two-month wait to see the other one. The foundations themselves didn’t have many answers to the Frosts’ initial questions about life expectancy or what course Annabel’s disease might take. The Frosts discovered that relatively few scientists and clinicians study AHC, and their focus seemed to be basic research and not developing a therapy. © 1996-2019 The Washington Post

Keyword: Movement Disorders
Link ID: 26565 - Posted: 09.03.2019

By Laura Sanders It’s baby’s first brain wave, sort of. As lentil-sized clusters of nerve cells grow in a lab dish, they begin to fire off rhythmic electrical signals. These oscillations share some features with those found in the brains of developing human babies, researchers report October 3 in Cell Stem Cell. Three-dimensional spheres of human brain cells, called cerebral organoids, are extremely simplistic models of the human brain. Still, these easy-to-obtain organoids may offer a better way to study how a brain is made, and how that process can go wrong (SN: 2/20/18). “The field is white-hot,” with fast progress in both making and understanding brain organoids, says John Huguenard, a neuroscientist at Stanford University not involved in the study. Finding this sort of coordinated electrical activity in organoids’ nerve cells, or neurons, is a first, he says. “The neurons are growing up and becoming mature enough where they can not only start to behave like neurons and fire individually, but now they can be coordinated.” For the study, researchers coaxed stem cells into forming some of the neurons that make up the outer layer of the brain. These cortical organoids grew in lab dishes that held arrays of electrodes printed along the bottom, allowing the scientists to monitor electrical activity as the organoids developed. © Society for Science & the Public 2000–2019

Keyword: Development of the Brain
Link ID: 26556 - Posted: 08.30.2019

By Lauren Aguirre, STAT Scientists who study Alzheimer’s disease have mostly ignored the role of seizures, but that is beginning to change, and new research suggests they may provide insight into the progression of the disease and pave the way for treatments. It’s no surprise to neurologists that some people experience convulsive seizures in the later stages of the disease. In fact, the second patient ever to receive an Alzheimer’s diagnosis more than a century ago suffered from them. But because brain damage can cause seizures, they were long thought to be just one more casualty of a deteriorating brain. Now evidence is accumulating that such abnormal electrical activity is far more common and occurs much earlier—and perhaps even precedes obvious signs of memory loss. This raises the possibility that seizures may be intimately tied up with the progression of the disease. New research that lends credence to this hypothesis was shared at the Alzheimer’s Association International Conference in Los Angeles this week. One study looked at 55 patients between the ages of 50 and 69 who were admitted to an Israeli medical center with their first known seizure. A quarter of them went on to develop dementia—with a mean time to the diagnosis of eight and a half years. Another study of nearly 300,000 U.S. veterans over the age of 55 found that seizures were associated with twice the risk for developing dementia between one and nine years later. © 2019 Scientific American,

Keyword: Alzheimers; Epilepsy
Link ID: 26441 - Posted: 07.23.2019

By Carl Zimmer In a laboratory at the Stanford University School of Medicine, the mice are seeing things. And it’s not because they’ve been given drugs. With new laser technology, scientists have triggered specific hallucinations in mice by switching on a few neurons with beams of light. The researchers reported the results on Thursday in the journal Science. The technique promises to provide clues to how the billions of neurons in the brain make sense of the environment. Eventually the research also may lead to new treatments for psychological disorders, including uncontrollable hallucinations. “This is spectacular — this is the dream,” said Lindsey Glickfeld, a neuroscientist at Duke University, who was not involved in the new study. In the early 2000s, Dr. Karl Deisseroth, a psychiatrist and neuroscientist at Stanford, and other scientists engineered neurons in the brains of living mouse mice to switch on when exposed to a flash of light. The technique is known as optogenetics. In the first wave of these experiments, researchers used light to learn how various types of neurons worked. But Dr. Deisseroth wanted to be able to pick out any individual cell in the brain and turn it on and off with light. So he and his colleagues designed a new device: Instead of just bathing a mouse’s brain in light, it allowed the researchers to deliver tiny beams of red light that could strike dozens of individual brain neurons at once. To try out this new system, Dr. Deisseroth and his colleagues focused on the brain’s perception of the visual world. When light enters the eyes — of a mouse or a human — it triggers nerve endings in the retina that send electrical impulses to the rear of the brain. There, in a region called the visual cortex, neurons quickly detect edges and other patterns, which the brain then assembles into a picture of reality. © 2019 The New York Times Company

Keyword: Vision
Link ID: 26433 - Posted: 07.19.2019

By Denise Grady The actor Cameron Boyce, 20, who died on Saturday, had epilepsy, and his death was caused by a seizure that occurred during his sleep, his family said in a statement. Mr. Boyce starred in shows on the Disney Channel, including “Descendants” and “Jessie,” and appeared in a number of movies. “Cameron’s tragic passing was due to a seizure as a result of an ongoing medical condition, and that condition was epilepsy,” a Boyce family spokesperson told ABC News in a statement on Tuesday night. The Los Angeles County coroner’s office conducted an autopsy, but said it was awaiting the results of additional tests before determining an official cause of death. The most likely cause of his death was Sudep, or sudden unexpected death in epilepsy, said Dr. Orrin Devinsky, director of NYU Langone’s Comprehensive Epilepsy Center in Manhattan. He was not involved in Mr. Boyce’s care. Each year, about one in 1,000 people with epilepsy die from this disorder. In the United States, there are about 2,600 such deaths a year, though neurologists suspect that figure is an undercount. “It can happen to anyone with epilepsy,” Dr. Devinsky said. “Even the first seizure could be the last one. The more uncontrolled the seizures, the more severe, and the more they occur in sleep, the higher the risk.” About 70 percent of cases occur during sleep, and the people are often found facedown in bed. Usually, they have been sleeping alone. The probable cause of death is that the person stops breathing. A severe seizure can temporarily shut down the brain, including the centers that control respiration, Dr. Devinsky said. © 2019 The New York Times Company

Keyword: Epilepsy
Link ID: 26408 - Posted: 07.11.2019

Two nationally renowned neurosurgeons at Washington University School of Medicine in St. Louis will present “BrainWorks,” a live theatrical performance that explores the wonders of the human brain by dramatizing real-life neurological cases. The performance, comprised of four one-act plays, will debut July 19-21 at the Loretto-Hilton Center for the Performing Arts at Webster University. Albert Kim, PhD, MD, associate professor of neurological surgery, and Eric C. Leuthardt, MD, professor of neurological surgery, will guide the audience through each scene as they explain the mysteries of the human brain and the neuroscience of diseases such as Alzheimer’s disease, epilepsy, brain tumors and stroke. Kim and Leuthardt teamed up with playwrights from the New Dramatists to write each one-act play; the scenarios are based on patients the doctors have treated. “We have involved conversations about what’s going to happen – the course of treatment, the risks and benefits,” Kim said. “We also ensure the families become involved in those conversations. Together, the patient and family members become a part of the process that transforms and heals them. It’s this kind of conversation we want to bring to others through ‘BrainWorks.’” ©2019 Washington University in St. Louis

Keyword: Alzheimers; Epilepsy
Link ID: 26386 - Posted: 07.04.2019

By Ryan Dalton In the dystopian world of George Orwell’s Nineteen Eighty-Four, the government of Oceania aims to achieve thought control through the restriction of language. As explained by the character ‘Syme’, a lexicologist who is working to replace the English language with the greatly-simplified ‘Newspeak’: “Don’t you see that the whole aim of Newspeak is to narrow the range of thought?” While Syme’s own reflections were short-lived, the merits of his argument were not: the words and structure of a language can influence the thoughts and decisions of its speakers. This holds for English and Greek, Inuktitut and Newspeak. It also may hold for the ‘neural code’, the basic electrical vocabulary of the neurons in the brain. Neural codes, like spoken languages, are tasked with conveying all manner of information. Some of this information is immediately required for survival; other information has a less acute use. To accommodate these different needs, a balance is struck between the richness of information being transferred and the speed or reliability with which it is transferred. Where the balance is set depends on context. In the example of language, the mention of the movie Jaws at a dinner party might result in a ranging and patient—if disconcerting—discussion around the emotional impact of the film. In contrast, the observation of a dorsal fin breaking through the surf at the beach would probably elicit a single word, screamed by many beachgoers at once: “shark!” In one context, the language used has been optimized for richness; in the other, for speed and reliability. © 2019 Scientific American

Keyword: Language
Link ID: 26383 - Posted: 07.03.2019

Strobe lighting at music festivals can increase the risk of epileptic seizures, researchers have warned. The Dutch team said even people who have not been diagnosed with epilepsy might be affected. Their study was prompted by the case of a 20-year-old, with no history of epilepsy, who suddenly collapsed and had a fit at a festival. The Epilepsy Society said festivals should limit lighting to the recommended levels. Epilepsy is a condition that affects the brain. There are many types, and it can start at any age. Around 3% of people with epilepsy are photosensitive, which means their seizures are triggered by flashing or flickering lights, or patterns. The Health and Safety Executive recommends strobe lighting should be kept to a maximum of four hertz (four flashes per second) in clubs and at public events. 'Life-affirming' The researchers studied electronic dance music festivals because they often use strobe lighting. They looked at data on people who needed medical care among the 400,000 visitors to 28 day and night-time dance music festivals across the Netherlands in 2015. The figures included 241,000 people who were exposed to strobe lights at night-time festivals. Thirty people at night-time events with strobe lighting had a seizure, compared with nine attending daytime events. The team, led by Newel Salet of the VU Medical Centre in Amsterdam, writing in BMJ Open, said other factors could increase the risk of seizures. But they added: "Regardless of whether stroboscopic lights are solely responsible or whether sleep deprivation and/or substance abuse also play a role, the appropriate interpretation is that large [electronic dance music] festivals, especially during the night-time, probably cause at least a number of people per event to suffer epileptic seizures." They advise anyone with photosensitive epilepsy to either avoid such events or to take precautionary measures, such as getting enough sleep and not taking drugs, not standing close to the stage, and leaving quickly if they experience any "aura" effects. © 2019 BBC

Keyword: Epilepsy; Vision
Link ID: 26323 - Posted: 06.12.2019

By MOISES VELASQUEZ-MANOFF When Catherine Jacobson first heard about the promise of cannabis, she was at wits’ end. Her 3-year-old son, Ben, had suffered from epileptic seizures since he was 3 months old, a result of a brain malformation called polymicrogyria. Over the years, Jacobson and her husband, Aaron, have tried giving him at least 16 different drugs, but none provided lasting relief. They lived with the grim prognosis that their son — whose cognitive abilities never advanced beyond those of a 1-year-old — would likely continue to endure seizures until the cumulative brain injuries led to his death. In early 2012, when Jacobson learned about cannabis at a conference organized by the Epilepsy Therapy Project, she felt a flicker of hope. The meeting, in downtown San Francisco, was unlike others she had attended, which were usually geared toward lab scientists and not directly focused on helping patients. This gathering aimed to get new treatments into patients’ hands as quickly as possible. Attendees weren’t just scientists and people from the pharmaceutical industry. They also included, on one day of the event, families of patients with epilepsy. The tip came from a father named Jason David, with whom Jacobson began talking by chance outside a presentation hall. He wasn’t a presenter or even very interested in the goings-on at the conference. He had mostly lost faith in conventional medicine during his own family’s ordeal. But he claimed to have successfully treated his son’s seizures with a cannabis extract, and now he was trying to spread the word to anyone who would listen. The idea to try cannabis extract came to David after he found out that the federal government held a patent on cannabidiol, a molecule derived from the cannabis plant that is commonly referred to as CBD. Unlike the better-known marijuana molecule delta-9-tetrahydrocannabinol, or THC, CBD isn’t psychoactive; it doesn’t get users high. But in the late 1990s, scientists at the National Institutes of Health discovered that it could produce remarkable medicinal effects. In test tubes, the molecule shielded neurons from oxidative stress, a damaging process common in many neurological disorders, including epilepsy.

Keyword: Drug Abuse; Epilepsy
Link ID: 26236 - Posted: 05.15.2019

By Benedict Carey The research on brain stimulation is advancing so quickly, and the findings are so puzzling, that a reader might feel tempted to simply pre-order a genius cap from Amazon, to make sense of it all later. In just the past month, scientists reported enhancing the working memory of older people, using electric current passed through a skullcap, and restoring some cognitive function in a brain-damaged woman, using implanted electrodes. Most recently, the Food and Drug Administration approved a smartphone-size stimulator intended to alleviate attention-deficit problems by delivering electric current through a patch placed on the forehead. Last year, another group of scientists announced that they, too, had created a brain implant that boosts memory storage. All the while, a do-it-yourself subculture continues to grow, of people who are experimenting with placing electrodes in their skulls or foreheads for brain “tuning.” Predicting where all these efforts are headed, and how and when they might converge in a grand methodology, is an exercise in rank speculation. Neuro-stimulation covers too many different techniques, for various applications and of varying quality. About the only certainties are the usual ones: that a genius cap won’t arrive anytime soon, and that any brain-zapping gizmo that provides real benefit also is likely to come with risk. Nevertheless, the field is worth watching because it hints at some elementary properties of brain function. Unlike psychiatric drugs, or psychotherapy, pulses of current can change people’s behavior very quickly, and reliably. Turn the current on and things happen; turn it off and the effect stops or tapers. © 2019 The New York Times Company

Keyword: Learning & Memory; Alzheimers
Link ID: 26232 - Posted: 05.14.2019

By Kelly Servick For a hair-thin probe penetrating the brain to listen in on neurons' electrical chatter, finesse is key. It's easy to rip tissue on the way in. And once in place, a probe can do further damage that muffles the signals it aims to detect. But recent reports describe a generation of finer probes that should prove less damaging. Just a few micrometers thick—comparable to neurons themselves—these tools may soon capture unprecedented long-term recordings from hard-to-reach parts of animal brains. And they may lead to more sophisticated brain-computer interfaces for people. Improved material fabrication techniques have helped labs create the exquisitely fine probes, says neural engineer Timothy Hanson, who developed a system for inserting tiny electrodes while at the University of California, San Francisco (UCSF). And lab tests have shown that brain research using ultrasmall electrodes "can be done, and that it's worthwhile." Conventional brain probes are already vanishingly tiny. Stiff electrodes known as Michigan probes, commonly used in neuroscience research, are pointed, ribbonlike shafts that can be as thin as 15 micrometers and are usually 60 micrometers wide or more. In a standard grid known as the Utah array, each spike is roughly 200 micrometers thick at its base. But in the months after either device is implanted, its connection to neurons typically weakens and its signal fades. A key reason is that the probe provokes an immune reaction in the brain. Its initial plunge into the tissue can tear blood vessels. And even after that damage heals, the probe continues to push and pull on surrounding tissue. In response, nonneuronal cells called glia multiply and form scars that push neurons away from the electrode. © 2019 American Association for the Advancement of Science.

Keyword: Brain imaging
Link ID: 26200 - Posted: 05.02.2019

James Hamblin The past two weeks have been frenetic for Bre Hushaw, who is now known to millions of people as the girl in the depression helmet. Hushaw has been hearing from people all around the world who want to try it, or at least want to know how it works. Her life as a meme began when she agreed to an on-camera interview with the local-news site AZfamily.com for a story headlined “Helmet Approved by FDA to Treat Depression Available in Arizona.” The feel-good tale of Hushaw’s miraculous recovery from severe depression was tossed into the decontextualizing maw of the internet and distilled down to a screenshot of a young woman looking like a listless Stormtrooper. Jokes poured in. Some of the most popular, each with more than 100,000 likes on Twitter, include: “If u see me with this ugly ass helmet mind ur business.” “Friend: hey everything alright? Me, wearing depression helmet: yeah I’m just tired.” “The depression helmet STAYS ON during sex.” Hushaw has been tracking the virality, sometimes cringing and sometimes laughing. She replies to as many serious inquiries as she can, while finishing up her senior year at Northern Arizona University before starting a job in marketing. A year ago, she didn’t think she was going to live to graduation. When she was 10 years old, her mother died. Her depression symptoms waxed and waned from then on, and they waxed especially when she heard the gunshots on her campus during a shooting at the school in 2015. She’s tried many medications over the years—14, by her count. (c) 2019 by The Atlantic Monthly Group.

Keyword: Depression
Link ID: 26163 - Posted: 04.22.2019