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

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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

By Gabriel Finkelstein Unlike Charles Darwin and Claude Bernard, who endure as heroes in England and France, Emil du Bois-Reymond is generally forgotten in Germany — no streets bear his name, no stamps portray his image, no celebrations are held in his honor, and no collections of his essays remain in print. Most Germans have never heard of him, and if they have, they generally assume that he was Swiss. But it wasn’t always this way. Du Bois-Reymond was once lauded as “the foremost naturalist of Europe,” “the last of the encyclopedists,” and “one of the greatest scientists Germany ever produced.” Contemporaries celebrated him for his research in neuroscience and his addresses on science and culture; in fact, the poet Jules Laforgue reported seeing his picture hanging for sale in German shop windows alongside those of the Prussian royal family. Those familiar with du Bois-Reymond generally recall his advocacy of understanding biology in terms of chemistry and physics, but during his lifetime he earned recognition for a host of other achievements. He pioneered the use of instruments in neuroscience, discovered the electrical transmission of nerve signals, linked structure to function in neural tissue, and posited the improvement of neural connections with use. He served as a professor, as dean, and as rector at the University of Berlin, directed the first institute of physiology in Prussia, was secretary of the Prussian Academy of Sciences, established the first society of physics in Germany, helped found the Berlin Society of Anthropology, oversaw the Berlin Physiological Society, edited the leading German journal of physiology, supervised dozens of researchers, and trained an army of physicians. © 2019 Scientific American

Keyword: Consciousness
Link ID: 26811 - Posted: 11.11.2019

By Kelly Servick CHICAGO, ILLINOIS—By harnessing the power of imagination, researchers have nearly doubled the speed at which completely paralyzed patients may be able to communicate with the outside world. People who are “locked in”—fully paralyzed by stroke or neurological disease—have trouble trying to communicate even a single sentence. Electrodes implanted in a part of the brain involved in motion have allowed some paralyzed patients to move a cursor and select onscreen letters with their thoughts. Users have typed up to 39 characters per minute, but that’s still about three times slower than natural handwriting. In the new experiments, a volunteer paralyzed from the neck down instead imagined moving his arm to write each letter of the alphabet. That brain activity helped train a computer model known as a neural network to interpret the commands, tracing the intended trajectory of his imagined pen tip to create letters (above). Eventually, the computer could read out the volunteer’s imagined sentences with roughly 95% accuracy at a speed of about 66 characters per minute, the team reported here this week at the annual meeting of the Society for Neuroscience. The researchers expect the speed to increase with more practice. As they refine the technology, they will also use their neural recordings to better understand how the brain plans and orchestrates fine motor movements. © 2019 American Association for the Advancement of Science.

Keyword: Robotics; Brain imaging
Link ID: 26745 - Posted: 10.24.2019

Ian Sample Science editor Doctors in the US have launched a clinical trial to see whether exposure to flickering lights and low frequency sounds can slow the progression of Alzheimer’s disease. A dozen patients enrolled in the trial will have daily one-hour sessions of the radical therapy which researchers hope will induce brain activity that protects against the disorder. Animal tests have shown that exposure to light and sound waves at 40Hz reinforces so-called gamma waves in the brain, with knock-on effects across the organ. In mice used to model the disease, the therapy appears to boost the activity of the brain’s immune cells, making them clear the aberrant proteins that build up in Alzheimer’s. Li-Huei Tsai, a neuroscientist who is leading the trial at MIT, told the Society for Neuroscience meeting in Chicago on Tuesday that the therapy improved the survival and health of the animals’ neurons, boosted their connectivity, and dilated blood vessels, all of which may benefit patients. “We would like to see if our approach slows Alzheimer’s disease,” Tsai told the Guardian. The patients enrolled on the trial will have cognitive tests every three months to assess their brain function and regular scans to measure their brain activity and the connectivity of neurons across the organ. © 2019 Guardian News & Media Limited

Keyword: Alzheimers; Brain imaging
Link ID: 26741 - Posted: 10.23.2019

Alexander D. Reyes Information in the brain is thought to be encoded as complex patterns of electrical impulses generated by thousands of neuronal cells. Each impulse, known as an action potential, is mediated by currents of charged ions flowing through a neuron’s membrane. But how the ions pass through the insulated membrane of the neuron remained a puzzle for many years. In 1976, Erwin Neher and Bert Sakmann developed the patch-clamp technique, which showed definitively that currents result from the opening of many channel proteins in the membrane1. Although the technique was originally designed to record tiny currents, it has since become one of the most important tools in neuroscience for studying electrical signals — from those at the molecular scale to the level of networks of neurons. By the 1970s, current flowing through the cell was generally accepted to result from the opening of many channels in the membrane, although the underlying mechanism was unknown. At that time, current was commonly recorded by impaling tissue with a sharp electrode — a pipette with a very fine point. Unfortunately, however, the signal recorded in this way was excessively noisy, and so only the large, ‘macroscopic’ current — the collective current mediated by many different types of channel — that flows through the tissue could be resolved. In 1972, Bernard Katz and Ricardo Miledi2, pioneers of the biology of the synaptic connections between cells, managed to infer from the macroscopic current certain properties of the membrane channels, but only after a heroic effort to exclude all possible confounding factors. The problem was that the macroscopic current could be influenced by factors not directly related to channel activity, such as cell geometry and modulatory processes that regulate cell excitability. Also troublesome was that interpretations of macroscopic-current features were based on unverified assumptions about the statistics of individual channel activity2,3. Despite Katz and Miledi’s careful analyses, there was a lingering doubt about whether their conclusions were correct. The crucial data were obtained by Neher and Sakmann using patch clamp. © 2019 Springer Nature Limited

Keyword: Brain imaging
Link ID: 26737 - Posted: 10.23.2019

By Laura Sanders CHICAGO — Light pulses from outside a monkey’s brain can activate nerve cells deep within. This external control, described October 20 at the annual meeting of the Society for Neuroscience, might someday help scientists treat brain diseases such as epilepsy. Controlling nerve cell behavior with light, a method called optogenetics, often requires thin optical fibers to be implanted in the brain (SN: 1/15/10). That invasion can cause infections, inflammation and tissue damage, says study coauthor Diego Mendoza-Halliday of MIT. He and his colleagues created a new light-responsive molecule, called SOUL, that detects extra dim light. After injecting SOUL into macaque monkeys’ brains, researchers shined blue light through a hole in the skull. SOUL-containing nerve cells, which were as deep as 5.8 millimeters in the brain, became active. A dose of orange light stopped this activity. SOUL can’t sense light coming from outside of the macaques’ skulls. But in mice, the system works through the skull, the researchers reported. LEDs implanted just under people’s skulls might one day be used to treat brain diseases. Such a system might be able to temporarily turn off nerve cells that are about to cause an epileptic seizure, for instance. “This is basically scooping out a piece of brain and then putting it back in a few seconds later,” when the risk of a seizure has dropped, Mendoza-Halliday says. © Society for Science & the Public 2000–2019.

Keyword: Brain imaging
Link ID: 26735 - Posted: 10.23.2019

Mengying Zhang While many people love colorful photos of landscapes, flowers or rainbows, some biomedical researchers treasure vivid images on a much smaller scale – as tiny as one-thousandth the width of a human hair. To study the micro world and help advance medical knowledge and treatments, these scientists use fluorescent nano-sized particles. Quantum dots are one type of nanoparticle, more commonly known for their use in TV screens. They’re super tiny crystals that can transport electrons. When UV light hits these semiconducting particles, they can emit light of various colors. One nanometer is one-millionth of a millimeter. RNGS Reuters/Nanosys That fluorescence allows scientists to use them to study hidden or otherwise cryptic parts of cells, organs and other structures. I’m part of a group of nanotechnology and neuroscience researchers at the University of Washington investigating how quantum dots behave in the brain. Common brain diseases are estimated to cost the U.S. nearly US$800 billion annually. These diseases – including Alzheimer’s disease and neurodevelopmental disorders – are hard to diagnose or treat. Nanoscale tools, such as quantum dots, that can capture the nuance in complicated cell activities hold promise as brain-imaging tools or drug delivery carriers for the brain. But because there are many reasons to be concerned about their use in medicine, mainly related to health and safety, it’s important to figure out more about how they work in biological systems. © 2010–2019, The Conversation US, Inc.

Keyword: Brain imaging
Link ID: 26708 - Posted: 10.16.2019

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