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

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

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

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

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

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

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

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

Keyword: Depression
Link ID: 27034 - Posted: 02.11.2020

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

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

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

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

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

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

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

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

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

Keyword: Epilepsy
Link ID: 26896 - Posted: 12.13.2019

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

Keyword: Epilepsy
Link ID: 26870 - Posted: 12.04.2019

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

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

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

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

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