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

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By Esther Landhuis On the heels of one failed drug trial after another, a recent study suggests people with early Alzheimer’s disease could reap modest benefits from a device that uses magnetic fields to produce small electric currents in the brain. Alzheimer’s is a degenerative brain disorder that afflicts more than 46 million people worldwide. At present there are no treatments that stop or slow its progression, although several approved drugs offer temporary relief from memory loss and other cognitive symptoms by preventing the breakdown of chemical messengers among nerve cells. The new study tested a regimen that combines computerized cognitive training with a procedure known as repetitive transcranial magnetic stimulation (rTMS). The U.S. Food and Drug Administration has cleared rTMS devices for some migraine sufferers as well as for people with depression who have not responded to antidepressant medications. Last month at the 13th International Conference on Alzheimer’s and Parkinson’s Diseases in Vienna, Israel-based Neuronix reported results of a phase III clinical trial of its therapy system, known as neuroAD, in Alzheimer’s patients. More than 99 percent of Alzheimer’s drug trials have failed. The last time a phase III trial for a wholly new treatment succeeded (not just a combination of two already approved drugs) was about 15 years ago. The recent study did not test a drug but rather a device, which usually has an easier time gaining FDA clearance. NeuroAD has been approved for use in Europe and the U.K., where six weeks of therapy costs about $6,700. The system is not commercially available in the U.S., but based on the latest results the company submitted an application for FDA clearance last fall. © 2017 Scientific American

Keyword: Alzheimers
Link ID: 23635 - Posted: 05.19.2017

Jon Hamilton Tiny, 3-D clusters of human brain cells grown in a petri dish are providing hints about the origins of disorders like autism and epilepsy. An experiment using these cell clusters — which are only about the size of the head of a pin — found that a genetic mutation associated with both autism and epilepsy kept developing cells from migrating normally from one cluster of brain cells to another, researchers report in the journal Nature. "They were sort of left behind," says Dr. Sergiu Pasca, an assistant professor of psychiatry and behavioral sciences at Stanford. And that type of delay could be enough to disrupt the precise timing required for an actual brain to develop normally, he says. The clusters — often called minibrains, organoids or spheroids — are created by transforming skin cells from a person into neural stem cells. These stem cells can then grow into structures like those found in the brain and even form networks of communicating cells. Brain organoids cannot grow beyond a few millimeters in size or perform the functions of a complete brain. But they give scientists a way to study how parts of the brain develop during pregnancy. "One can really understand both a process of normal human brain development, which we frankly don't understand very well, [and] also what goes wrong in the brain of patients affected by diseases," says Paola Arlotta, a professor of stem cell and regenerative biology at Harvard who was not involved in the cell migration study. Arlotta is an author of a second paper in Nature about creating a wide variety of brain cells in brain organoids. © 2017 npr

Keyword: Development of the Brain; Autism
Link ID: 23545 - Posted: 04.27.2017

By KAREN BARROW The World Health Organization estimates that more than 50 million people worldwide have some form of epilepsy, a neurological disorder that is characterized by recurring episodes of seizure. While seizures come in various forms, those with epilepsy cope with similar issues: social stigma, complex treatment options and a feeling of powerlessness. Here, eight men, women and children discuss what it’s like to live with epilepsy. Denise L. Pease, an assistant comptroller for New York City, began having complex partial seizures after a car accident in which she suffered a traumatic brain injury. But because Ms. Pease lives alone, it wasn’t until a relative saw her having a tonic-clonic seizure, what used to be known as a grand mal seizure, that she realized she had developed epilepsy. Tonic-clonic seizures typically involve the whole body and can be very dramatic. Ms. Pease began to notice that she would get a strange taste in her mouth before a seizure, so whenever that happened she made sure she was seated in a safe location and waited for the seizure to pass. This sensation of an oncoming seizure, called an aura, is common among people with epilepsy. After eight years of trying different medications to control her epilepsy, Ms. Pease is happy to be back at work and no longer lives in fear of an imminent seizure. Ms. Pease is hopeful that she will soon be able to drive, and she continues to plan for her future. “When you have epilepsy, you have to be your own advocate,” she said. Sallie Gallagher’s son, Michael, started having complex partial seizures at age 4. This type of seizure doesn’t cause the full-body twitching associated with tonic-clonic seizure, but it can cause a person to start to act strangely or be completely unaware of his surroundings. © 2017 The New York Times Company

Keyword: Epilepsy
Link ID: 23544 - Posted: 04.27.2017

By BENEDICT CAREY Well-timed pulses from electrodes implanted in the brain can enhance memory in some people, scientists reported on Thursday, in the most rigorous demonstration to date of how a pacemaker-like approach might help reduce symptoms of dementia, head injuries and other conditions. The report is the result of decades of work decoding brain signals, helped along in recent years by large Department of Defense grants intended to develop novel treatments for people with traumatic brain injuries, a signature wound of the Iraq and Afghanistan wars. The research, led by a team at the University of Pennsylvania, is published in the journal Current Biology. Previous attempts to stimulate human memory with implanted electrodes had produced mixed results: Some experiments seemed to sharpen memory, but others muddled it. The new paper resolves this confusion by demonstrating that the timing of the stimulation is crucial. Zapping memory areas when they are functioning poorly improves the brain’s encoding of new information. But doing so when those areas are operating well — as they do for stretches of the day in most everyone, including those with deficits — impairs the process. “We all have good days and bad days, times when we’re foggy, or when we’re sharp,” said Michael Kahana, who with Youssef Ezzyat led the research team. “We found that jostling the system when it’s in a low-functioning state can jump it to a high-functioning one.” Researchers cautioned that implantation is a delicate procedure and that the reported improvements may not apply broadly. The study was of epilepsy patients; scientists still have much work to do to determine whether this approach has the same potential in people with other conditions, and if so how best to apply it. But in establishing the importance of timing, the field seems to have turned a corner, experts said. © 2017 The New York Times Company

Keyword: Learning & Memory; Epilepsy
Link ID: 23520 - Posted: 04.21.2017

By David Noonan Like many people with epilepsy, Richard Shane, 56, has some problems with memory. But he can easily recall his first seizure, 34 years ago. “I was on the phone with my father, and I noticed that I started moaning, and I lost some level of consciousness,” Shane says. After experiencing a similar episode three weeks later, he went to a doctor and learned he had epilepsy, a neurological disorder caused by abnormal electrical activity in the brain. The first medication he was prescribed, Dilantin (phenytoin), failed to stop or even reduce his seizures. So did the second and the third. His epilepsy, it turned out, was drug-resistant. Over the next 22 years Shane suffered two to five or more seizures a week. He and his doctors tried every new antiseizure drug that came along, but none worked. Finally, in 2004, as a last resort, a neurosurgeon removed a small part of Shane's brain where his seizures originated. “It was a matter of what sucks less,” Shane says, “having brain surgery or having epilepsy.” Shane has been seizure-free ever since. As many as three million people in the U.S. live with epilepsy, and more than 30 percent of them receive inadequate relief from medication, a number that persists despite the introduction of more than a dozen new antiepileptic drugs since 1990. Although surgery has helped some patients such as Shane, uncontrollable epilepsy remains a living nightmare for patients and an intractable foe for clinicians and researchers. “I hate to say it, but we do not know why” some people respond to medications and others do not, says neurologist Michael Rogawski, who studies epilepsy treatments at the University of California, Davis. And yet if the central conundrum continues, so does the determined quest for new and different approaches to treating the toughest cases. © 2017 Scientific American

Keyword: Epilepsy
Link ID: 23495 - Posted: 04.15.2017

Consider two children who have childhood absence epilepsy (CAE), the most common form of pediatric epilepsy. They both take the same drug — one child sees an improvement in their seizures, but the other does not. A new study in the Annals of Neurology identified the genes that may underlie this difference in treatment outcomes, suggesting there may be potential for using a precision medicine approach to help predict which drugs will be most effective to help children with CAE. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS) and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), both part of the National Institutes of Health. “A better understanding of genetic factors underlying a disease and the way that people respond to treatments may help healthcare providers select the best therapies for children with CAE,” said Vicky Whittemore, Ph.D., program director at NINDS. A team led by Tracy A. Glauser, M.D., director of the Comprehensive Epilepsy Center at Cincinnati Children’s Hospital Medical Center and professor of pediatrics in the University of Cincinnati College of Medicine, investigated whether there may be a genetic basis for different responses to three drugs used for CAE (ethosuximide, valproic acid, and lamotrigine). The experiments focused on three genes that code for T-type calcium channels that are involved in CAE and one gene that codes for a transporter that shuttles the drugs out of the brain. T-type calcium channels help control the firing rate of brain cells. The current study is part of a 32-center, randomized, controlled clinical trial that compared the effects of the three most commonly used drugs in 446 children who were recently diagnosed with CAE.

Keyword: Epilepsy; Genes & Behavior
Link ID: 23480 - Posted: 04.12.2017

By Jia Naqvi An experimental technique reduces the tics, or involuntary movements and vocal outbursts, associated with severe Tourette's syndrome in young adults, a study published Friday found. The surgical technique, called thalamic deep brain stimulation (DBS), sends electrical impulses to a specific area of the brain that reduces the tics, according to the study published in the Journal of Neurosurgery. The finding adds to the growing body of evidence about the safety and effectiveness of deep brain stimulation, which might eventually lead the Food and Drug Administration to approve the treatment for Tourette's syndrome, according to the researchers. “Our study shows that deep brain stimulation is a safe, effective treatment for young adults with severe Tourette syndrome that cannot be managed with current therapies,” said Alon Mogilner, an associate professor in the departments of neurosurgery and anesthesiology at New York University Langone and director of its Center for Neuromodulation, in a news release. “This treatment has the potential to improve the quality of life for patients who are debilitated through their teenage years and young adulthood.” Tourette's syndrome, a type of neurological disorder, according to various studies afflicts from 0.3 to 0.6 percent of children in the United States, with around 138,000 ages 6 to 17 being diagnosed with the condition. The causes for the syndrome are not well known and are thought to be largely genetic, with unidentified environmental factors increasing the likelihood of the condition. Usually the syndrome begins in childhood and the condition improves with age for some people, but for others the symptoms become more severe to the point that people become socially isolated and unable to work or attend school. © 1996-2017 The Washington Post

Keyword: Tourettes
Link ID: 23468 - Posted: 04.08.2017

Sallie Baxendale, Temporal lobe epilepsy—a common form of epilepsy characterized by seizures that begin in the memory-regulating temporal lobe—does appear to influence personality, though not in the way many may think and certainly not in the way people have believed throughout history. The idea of the epileptic personality is an ancient one. Thousands of years ago people with epilepsy were thought to be possessed by either divine beings or demons. In fact, the notion that a seizure represents a kind of communion with another spiritual realm still holds sway in some societies today. In more recent history, Westerners largely perceived epilepsy as a punishment for morally lax behavior. In one 1892 paper, the author claimed that debauchery and excessive lust frequently led to epilepsy and that a person could trigger a seizure by listening to love songs and eating chocolate. More recently, scientists began investigating whether epilepsy, in fact, altered personality. In 1975 neurologists Stephen Waxman and Norman Geschwind, both then at Harvard University, published an analysis based on observations of their patients with temporal lobe epilepsy in which they reported that many patients had a tendency toward religiosity, intense emotions, detailed thoughts, and a compulsion to write or draw. This cluster of characteristics became known as the epileptic personality. Over the next decade other researchers added hostility, aggression, lack of humor and obsessiveness to the list of personality traits supposedly associated with the condition. © 2017 Scientific American

Keyword: Epilepsy; Emotions
Link ID: 23464 - Posted: 04.08.2017

Katherine Whalley The mammalian suprachiasmatic nucleus (SCN) can autonomously generate circadian oscillations in gene expression and neuronal activity, enabling it to fulfil its role as the brain's 'master circadian clock'. Although the contributions of specific neuronal populations to SCN function have begun to be elucidated, the potential influences of SCN astrocytes are relatively unexplored. Brancaccio et al. now reveal an important role for astrocyte–neuron signalling in SCN timekeeping. SCN neurons exhibit circadian oscillations in their intracellular calcium level ([Ca2+]i), peaking during the circadian 'day'. To determine whether similar fluctuations in activity are observed in astrocytes, the authors expressed a genetically encoded reporter of astrocytic [Ca2+]i in organotypic SCN slices. Long-term imaging revealed the presence of circadian oscillations in astrocytic [Ca2+]i, which was at its highest during the circadian 'night' and thus was anti-phasic to that of neurons. Astrocytes release 'gliotransmitters', including glutamate, in response to an increase in [Ca2+]i. When the authors expressed a genetically encoded sensor of the extracellular glutamate concentration ([Glu]e) in SCN slices, they observed circadian oscillations in [Glu]e that were in phase with astrocytic [Ca2+]i. oscillations. That astrocytes were the source of the measured [Glu]e was supported by the fact that the pharmacological inhibition of astrocytic glutamate catabolism or the genetic ablation of astrocytes, respectively, increased or reduced [Glu]e. © 2017 Macmillan Publishers Limited,

Keyword: Biological Rhythms; Glia
Link ID: 23436 - Posted: 04.01.2017

By KATIE THOMAS The Food and Drug Administration approved on Tuesday the first drug to treat a severe form of multiple sclerosis, offering hope to patients who previously had no other options to combat a relentless disease that leads to paralysis and cognitive decline. The federal agency also cleared the drug to treat people with the more common, relapsing form of the disease. “I think that this is a very big deal,” said Dr. Stephen Hauser, the chairman of the neurology department at the University of California, San Francisco, and leader of the steering committee that oversaw the late-stage clinical trials of the drug, ocrelizumab. “The magnitude of the benefits that we’ve seen with ocrelizumab in all forms of M.S. are really quite stunning.” The drug, which will be sold under the brand name Ocrevus by Genentech, showed the most notable results in patients with relapsing multiple sclerosis, appearing to halt progression of the disease with few serious side effects. In patients with the more severe form, primary progressive multiple sclerosis, the drug only modestly slowed patients’ decline, but medical experts described it as an important first step. “This sort of opens the door for us,” said Dr. Fred D. Lublin, who was a crucial investigator for the clinical trial and is director of the Corinne Goldsmith Dickinson Center for Multiple Sclerosis at Mount Sinai Hospital in New York. “Once we open that door, then we do better and better and better. It’s a very encouraging result.” Genentech, which is owned by the Swiss pharmaceutical giant Roche, said Tuesday that it would charge a list price of $65,000 a year, which — though expensive — is 25 percent less than an existing drug, Rebif, that was shown to be clinically inferior to Ocrevus in the two clinical trials that led to Ocrevus’s approval. © 2017 The New York Times Company

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 23421 - Posted: 03.29.2017

By Erik Vance The world’s smallest arachnid, the Samoan moss spider, is at a third of a millimeter nearly invisible to the human eye. The largest spider in the world is the goliath birdeater tarantula, which weighs 5 ounces and is about the size of a dinner plate. For reference, that is about the same difference in scale between that same tarantula and a bottlenose dolphin. And yet the bigger spider does not act in more complex ways than its tiny counterpart. “Insects and spiders and the like—in terms of absolute size—have among the tiniest brains we’ve come across,” says William Wcislo, a scientist at the Smithsonian Tropical Research Institute in Panama City. “But their behavior, as far as we can see, is as sophisticated as things that have relatively large brains. So then there’s the question: How do they do that?” No one would argue that a tarantula is as smart as a dolphin or having a really big brain is not an excellent way to perform complicated tasks. But a growing number of scientists are asking the question: Is it the only way? Do you need a big brain to hunt elusive prey, design complicated structures or produce complex social dynamics? For generations scientists have wondered how intelligent creatures developed large brains to perform complicated tasks. But Wcislo is part of a small community of scientists less interested in how brains have grown than how they have shrunk and yet shockingly still perform tasks as well or better than similar species that are much larger in size. In other words, it’s what scientists call brain miniaturization, not unlike the scaling down in size of the transistors in a computer chip. This research, in fact, may hold clues to innovative design strategies that engineers might incorporate in future generations of computers. © 2017 Scientific American

Keyword: Miscellaneous
Link ID: 23418 - Posted: 03.29.2017

Many epilepsy patients in Australia are turning to medicinal cannabis to manage their seizures, a survey has shown. The nationwide survey found 14% of people with epilepsy had used cannabis products to manage the condition. Of those, 90% of adults and 71% of children with epilepsy, according to their parents, reported success in managing seizures. GW Pharmaceuticals doubles in value after cannabis drug success in epilepsy trial Read more Published in the journal Epilepsy & Behaviour, the Epilepsy Action Australia study, in partnership with the Lambert Initiative at the University of Sydney, surveyed 976 respondents to examine cannabis use in people with epilepsy, reasons for use and any perceived benefits self-reported by consumers. The main reason given for trying cannabis products was to seek a treatment with “more favourable” side-effects compared with standard antiepileptic drugs. The lead author of the study, Anastatsia Suraeve from the Lambert Initiative, said researchers had gained further insight into the reasons that influence use. “Despite the limitations of a retrospective online survey, we cannot ignore that a significant proportion of adults and children with epilepsy are using cannabis-based products in Australia, and many are self-reporting considerable benefits to their condition,” Suraeve said. “More systematic clinical studies are urgently needed to help us better understand the role of cannabinoids in epilepsy,” she said. © 2017 Guardian News and Media Limited

Keyword: Epilepsy; Drug Abuse
Link ID: 23342 - Posted: 03.11.2017

By Ruth Williams Scientists at New York University’s School of Medicine have probed the deepest layers of the cerebral cortices of mice to record the activities of inhibitory interneurons when the animals are alert and perceptive. The team’s findings reveal that these cells exhibit different activities depending on the cortical layer they occupy, suggesting a level of complexity not previously appreciated. In their paper published in Science today (March 2), the researchers also described the stimulatory and inhibitory inputs that regulate these cells, adding further details to the picture of interneuron operations within the cortical circuitry. “It is an outstanding example of circuit analysis and a real experimental tour de force,” said neuroscientist Massimo Scanziani of the University of California, San Diego, who was not involved in the work. Christopher Moore of Brown University in Providence, Rhode Island, who also did not participate in the research, echoed Scanziani’s sentiments. “It’s just a beautiful paper,” he said. “They do really hard experiments and come up with what seem to be really valid [observations]. It’s a well-done piece of work.” The mammalian cerebral cortex is a melting pot of information, where signals from sensory inputs, emotions, and memories are combined and processed to produce a coherent perception of the world. Excitatory cells are the most abundant type of cortical neurons and are thought to be responsible for the relay and integration of this information, while the rarer interneurons inhibit the excitatory cells to suppress information flow. Interneurons are “a sort of gatekeeper in the cortex,” said Scanziani. © 1986-2017 The Scientist

Keyword: Attention
Link ID: 23314 - Posted: 03.04.2017

By Matt Reynolds If you’re happy and you know it, clap someone else’s hands. A muscle stimulation system aims to evoke empathy by triggering involuntary hand gestures in one person in response to mood changes in another. “If you’re moving in the same way as another person you might understand that person better,” says Max Pfeiffer at the University of Hannover in Germany. Pfeiffer and his team wired up four people to an EEG machine that measured changes in the electrical activity in their brain as they watched film clips intended to provoke three emotional responses: amusement, anger and sadness. These people were the “emotion senders”. Each sender was paired with an “emotion recipient” who wore electrodes on their arms that stimulated their muscles and caused their arms and hands to move when the mood of their partner changed. The gestures they made were based on American Sign Language for amusement, anger and sadness. To express amusement, volunteers had their muscles stimulated to raise one arm, to express anger they raised an arm and made a claw gesture, and to express sadness they slowly slid an arm down their chest. These resemble natural movements associated with the feelings, so the team hypothesised that they would evoke the relevant emotion. Asked to rate how well the gestures corresponded to the emotions, the volunteers largely matched the gestures to the correct mood. © Copyright Reed Business Information Ltd.

Keyword: Brain imaging
Link ID: 23302 - Posted: 03.02.2017

By Michelle Roberts A multiple sclerosis treatment being tested in patients can stop the disease for at least five years, say doctors. The risky therapy involves wiping out the person's immune system with strong cancer drugs and then rebooting it with a stem cell transplant. Doctors say only some patients will be suitable to try it, particularly because it is so high risk. Out of 281 people who had the treatment, nearly half benefited, but eight died shortly afterwards. The work in JAMA Neurology is one of the largest and longest investigations of this aggressive MS treatment. Mark Rye, 41 and from Surrey, had his transplant just before Christmas 2016. Two months on he is doing well. "It was a hard decision, knowing what could go wrong. My wife and I discussed it for many, many hours. We've got small children and I didn't want my MS to get worse and end up in a wheelchair. "I did this to halt the condition and so that I can be there for my children, who are still so young. I want to be able to play rugby and football with them as they grow up." What is not clear is for how long the therapy might ultimately work. Freeze frame MS is not fatal, but it is incurable. The disease causes the immune system to attack the protective coating of nerves in the brain and spinal cord, which can create problems with a person's vision, walking and balance. © 2017 BBC

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 23263 - Posted: 02.21.2017

Jon Hamilton Scientists may have solved the mystery of nodding syndrome, a rare form of epilepsy that has disabled thousands of children in East Africa. The syndrome seems to be caused by the immune system's response to a parasitic worm, an international team reports in the journal Science Translational Medicine. And they think it's the same worm responsible for river blindness, an eye infection that's also found in East Africa. The finding means that current efforts to eliminate river blindness should also reduce nodding syndrome, says Avi Nath, an author of the study and chief of the section of infections of the nervous system at the National Institute of Neurological Disorders and Stroke. "We can prevent new infections even if we can't treat the ones who already have nodding syndrome," Nath says. Drugs can kill the parasite in its early stages. Nodding syndrome usually strikes children between 5 and 16 who live in rural areas of northern Uganda and South Sudan. Their bodies and brains stop growing. And they experience frequent seizures. "These are kids, young kids, you would expect that they should be running around playing," says Nath, who visited Uganda several years ago. "Instead, if you go to these villages they are just sitting there in groups," so villagers can keep an eye on them. © 2017 npr

Keyword: Epilepsy; Neuroimmunology
Link ID: 23237 - Posted: 02.16.2017

“Bench-to-bedside” describes research that has progressed from basic science in animal models that has led to therapies used in patients. Now, a study in the journal Brain describes what could be considered a direct “aquarium-to-bedside” approach, taking a drug discovered in a genetic zebrafish model of epilepsy and testing it, with promising results, in a small number of children with the disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This is the first time that scientists have taken a potential therapy discovered in a fish model directly into people in a clinical trial,” said Vicky Whittemore, Ph.D., program director at the NINDS. “These findings suggest that it may be possible to treat neurological disorders caused by genetic mutations through an efficient and precision medicine-style approach.” Scott C. Baraban, Ph.D., the William K. Bowes Jr. Endowed Chair in Neuroscience Research and professor of neurological surgery at the University of California, San Francisco (UCSF), postdoctoral fellow Aliesha Griffin, Ph.D., and colleagues used a zebrafish model of Dravet syndrome to test the drug lorcaserin and found that it suppressed seizure activity in the fish. Dravet syndrome is a severe form of pediatric epilepsy characterized by frequent daily drug-resistant seizures and developmental delays. It is caused by a genetic mutation, which Dr. Baraban’s group was able to introduce into the zebrafish to cause epilepsy. Dr. Baraban and his colleague Kelly Knupp, M.D. at the University of Colorado, Denver, then tested lorcaserin in five children with Dravet syndrome. The children were resistant to other anti-epileptic drugs and participated in this study through a compassionate use, off-label program.

Keyword: Epilepsy; Development of the Brain
Link ID: 23209 - Posted: 02.10.2017

New clinical trial results provide evidence that high-dose immunosuppressive therapy followed by transplantation of a person's own blood-forming stem cells can induce sustained remission of relapsing-remitting multiple sclerosis (MS), an autoimmune disease in which the immune system attacks the central nervous system. Five years after receiving the treatment, called high-dose immunosuppressive therapy and autologous hematopoietic cell transplant (HDIT/HCT), 69 percent of trial participants had survived without experiencing progression of disability, relapse of MS symptoms or new brain lesions. Notably, participants did not take any MS medications after receiving HDIT/HCT. Other studies have indicated that currently available MS drugs have lower success rates. The trial, called HALT-MS, was sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and conducted by the NIAID-funded Immune Tolerance Network (link is external) (ITN). The researchers published three-year results from the study in December 2014, and the final five-year results appear online Feb. 1 in Neurology, the medical journal of the American Academy of Neurology. “These extended findings suggest that one-time treatment with HDIT/HCT may be substantially more effective than long-term treatment with the best available medications for people with a certain type of MS,” said NIAID Director Anthony S. Fauci, M.D. “These encouraging results support the development of a large, randomized trial to directly compare HDIT/HCT to standard of care for this often-debilitating disease.”

Keyword: Multiple Sclerosis; Stem Cells
Link ID: 23177 - Posted: 02.02.2017

Ian Sample Science editor Doctors have used a brain-reading device to hold simple conversations with “locked-in” patients in work that promises to transform the lives of people who are too disabled to communicate. The groundbreaking technology allows the paralysed patients – who have not been able to speak for years – to answer “yes” or “no” to questions by detecting telltale patterns in their brain activity. Three women and one man, aged 24 to 76, were trained to use the system more than a year after they were diagnosed with completely locked-in syndrome, or CLIS. The condition was brought on by amyotrophic lateral sclerosis, or ALS, a progressive neurodegenerative disease which leaves people totally paralysed but still aware and able to think. “It’s the first sign that completely locked-in syndrome may be abolished forever, because with all of these patients, we can now ask them the most critical questions in life,” said Niels Birbaumer, a neuroscientist who led the research at the University of Tübingen. “This is the first time we’ve been able to establish reliable communication with these patients and I think that is important for them and their families,” he added. “I can say that after 30 years of trying to achieve this, it was one of the most satisfying moments of my life when it worked.” © 2017 Guardian News and Media Limited

Keyword: Consciousness; Brain imaging
Link ID: 23176 - Posted: 02.01.2017

NEUROSCIENCE, like many other sciences, has a bottomless appetite for data. Flashy enterprises such as the BRAIN Initiative, announced by Barack Obama in 2013, or the Human Brain Project, approved by the European Union in the same year, aim to analyse the way that thousands or even millions of nerve cells interact in a real brain. The hope is that the torrents of data these schemes generate will contain some crucial nuggets that let neuroscientists get closer to understanding how exactly the brain does what it does. But a paper just published in PLOS Computational Biology questions whether more information is the same thing as more understanding. It does so by way of neuroscience’s favourite analogy: comparing the brain to a computer. Like brains, computers process information by shuffling electricity around complicated circuits. Unlike the workings of brains, though, those of computers are understood on every level. Eric Jonas of the University of California, Berkeley, and Konrad Kording of Northwestern University, in Chicago, who both have backgrounds in neuroscience and electronic engineering, reasoned that a computer was therefore a good way to test the analytical toolkit used by modern neuroscience. Their idea was to see whether applying those techniques to a microprocessor produced information that matched what they already knew to be true about how the chip works. © The Economist Newspaper Limited 2017.

Keyword: Brain imaging
Link ID: 23126 - Posted: 01.21.2017