Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
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Kerri Smith Researchers have both created and relieved symptoms of obsessive-compulsive disorder (OCD) in genetically modified mice using a technique that turns brain cells on and off with light, known as optogenetics. The work, by two separate teams, confirms the neural circuits that contribute to the condition and points to treatment targets. It also provides insight into how quickly compulsive behaviours can develop — and how quickly they might be soothed. The results of the studies are published in Science1, 2. Brain scanning in humans with OCD has pointed to two areas — the orbitofrontal cortex, just behind the eyes, and the striatum, a hub in the middle of the brain — as being involved in the condition's characteristic repetitive and compulsive behaviours. But “in people we have no way of testing cause and effect”, says Susanne Ahmari, a psychiatrist and neuroscientist at Columbia University in New York who led one of the studies. It is not clear, for example, whether abnormal brain activity causes the compulsions, or whether the behaviour simply results from the brain trying to hold symptoms at bay by compensating. “There’s been a big debate in the field,” says Satinder Kaur Singh of Yale University in New Haven, Connecticut, who studies molecules involved in OCD-like disorders but was not involved in the new studies. “What the Ahmari paper shows is that it is causative.” © 2013 Nature Publishing Group
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 18248 - Posted: 06.08.2013
By James Gallagher Health and science reporter, BBC News An experimental treatment to stop the body attacking its own nervous system in patients with multiple sclerosis (MS) appears safe in trials. The sheath around nerves cells, made of myelin, is destroyed in MS, leaving the nerves struggling to pass on messages. A study on nine patients, reported in Science Translational Medicine, tried to train the immune system to cease its assault on myelin. The MS Society said the idea had "exciting potential". As nerves lose their ability to talk to each other, the disease results in problems moving and balancing and can affect vision. There are drugs that can reduce number and severity of attacks, but there is no cure. The disease is caused by the body's immune system thinking that myelin is a foreign body like a flu virus. Researchers at the Northwestern University Feinberg School of Medicine developed a technique to retrain the immune system. They took blood samples and coupled white blood cells, a part of the immune system, to fragments of myelin. This was injected back into the patients to make them tolerate myelin. BBC © 2013
By Geoffrey Mohan Hyperactive brain cells firing together could be an early indicator of autism and developmental disabilities, a team of UCLA researchers has found. Networks of neurons were found to be firing in a highly synchronized and seemingly unrelenting fashion, even through sleep, in the brains of juvenile mice that have a genetic abnormality similar to one that causes mental retardation and autism symptoms in humans, according to the research published online Monday in Nature Neuroscience. Without independently firing neurons, the human brain would be about as functionally complicated as a digital switch. With it, we compose poetry and send robotic carts to Mars. "If you want to code information, you can’t just have all the cells fire together or not, because then that’s just binary. It goes up and down," said UCLA neuroscientist Carlos Portera-Cailliau, a lead author of the report. “But if you have billions of neurons, all firing independently or in small clusters, then you can code a lot of information.” That “de-synchronization” was greatly diminished in the neocortex of the juvenile mice that had been altered so that they lack the same protein known to cause mental retardation and autistic behaviors in humans. These so-called Fmr1 Knockout mice, named for the gene that is knocked out, exhibit autism behaviors, among them social deficits – they don’t go over and sniff and examine a new mouse introduced to the cage, like wild mice would. Copyright 2013
Link ID: 18235 - Posted: 06.05.2013
Kerri Smith When Karl Deisseroth moved into his first lab in 2004, he found himself replacing a high-profile tenant: Nobel-prizewinning physicist Steven Chu. “His name was still on the door when I moved in,” says Deisseroth, a neuroscientist, of the basement space at Stanford University in California. The legacy has had its benefits. When chemistry student Feng Zhang dropped by looking for Chu, Deisseroth convinced him to stick around. “I don't think he knew who I was. But he got interested enough.” Deisseroth is now a major name in science himself. He is associated with two blockbuster techniques that allow researchers to show how intricate circuits in the brain create patterns of behaviour. The development of the methods, he says, came from a desire to understand mechanisms that give rise to psychiatric disease — and from the paucity of techniques to do so. “It was extremely clear that for fundamental advances in these domains I would have to spend time developing new tools,” says Deisseroth. His measured tone and laid-back demeanour belie the frenzy that his lab's techniques are generating in neuroscience. First came optogenetics1, which involves inserting light-sensitive proteins from algae into neurons, allowing researchers to switch the cells on and off with light. Deisseroth developed the method shortly after starting his lab, working with Zhang and Edward Boyden, a close collaborator at the time. Optogenetics has since been adopted by scientists around the world to explore everything from the functions of neuron subtypes to the circuits altered in depression or autism. Deisseroth has lost count of how many groups are using it. “We sent clones to thousands of laboratories,” he says. © 2013 Nature Publishing Group
Keyword: Brain imaging
Link ID: 18210 - Posted: 05.30.2013
By Nathan Seppa Multiple sclerosis, long considered a disease of white females, has affected more black women in recent years, a new study finds. Hispanic and Asian women, who have previously seemed to be at less risk of MS, remain so, researchers report May 7 in Neurology. The findings bolster a theory that vitamin D deficiency, which is common in people with dark skin in northern latitudes, contributes to MS. MS is a debilitating condition in which the protective coatings on nerves in the central nervous system get damaged, resulting in a loss of motor control, muscle weakness, vision complications and other problems. The National Multiple Sclerosis Society estimates that 2.1 million people worldwide have the condition. The researchers scanned medical information from 3.5 million people who were members of the health maintenance organization Kaiser Permanente Southern California and found that 496 people received diagnoses of MS from 2008 through 2010. Of these patients, women comprised 70 percent, not an unusual fraction for people with MS. Surprisingly, the patients included 84 black women. That means the annual incidence of MS in black women was 10.2 cases per 100,000 people. That’s not a great risk for an individual, but it was higher than the annual rates for white, Hispanic and Asian women, which were 6.9, 2.9 and 1.4 per 100,000 people, respectively. Among blacks, women had three times the incidence as men; in the other racial and ethnic groups, the MS rate in women was roughly double that of men. © Society for Science & the Public 2000 - 2013
By Ingrid Wickelgren I have seen the invisible arms of multiple sclerosis, a potentially devastating disease of the nervous system, touch friends, relatives and acquaintances. They perturbed the personality of a father of a close friend and left him unable to keep a job and support the family. They forced a young woman I met years ago to walk tentatively, watching her step. They put one beloved member of my extended family with two small children in a wheelchair and took away his voice. Nowadays, many people with MS find that new medications can mitigate the progression of their disease (see “New Treatments Tackle Multiple Sclerosis,” by James D. Bowen, Scientific American Mind, July/August 2013). But many mysteries remain about the cause of the disorder and no one knows how to prevent or cure it. About a decade ago, a technology entrepreneur named Art Mellor, who was diagnosed with MS in 2000, founded an organization called Accelerated Cure Project based in Waltham, Massachusetts to help speed progress on solving these mysteries, in part through greater collaboration among scientists. In one of its efforts, it maintains a repository of thousands of blood samples from patients who visited any of 10 U.S. clinics. The samples are made available to anyone willing to share their data with the Project. Scientists have used these samples in more than 70 different studies into the causes of MS and how to diagnose and treat it. A number of these experiments involve trying to identify molecular signs of the disease in the blood, in hopes of developing a simple blood test for the disorder. Such a test might reduce the time and cost of an MS diagnosis. The primary tool for spotting MS today is magnetic resonance imaging (MRI), which can reveal inflammation in the brain characteristic of the disorder. © 2013 Scientific American
Keyword: Multiple Sclerosis
Link ID: 18132 - Posted: 05.08.2013
National Institutes of Health researchers used the popular anti-wrinkle agent Botox to discover a new and important role for a group of molecules that nerve cells use to quickly send messages. This novel role for the molecules, called SNARES, may be a missing piece that scientists have been searching for to fully understand how brain cells communicate under normal and disease conditions. "The results were very surprising,” said Ling-Gang Wu, Ph.D., a scientist at NIH’s National Institute of Neurological Disorders and Stroke. “Like many scientists we thought SNAREs were only involved in fusion." Every day almost 100 billion nerve cells throughout the body send thousands of messages through nearly 100 trillion communication points called synapses. Cell-to-cell communication at synapses controls thoughts, movements, and senses and could provide therapeutic targets for a number of neurological disorders, including epilepsy. Nerve cells use chemicals, called neurotransmitters, to rapidly send messages at synapses. Like pellets inside shotgun shells, neurotransmitters are stored inside spherical membranes, called synaptic vesicles. Messages are sent when a carrier shell fuses with the nerve cell’s own shell, called the plasma membrane, and releases the neurotransmitter “pellets” into the synapse. SNAREs (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) are three proteins known to be critical for fusion between carrier shells and nerve cell membranes during neurotransmitter release.
by Sara Reardon People with epilepsy have to learn to cope with the unpredictable nature of seizures – but that could soon be a thing of the past. A new brain implant can warn of seizures minutes before they strike, enabling them to get out of situations that could present a safety risk. Epileptic seizures are triggered by erratic brain activity. The seizures last for seconds or minutes, and their unpredictability makes them hazardous and disruptive for people with epilepsy, says Mark Cook of the University of Melbourne in Australia. Like earthquakes, "you can't stop them, but if you knew when one was going to happen, you could prepare", he says. With funding from NeuroVista, a medical device company in Seattle, Cook and his colleagues have developed a brain implant to do just that. The device consists of a small patch of electrodes that measure brain wave activity. Warning light Over time, the device's software learns which patterns of brainwave activity indicate that a seizure is about to happen. When it detects such a pattern, the implant then transmits a signal through a wire to a receiver implanted under the wearer's collarbone. This unit alerts the wearer by wirelessly activating a handheld gadget with coloured lights – a red warning light, for example, signals that a seizure is imminent. © Copyright Reed Business Information Ltd.
by Sara Reardon An electronic patch can analyse complex brainwaves and listen in on a fetus’s heart MIND reading can be as simple as slapping a sticker on your forehead. An "electronic tattoo" containing flexible electronic circuits can now record some complex brain activity as accurately as an EEG. The tattoo could also provide a cheap way to monitor a developing fetus. The first electronic tattoo appeared in 2011, when Todd Coleman at the University of California, San Diego, and colleagues designed a transparent patch containing electronic circuits as thin as a human hairMovie Camera. Applied to skin like a temporary tattoo, these could be used to monitor electrophysiological signals associated with the heart and muscles, as well as rudimentary brain activity. To improve its usefulness, Coleman's group has now optimised the placement of the electrodes to pick up more complex brainwaves. They have demonstrated this by monitoring so-called P300 signals in the forebrain. These appear when you pay attention to a stimulus. The team showed volunteers a series of images and asked them to keep track of how many times a certain object appeared. Whenever volunteers noticed the object, the tattoo registered a blip in the P300 signal. The tattoo was as good as conventional EEG at telling whether a person was looking at the target image or another stimulus, the team told a recent Cognitive Neuroscience Society meeting in San Francisco. © Copyright Reed Business Information Ltd.
Kristoffer Famm, et al. Imagine a day when electrical impulses are a mainstay of medical treatment. Your clinician will administer 'electroceuticals' that target individual nerve fibres or specific brain circuits to treat an array of conditions. These treatments will modulate the neural impulses controlling the body, repair lost function and restore health. They could, for example, coax insulin from cells to treat diabetes, regulate food intake to treat obesity and correct balances in smooth-muscle tone to treat hypertension and pulmonary diseases. All this is within reach if researchers from disparate disciplines in academia and industry work together. Here, we outline what needs to be done to bring about electroceuticals and unveil a public–private research initiative and an award that we hope will catalyse the field. Electrical impulses — action potentials — are the language of the body's nervous system. Virtually all organs and functions are regulated through circuits of neurons communicating through such impulses1. Two features make these circuits excellent targets for therapeutic intervention. First, they comprise discrete components — interconnected cells, fibre tracts and nerve bundles — allowing for pinpoint intervention. Second, they are controlled by patterns of action potentials, which can be altered for treatment. Already, devices that harness electrical impulses are used to treat disease. Pacemakers and defibrillators save millions of lives each year; deep-brain stimulation dramatically improves the quality of life for people with Parkinson's disease and depression; sacral-nerve stimulation restores some bladder control in people with paraplegia, and vagus-nerve stimulation shows clinical benefits in diseases ranging from epilepsy to rheumatoid arthritis2. But these devices do not target specific cells within circuits. © 2013 Nature Publishing Group
By Scicurious In his State of the Union this year, President Obama referred to increasing support for science and technology, and mentioned the “Brain Activity Map”. Of course neuroscientists were instantly atwitter. It was the first we’d all heard of any Brain Activity Map. What is it? What did it mean? After a lot of speculation and some quickly formed opinions about whether or not it was a good idea…the White House has now unveiled what the project actually is: BRAIN, Brain Research through Advancing Innovative Neurotechnologies. And what is the project exactly? Will the BRAIN project end up as a BAM (Brain Activity Map)? Or a BUST (Badly Underfunded S**T)? I’d like to explore what I know, and I’d like to hear what everyone else knows as well. Am I wrong? Am I too optimistic? Too pessimistic? Have at. What is the BRAIN Project about? What are its goals? Well, nobody knows, actually. I certainly don’t know. But it appears that no one else knows either. “This working group, co-chaired by Dr. Cornelia “Cori” Bargmann (The Rockefeller University) and Dr. William Newsome (Stanford University), is being asked to articulate the scientific goals of the BRAIN initiative and develop a multi-year scientific plan for achieving these goals, including timetables, milestones, and cost estimates.” So basically, BRAIN is a very fancy initiative, with a fancy name…and so far, no goals. And of course, we’re all excited and trying to figure out what it’s going to be and whether or not it will work. Maybe it would have been in the better interest of the White House to wait until there were…you know, goals. But there is one goal that seems established here: new technologies. © 2013 Scientific American
Keyword: Brain imaging
Link ID: 18004 - Posted: 04.09.2013
By Sara Reardon and Bob Holmes, When President Obama called for $100 million in federal funding last week to map the human brain, he said he was hoping to “unlock the mystery of the three pounds of matter that sits between our ears.” Scientists hope that tracking brain activity neuron by neuron — an effort now called the Brain Research Through Advancing Innovative Neurotechnologies (BRAIN) Initiative — will revolutionize our understanding of brain function in the same way that the Human Genome Project is transforming our understanding of our genes. But just how do you go about mapping a brain? This is a question that two projects with similar lofty goals are already grappling with. The Human Brain Project aims to do it by creating a computer simulation of the entire brain. The Human Connectome Project is using magnetic resonance imaging to track the fibers that connect different regions of the brain on the millimeter scale, giving a rough-grained road map of the brain. To succeed, researchers will need to find noninvasive ways to record the firing of individual neurons, because all current methods involve opening the skull and, often, sticking electrodes into brain tissue. “Right now, you’re literally driving posts into the brain. It’s not very sophisticated,” says neurobiologist John Ngai of the University of California at Berkeley. A few groups are working on new approaches. The MindScope project at the Allen Institute for Brain Science in Seattle aims to map the visual cortex of mice. The team identifies where neurons are firing by injecting the brain with dyes or using genetically engineered proteins that bind to calcium molecules. When a neuron fires, calcium flows into the cell and activates the dye or protein. © 1996-2013 The Washington Post
Keyword: Brain imaging
Link ID: 18003 - Posted: 04.09.2013
By Meghan Rosen Save the clunky tricorders for Star Trek. One day, tiny biological computers with DNA-based circuitry could diagnose diseases. Using snippets of DNA and DNA-clipping chemicals, researchers have created one key component of a computer’s brain: the transistor, a switch that helps electronics perform logic. The biological switch, dubbed a transcriptor, could be plugged together with other biological devices to boost the power of DNA-based computers, researchers report March 28 in Science. With these switches, researchers might be able to program probiotic bacteria — the kind found in yogurt — to detect signs of colon cancer and then spit out warning signals, says study coauthor Jerome Bonnet of Stanford University. “The bacteria could actually travel through your gut and make a color in your poop,” he says. Inside every smartphone, television and iPod, a computer chip holds circuits loaded with millions of transistors. By flipping on or off, the tiny switches direct electrical current to different parts of the chip. But inside cells, even just a few linked-up switches could be powerful, says synthetic biologist Timothy Lu of MIT. The simple circuits “probably wouldn’t be able to compute square roots,” he says, “but you don’t need to put a MacBook chip inside a cell to get some really interesting functions.” And genetic computers can go places conventional electronics can’t. Instead of controlling the flow of electrons across metal circuit wires, the biological switches control the flow of a protein along a “wire” of DNA in living bacteria. As the protein chugs along the wire, it sends out messages telling the cell to make specific molecules — molecules that color a person’s poop green, for example. © Society for Science & the Public 2000 - 2013
Link ID: 17986 - Posted: 04.03.2013
By DENISE GRADY A treatment that many people with multiple sclerosis had hoped would prove effective has failed its first rigorous test, according to a new study. The treatment uses balloons — the type commonly employed to open blocked arteries in people with heart disease — to widen veins in the head and neck. The technique is based on the unproven theory that narrowed veins cause multiple sclerosis by stopping blood from draining out of the brain properly, which is thought to damage nerves and the fatty sheath, myelin, that insulates them. A vascular surgeon from Italy, Dr. Paolo Zamboni, is the leading proponent of the idea. In recent years, 30,000 people around the world have flocked to clinics offering the balloon treatment, despite the lack of solid evidence for it. Many patients want it because the standard drug treatments have not helped. Multiple sclerosis is incurable and causes progressive disability that eventually forces many patients to use wheelchairs. Some people think the balloon treatment has helped them, and testimonials on the Internet have helped create a powerful demand for the procedure. Researchers at the University at Buffalo recruited 20 patients with the disease to test the theory. Half were picked at random to receive the treatment, and the other half underwent a “sham” procedure in which doctors did not actually use balloons. The patients did not know whether their veins had been expanded, and neither did the people who assessed them later. The patients were monitored for six months. There were no significant differences between the two groups in symptoms or tests used to measure the quality of life, the researchers reported last month at a meeting of the American Academy of Neurology in San Diego. In a few cases, brain lesions associated with the disease actually seemed to worsen after the treatment. © 2013 The New York Times Company
Keyword: Multiple Sclerosis
Link ID: 17977 - Posted: 04.02.2013
by Anil Ananthaswamy, A YOUNG man lies unconscious on the table, his head clamped firmly in place. His eyes are closed. The hair over his left temple has been shaved. I'm in the operating room at University Hospital Zurich in Switzerland with neurologist Thomas Grunwald, who has diagnosed 22-year-old Jeremy Künzler with drug-resistant temporal lobe epilepsy. His symptoms during fits suggest that the seizures begin in the left temporal lobe. Often, this condition can only be treated by surgically removing the errant brain tissue. Unfortunately, brain scans have revealed nothing that would point to the source of Künzler's seizures – no obvious tumour, scar or lesion. In ordinary circumstances, Künzler would have to undergo exploratory brain surgery. But instead of this drastic operation, Grunwald is pioneering a technique to pinpoint the problem area. He has asked neurosurgeon Niklaus Krayenbühl to implant electrodes inside Künzler's skull: a grid electrode over his left temporal lobe, and two strip electrodes beneath the left and right lobes, used to monitor activity bilaterally in the hippocampi and amygdalae. Once they are in place, Grunwald will record brain signals in real time during seizures and use the information to try to identify the epileptogenic tissue. It's my first time inside an operating room. I'm anxious, as I have been told not to touch a thing for fear of contamination, especially the giant surgical microscope covered in clear, sterile plastic. "The nurses are very strict," says Grunwald. "If you touch this, even with your head, they get really angry." © Copyright Reed Business Information Ltd.
Link ID: 17953 - Posted: 03.27.2013
Two years after New Brunswick decided to help multiple sclerosis patients pay for an unproven treatment that's only offered outside the country, the number of patients who have sought the so-called liberation treatment has fallen short of expectations. A leading authority on MS says he's not surprised the numbers are falling off. The Finance Department says since April 1, 2011, 82 people who wanted the treatment that widens constricted veins in the neck have been approved for payments of $2,500 each. Applicants get the government funding if a community group raises matching funds. The provincial government budgeted $400,000 for the program in its first two years of operation — or enough to help 160 people seek the treatment. The government approved 25 applications in the first four months the money was available, but interest has tapered off and there have been no applications in the last two months. “It's getting fewer and fewer because every month a negative study is coming out," said Dr. Jock Murray, a neurologist at Dalhousie University in Halifax. Italian vascular specialist Paolo Zamboni reported dramatic improvements in his patients after he pioneered the procedure, but Murray said none of the subsequent studies done around the world have had the same results. “Every study has tended to be negative," he said. © CBC 2013
Keyword: Multiple Sclerosis
Link ID: 17944 - Posted: 03.25.2013
Monya Baker At first glance, it looks like an oddly shaped campfire: smoky grey shapes light up with red sparks and flashes. But the video actually represents a different sort of crackle — the activity of individual neurons across a larval fish brain. It is the first time that researchers have been able to image an entire vertebrate brain at the level of single cells. “We see the big picture without losing resolution,” says Phillipp Keller, a microscopist at the Howard Hughes Medical Institute's Janelia Farm Research Campus in Ashburn, Virginia, who developed the system with Janelia neurobiologist Misha Ahrens. The researchers are able to record activity across the whole fish brain almost every second, detecting 80% of its 100,000 neurons. (The rest lie in hard-to-access areas, such as between the eyes; their activity is visible but cannot be pinned down to single cells.) The work is published today in Nature Methods1. “It’s phenomenal,” says Rafael Yuste, a neuroscientist at Columbia University in New York. “It is a bright star now in the literature, suggesting that it is not crazy to map every neuron in the brain of an animal.” Yuste has been leading the call for a big biology project2 that would do just that in the human brain, which contains about 85,000 times more neurons than the zebrafish brain. The resolution offered by the zebrafish study will enable researchers to understand how different regions of the brain work together, says Ahrens. With conventional techniques, imaging even 2,000 neurons at once is difficult, so researchers must pick and choose which to look at, and extrapolate. Now, he says, “you don't need to guess what is happening — you can see it”. © 2013 Nature Publishing Group
Keyword: Brain imaging
Link ID: 17922 - Posted: 03.19.2013
A clinical trial test of a vein-opening procedure for multiple sclerosis suggests it does not improve symptoms, and in a few patients symptoms worsened. The small pilot study was designed to test the safety and effectiveness of using balloons to unblock veins in the neck and chest of people with MS. Dr. Paolo Zamboni, left, and Dr. Robert Zivadinov have studied whether multiple sclerosis is triggered by vascular problems and have suggested it can be treated by using angioplasty to unblock vessels.Dr. Paolo Zamboni, left, and Dr. Robert Zivadinov have studied whether multiple sclerosis is triggered by vascular problems and have suggested it can be treated by using angioplasty to unblock vessels. Chronic cerebro-spinal venous insufficiency or CCSVI is a hypothesis put forward by Italian vascular surgeon Dr. Paolo Zamboni. He suspects that narrowed neck veins create a backup of blood that can lead to lesions in the brain and inflammation. On Friday, researchers at the University of Buffalo discussed the findings of their clinical trial involving 10 MS patients in an initial safety trial of the real and fake procedures and 20 who were randomized to receive treatment or a placebo. "All the outcomes that we looked at — which had to do with clinical disease, functional status, quality of life, cognition — there was no appreciable difference between the two arms," principal investigator Dr. Adnan Siddiqui, an assistant professor of neurosurgery at the University of Buffalo, said in an interview. When the investigators reviewed the MRI data, Siddiqu said they found new activity in patients who received the balloon angioplasty treatment. © CBC 2013
Keyword: Multiple Sclerosis
Link ID: 17914 - Posted: 03.18.2013
by Andy Coghlan Stimulating the brain with electrical signals can sharpen some of your faculties, but now it seems it can dim others at the same time. Transcranial electrical stimulation (TES), delivered by electrodes on the surface of the head, has been shown to double people's speed of learning. Now the first evidence has emerged that improvements in one aspect of learning might come at the expense of other abilities. Roi Cohen Kadosh of the University of Oxford, showed volunteers pairs of unfamiliar symbols. Each symbol had a secret numerical value, and the volunteers' task was to state – as quickly as possible while avoiding mistakes – which symbol in a pair had the bigger value. The correct answer was then displayed. Over six sessions in one week, it was possible to measure how quickly and efficiently the volunteers learned the value of each symbol. Second task In a second task, participants had to register which of each pair of symbols was physically larger, a measure of automatic thinking. "Automaticity is the skill of doing things without thinking about them, such as reading, driving or mounting stairs," says Cohen Kadosh, who conducted the experiment with Teresa Iucalano of the Stanford Cognitive and Systems Neuroscience Laboratory in Palo Alto, California. During the experiments, volunteers received TES to their posterior parietal cortex – vital for numerical learning – or their dorsolateral prefrontal cortex – vital for automaticity. Some unknowingly received a sham treatment. © Copyright Reed Business Information Ltd.
Keyword: Learning & Memory
Link ID: 17877 - Posted: 03.09.2013
By James Gallagher Health and science reporter, BBC News It may be possible to use a patient's own skin to repair the damage caused by multiple sclerosis (MS), which is currently incurable, say researchers. Nerves struggle to communicate in MS as their insulating covering is attacked by the immune system - causing fatigue and damaging movement. Animal tests, described in the journal Cell Stem Cell, have now used modified skin cells to repair the insulation. Experts said there was an "urgent need" for such therapies. Just like electrical wires, nerves have insulation - but instead of plastic, the body uses a protein called myelin. However, diseases that result in damage to the myelin, including MS, leave the nerves exposed and electrical signals struggle to travel round the body. A team of scientists at the University of Rochester Medical Center, in the US, used advances in stem-cell research to attempt to repair the myelin. They took a sample of human skin cells and converted it into stem cells, which are capable of becoming any other type of cell in the body. The next step was to transform the stem cells into immature versions of cells in the brain that produce myelin. When these cells had been injected into mice born without any myelin it had had a significant effect, said researchers. BBC © 2013