Chapter 11. Motor Control and Plasticity

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Ian Sample Science editor Rats with spinal cord injuries have regained the use of their paws after being given a groundbreaking gene therapy that helps to mend damaged nerves in the spine. The new therapy works by dissolving the dense scar tissue that forms a thick barrier between severed nerves when the spinal column is broken. Animals that were given the treatment produced an enzyme called chondroitinase which breaks down scar tissue and allows the broken nerves to reconnect with each other. Tests showed that when the therapy was given for two months, rats relearned the kinds of skilled movements they needed to grab little sugar balls from a platform. “The gene therapy has enabled us to treat large areas of the spinal cord with only one injection,” said Elizabeth Bradbury, who led the research at King’s College London. “This is important because the spinal cord is long and the pathology spreads down its whole length after injury.” While more animal studies are needed before the therapy can go into human trials, researchers hope that ultimately the treatment will help people with spinal injuries who have lost the ability to perform daily tasks, such as using a knife and fork, picking up a mug, and writing. © 2018 Guardian News and Media Limited

Keyword: Regeneration
Link ID: 25095 - Posted: 06.16.2018

By James Gallagher Health and science correspondent, BBC News Scientists say they have taken a significant step towards the goal of giving paralysed people control of their hands again. The team at King's College London used gene therapy to repair damage in the spinal cord of rats. The animals could then pick up and eat sugar cubes with their front paws. It is early stage research, but experts said it was some of the most compelling evidence that people's hand function could one day be restored. The spinal cord is a dense tube of nerves carrying instructions from the brain to the rest of the body. The body repairs a wounded spinal cord with scar tissue. However, the scar acts like a barrier to new connections forming between nerves. How the gene therapy works The researchers were trying to dissolve components of the scar tissue in the rats' spinal cord. They needed to give cells in the cord a new set of genetic instructions - a gene - for breaking down the scar. The instructions they gave were for an enzyme called chondroitinase. And they used a virus to deliver them. Finally, a drug was used to activate the instructions. The animals regained use of their front paws after the gene therapy had been switched on for two months. Dr Emily Burnside, one of the researchers, said: "The rats were able to accurately reach and grasp sugar pellets. "We also found a dramatic increase in activity in the spinal cord of the rats, suggesting that new connections had been made in the networks of nerve cells." The researchers hope their approach will work for people injured in car crashes or falls. © 2018 BBC.

Keyword: Regeneration
Link ID: 25092 - Posted: 06.15.2018

by Cleve R. Wootson Jr. Kailyn Griffin, 5, experienced temporary paralysis following a tick bite in Grenada, Miss., discovered on June 6. (WLBT) As soon as Kailyn Griffin's feet hit the floor Wednesday morning, she collapsed in a heap. The 5-year-old kept trying to stand but fell every time. She was also struggling to speak, said her mother, Jessica Griffin. Her daughter had been fine when the family went out to a T-ball game the night before, NBC-affiliate WLBT in Jackson, Miss., reported. Maybe Kailyn was having a hard time waking up Wednesday morning, or perhaps her legs were asleep. Then Griffin saw the tick. She had gathered Kailyn's hair to put it in a ponytail when she spotted the arachnid, embedded in the girl's scalp, swelled with the girl's blood. She pulled the tick out and placed it in a plastic bag, then rushed to the hospital with Kailyn, WTXL reported. Doctors told Griffin it was an uncommon condition called tick paralysis. “After tons of bloodwork and a CT of the head UMMC has ruled it as tick paralysis! PLEASE for the love of god check your kids for ticks! It’s more common in children than it is adults!” Griffin, of Grenada, Miss., wrote in a Facebook post Wednesday that seemed a mixture of worry and relief. “Scary is a UNDERSTATEMENT!” Griffin could not be immediately reached for comment. It was unclear where or when she thought her daughter had acquired the tick, or how long it had been on her body. Ticks are most active from April through September, The Washington Post has reported. Tick paralysis is caused by female ticks on the verge of laying eggs. After the tick eats a blood meal and is engorged, it secretes a neurotoxin into the host, according to the American Lyme disease Foundation. The symptoms can occur five to seven days after the tick starts feeding. © 1996-2018 The Washington Post

Keyword: Movement Disorders
Link ID: 25081 - Posted: 06.12.2018

By Ruth Williams Four patients with chronic spinal damage and a complete loss of motor and sensory functions below their waists have received transplants of human neural stem cells in a first-of-its-kind clinical trial. A report in Cell Stem Cell today (June 1) documents the procedure and the subsequent clinical follow up of the patients, who exhibit no signs of untoward effects but rather tiny hints of improvement. “It’s an extremely interesting and important piece of work,” says neurologist Eva Feldman of the University of Michigan who was not involved with the work. “The rodent model results were very compelling and . . . laid the groundwork for this very small, proof-of-concept safety trial.” While these results seem tantalizing, “the numbers [of patients] are extremely small,” says Feldman, and “the patients themselves notice no change in function or quality of life.” Severe spinal injuries can have devastating consequences, often leaving patients with complete paralysis below the injury site and with little hope of recovery. While there is currently no therapy that can promote neuronal repair in such patients, evidence from animal studies, including those carried out in primates, has indicated that transplantation of human-derived neural stem cells to the site of injury can promote some functional recovery of downstream musculature. © 1986-2018 The Scientist

Keyword: Regeneration; Stem Cells
Link ID: 25059 - Posted: 06.05.2018

By Robert F. Service Prosthetics may soon take on a whole new feel. That’s because researchers have created a new type of artificial nerve that can sense touch, process information, and communicate with other nerves much like those in our own bodies do. Future versions could add sensors to track changes in texture, position, and different types of pressure, leading to potentially dramatic improvements in how people with artificial limbs—and someday robots—sense and interact with their environments. “It’s a pretty nice advance,” says Robert Shepherd, an organic electronics expert at Cornell University. Not only are the soft, flexible, organic materials used to make the artificial nerve ideal for integrating with pliable human tissue, but they are also relatively cheap to manufacture in large arrays, Shepherd says. Modern prosthetics are already impressive: Some allow amputees to control arm movement with just their thoughts; others have pressure sensors in the fingertips that help wearers control their grip without the need to constantly monitor progress with their eyes. But our natural sense of touch is far more complex, integrating thousands of sensors that track different types of pressure, such as soft and forceful touch, along with the ability to sense heat and changes in position. This vast amount of information is ferried by a network that passes signals through local clusters of nerves to the spinal cord and ultimately the brain. Only when the signals combine to become strong enough do they make it up the next link in the chain. © 2018 American Association for the Advancement of Science.

Keyword: Robotics; Pain & Touch
Link ID: 25048 - Posted: 06.01.2018

Deep brain stimulation has been used to treat Parkinson’s disease symptoms for 25 years, but limitations have led researchers to look for ways to improve the technique. This study describes the first fully implanted DBS system that uses feedback from the brain itself to fine-tune its signaling. The study was supported by the National Institutes of Health’s Brain Research through Advancing Innovative Technologies (BRAIN) Initiative and the National Institute of Neurological Disorders and Stroke (NINDS). “The novel approach taken in this small-scale feasibility study may be an important first step in developing a more refined or personalized way for doctors to reduce the problems patients with Parkinson’s disease face every day,” said Nick B. Langhals, Ph.D., program director at NINDS and team lead for the BRAIN Initiative. Deep brain stimulation is a method of managing Parkinson’s disease symptoms by surgically implanting an electrode, a thin wire, into the brain. Traditional deep brain stimulation delivers constant stimulation to a part of the brain called the basal ganglia to help treat the symptoms of Parkinson’s. However, this approach can lead to unwanted side effects, requiring reprogramming by a trained clinician. The new method described in this study is adaptive, so that the stimulation delivered is responsive in real time to signals received from the patient’s brain. “This is the first time a fully implanted device has been used for closed-loop, adaptive deep brain stimulation in human Parkinson’s disease patients,” said Philip Starr, M.D., Ph.D., professor of neurological surgery, University of California, San Francisco, and senior author of the study, which was published in the Journal of Neural Engineering.

Keyword: Parkinsons
Link ID: 25034 - Posted: 05.30.2018

A new neck brace for people with motor neurone disease (MND) makes a "substantial difference" to their quality of life, a patient has said. The disease causes muscle wasting, eventually leaving people with the condition unable to support their head. MND patient Philip Brindle said the collar, designed in Sheffield, "opened up opportunities that I do not think I would have had otherwise". The device is now being used by 25 NHS Trusts, according to its designers. MND is a progressive and terminal disease that damages the function of nerves and leads to muscle wasting and mobility problems, among other symptoms. It affects up to 5,000 adults in the UK, according to charity the MND Association. Dr Brian Dickie, director of research development at the association, said the collar has been "preferred by the majority of people who tried it". Image caption Mr Brindle's MND has left him unable to hold his head up independently Mr Brindle, 72, from Chesterfield, said since he was diagnosed with MND in 2015 his head had begun to drop and he did not want to be seen in public. "I just do not have the strength to hold [my head] up anymore and that makes life extremely unpleasant," he said. "You can't read, you can't watch TV, you can't have a conversation with anyone and you can't eat or drink with your head in that position." Image caption The Head Up collar is made from the same material used in space suits The new collar was designed by researchers at the University of Sheffield and Sheffield Hallam University, together with patients and clinicians at Sheffield Teaching Hospital. It has a soft fabric base, made from a material used by NASA to make space suits, on to which a series of shaped supports can be added to provide additional stability. © 2018 BBC

Keyword: ALS-Lou Gehrig's Disease
Link ID: 25033 - Posted: 05.30.2018

Prion diseases are slow degenerative brain diseases that occur in people and various other mammals. No vaccines or treatments are available, and these diseases are almost always fatal. Scientists have found little evidence of a protective immune response to prion infections. Further, microglia — brain cells usually involved in the first level of host defense against infections of the brain — have been thought to worsen these diseases by secreting toxic molecules that can damage nerve cells. Now, scientists have used an experimental drug, PLX5622, to test the role of microglia against scrapie, a prion disease of sheep. PLX5622 rapidly kills most of the microglia in the brain. When researchers gave the drug to mice infected with scrapie, microglia were eliminated and the mice died one month faster than did untreated mice. The results, published in the Journal of Virology by researchers from the National Institute of Allergy and Infectious Diseases at the National Institutes of Health, suggest that microglia can defend against a prion infection and thus slow the course of disease. The scientists hypothesize that microglia trap and destroy the aggregated prion proteins that cause brain damage. The findings suggest that drugs that increase the helpful activity of microglia may have a role in slowing the progression of prion diseases. Researchers are now studying the details of how microglia may be able to destroy prions in the brain. The scientists note that microglia could have a similar beneficial effect on other neurodegenerative diseases associated with protein aggregation, such as Alzheimer’s disease and Parkinson’s disease.

Keyword: Prions; Glia
Link ID: 24991 - Posted: 05.18.2018

By Shawna Williams Even as patients with Parkinson’s disease, obsessive-compulsive disorder, and other conditions turn to deep brain stimulation (DBS) to keep their symptoms in check, it’s been unclear to scientists why the therapy works. Now, researchers in Texas report that in mice, the treatment dials the activity of hundreds of genes up or down in brain cells. Their results, published in eLife March 23, hint that DBS’s use could be expanded to include improving learning and memory in people with intellectual disabilities. “The paper is very well done. . . . It’s really a rigorous study,” says Zhaolan “Joe” Zhou, a neuroscientist at the University of Pennsylvania’s Perelman School of Medicine who reviewed the paper for eLife. Now that the genes and pathways DBS affects are known, researchers can home in on ways to improve the treatment, or perhaps combine the therapy with pharmacological approaches to boost its effect, he says. In DBS, two electrodes are surgically implanted in a patient’s brain (the area depends on the disorder being treated), and connected to generators that are placed in the chest. Gentle pulses of electricity are then passed continuously through the electrodes. The treatment reduces motor symptoms in many people with Parkinson’s, and allows some patients to reduce their use of medications, but it does not eliminate symptoms or slow the disease’s progression. In addition to its use in movement disorders, DBS is being explored as a potential therapy for a range of other brain-related disorders. For instance, as a way to boost learning and memory in people with Alzheimer’s disease, researchers are looking into stimulating the fimbria-fornix, a brain region thought to regulate the activity of the memory-storing hippocampus. © 1986-2018 The Scientist

Keyword: Parkinsons; Epigenetics
Link ID: 24982 - Posted: 05.16.2018

A new tool developed by researchers at the National Institutes of Health has determined, for the first time, how two distinct sets of neurons in the mouse brain work together to control movement. The method, called spectrally resolved fiber photometry (SRFP), can be used to measure the activity of these neuron groups in both healthy mice and those with brain disease. The scientists plan to use the technique to better understand what goes wrong in neurological disorders, such as Parkinson’s disease. The study appeared online in the journal Neuron. According to Guohong Cui, M.D., Ph.D., head of the In Vivo Neurobiology Group at the National Institute of Environmental Health Sciences (NIEHS), part of NIH, the project began because he wanted to find out why patients with Parkinson’s disease have problems with movement. Typically, the disease motor symptoms include tremor, muscle stiffness, slowness of movement, and impaired balance. Cui explained that an animal’s ability to move was controlled by two groups of neurons in the brain called the direct pathway (D1) and indirect pathway (D2). Based on clinical studies of patients with Parkinson’s and primate models, some researchers hypothesized that the loss of the neurotransmitter dopamine in the midbrain resulted in an imbalance of neural activities between D1 and D2. Since previous methods could not effectively distinguish different cell types in the brain, the hypothesis remained under debate. However, using SRFP, Cui’s team was able to label D1 and D2 neurons with green and red fluorescent sensors to report their neural activity.

Keyword: Parkinsons; Movement Disorders
Link ID: 24976 - Posted: 05.15.2018

By Ashley Yeager At first glance, neurons and muscle cells are the stars of gross motor function. Muscle movement results from coordination between nerve and muscle cells: when an action potential arrives at the presynaptic neuron terminal, calcium ions flow, causing proteins to fuse with the cell membrane and release some of the neuron’s contents, including acetylcholine, into the cleft between the neuron and muscle cell. Acetylcholine binds to receptors on the muscle cell, sending calcium ions into it and causing it to contract. But there’s also a third kind of cell at neuromuscular junctions, a terminal/perisynaptic Schwann cell (TPSC). These cells are known to aid in synapse formation and in the repair of injured peripheral motor axons, but their possible role in synaptic communications has been largely ignored. Problems with synaptic communication can underlie muscle fatigue, notes neuroscientist Thomas Gould of the University of Nevada, Reno, in an email to The Scientist. “Because these cells are activated by synaptic activity, we wondered what the role of this activation was.” To investigate, he and his colleagues stimulated motor neurons from neonatal mouse diaphragm tissue producing a calcium indicator, and found that TPSCs released calcium ions from the endoplasmic reticulum into the cytosol and could take in potassium ions from the synaptic cleft between neurons and muscle cells. However, TPSCs lacking the protein purinergic 2Y1 receptor (P2Y1R) didn’t release calcium or appear to take in potassium ions. © 1986-2018 The Scientist

Keyword: Glia; Muscles
Link ID: 24964 - Posted: 05.12.2018

By LISA SANDERS, M.D. The young woman rubbed her eyes. The numbers and letters on her computer screen jumped erratically. So did the world around her. This had happened before, but late at night when she was tired, never in the middle of the day. The light from the screen suddenly seemed too bright. And her headache, the one that was always present these days, tightened from a dull ache to a squeezing pressure on the back of her head and neck. Nearly in tears from pain and frustration, the 19-year-old called her mother. She couldn’t see; she couldn’t drive. Could her mother pick her up from work? The problems with her eyes began in grade school. Two years earlier, she nearly went blind. All she could see on the left was a rim of light. Everything else was blocked by a big black spot. And then a black dot appeared in her right eye as well. Her parents took her to see many eye doctors, only to be told that there was nothing wrong. One doctor told them that she had “emotional blindness.” The young woman’s vision somehow got a lot better on its own, and though the black dot still obstructed some of her vision, for the last eight months she’d been able to drive — so important in this small mountain town an hour north of San Diego. Now she couldn’t see for what seemed like a different reason. The young woman’s mother arranged for her to go to San Diego to see a neuro-ophthalmologist — a doctor who specializes in vision problems that originate in the brain. When they got to the office, though, the young woman’s vision and headache had returned to their imperfect but baseline state. She told the doctor that her symptoms were least intrusive in the morning; standing and walking seemed to make everything worse. Come back later, the doctor instructed. Mother and daughter walked around and shopped. When a couple of hours later the daughter’s eyes started jumping and her headache worsened, they hurried back to the office. © 2018 The New York Times Company

Keyword: Vision; Movement Disorders
Link ID: 24946 - Posted: 05.07.2018

By GRETCHEN REYNOLDS Small amounts of exercise could have an outsize effect on happiness. According to a new review of research about good moods and physical activity, people who work out even once a week or for as little as 10 minutes a day tend to be more cheerful than those who never exercise. And any type of exercise may be helpful. The idea that moving can affect our moods is not new. Many of us would probably say that we feel less cranky or more relaxed after a jog or visit to the gym. Science would generally agree with us. A number of past studies have noted that physically active people have much lower risks of developing depression and anxiety than people who rarely move. But that research centered on the relationships between exercise and psychological problems like depression and anxiety. Fewer past studies explored links between physical activity and upbeat emotions, especially in people who already were psychologically healthy, and those studies often looked at a single age group or type of exercise. On their own, they do not tell us much about the amounts or types of exercise that might best lift our moods, or whether most of us might expect to find greater happiness with regular exercise or only certain groups of people. So for the new review, which was published last month in The Journal of Happiness Studies, researchers at the University of Michigan decided to aggregate and analyze multiple past studies of working out and happiness. © 2018 The New York Times Company

Keyword: Depression
Link ID: 24930 - Posted: 05.02.2018

Aided by advanced stem cell technology and tissue chips, National Institutes of Health-funded researchers used stem cells originally derived from a person’s skin to recreate interactions between blood vessels and neurons that may occur early in the formation of the fetal human spinal cord. The results published in Stem Cell Reports suggest that the system can mimic critical parts of the human nervous system, raising the possibility that it may one day, be used to test personalized treatments of neurological disorders. Led by Samuel Sances, Ph.D., and Clive N. Svendsen, Ph.D., Cedars-Sinai Board of Governors Regenerative Medicine Institute, Los Angeles, CA, the researchers first converted the stem cells into newborn spinal cord neurons or epithelial cells that line walls of brain blood vessels. In most experiments, each cell type was then injected into one of two chambers embedded side-by-side in thumb-sized, plastic tissue chips and allowed to grow. Six days after injections, the researchers found that the growing neurons exclusively filled their chambers while the growing blood vessel cells not only lined their chamber in a cobblestone pattern reminiscent of vessels in the body, but also snuck through the perforations in the chamber walls and contacted the neurons. This appeared to enhance maturation of both cell types, causing the neurons to fire more often and both cell types to be marked by some gene activity found in fetal spinal cord cells. Tissue chips are relatively new tools for medical research and since 2012 the NIH has funded several tissue-chip projects. Unlike traditional petri dish systems, tissue chips help researchers grow cells in more life-like environments. Using microprocessor manufacturing techniques, the chambers can be built to recreate the three-dimensional shapes of critical organ parts and the tight spaces that mimic the way viscous, bodily fluids normally flow around the cells.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 24915 - Posted: 04.28.2018

Amina Zafar · CBC News Exercise helps protect against depression regardless of age or location in the world, a large new analysis suggests. Researchers pooled data from 49 studies to create a sample of more than 266,000 people on four continents to examine the role of physical activity in preventing depression. "The key message is that really when it comes to exercise and our mental health that something is better than nothing," said study author Simon Rosenbaum, senior research fellow in the School of Psychiatry at the University of New South Wales in Australia. "And if you're doing something, try to add a little bit more." The findings were published in Tuesday's issue of the American Journal of Psychiatry. Rosenbaum said the meta-analysis builds on a growing body of evidence on how exercise can also be an important part of treatment for people living with mental illness. Those who followed weekly guidelines to get 150 minutes of moderate aerobic activity, such as cycling or brisk walking, were less likely to develop depression over nearly eight years of followup compared with those who didn't meet the guideline. Rosenbaum, an exercise physiologist, said the challenge is to support people to take the first step to get active by offering enough social support, access and the right environment. Rosenbaum, who enjoys kayaking and rock climbing, suggested that people should do physical activity that they enjoy and are able to fit into their routine. That way, they're more likely to keep it up in the long term. ©2018 CBC/Radio-Canada.

Keyword: Depression
Link ID: 24898 - Posted: 04.25.2018

/ By Madeline Bodin This winter was a little quieter than usual for the folks at Silver Creek Specialty Meats in Oshkosh, Wisconsin. For generations, winter was when hunters would make regular visits to the low-rise white brick facility near the shore of Lake Winnebago, carrying the odds and ends of the deer they had killed the previous fall so it could be turned into venison sausages. This year, though, no hunters came. “It’s not quite black and white. What do we do in the meantime?” In August, Silver Creek Specialty Meats sent out a letter notifying customers that it would no longer accept venison for processing. “As you are probably aware,” the letter said, “chronic wasting disease in the wild deer population of the State of Wisconsin has been steadily spreading. The disease has now been found in wild deer in 19 counties throughout the state. Due to the spread of the disease it has become extremely difficult to screen out any venison coming from CWD infected areas.” Deer with chronic wasting disease, or CWD, tremble and drool. They often cannot hold their heads up. Eventually, they lose so much weight that they are little more than hide and bone. The disease arises from a particular prion — single-protein infectious agents linked to various neurodegenerative diseases in mammals. And prion diseases are always fatal. Copyright 2018 Undark

Keyword: Prions
Link ID: 24880 - Posted: 04.19.2018

By NICHOLAS BAKALAR A traumatic brain injury, even a mild concussion, increases the risk for Parkinson’s disease, a new study reports. Researchers identified all patients diagnosed with T.B.I. in a Veterans Health Administration database — 162,935 men and women — and matched them with the same number of people with similar health and behavioral characteristics but who had not had a brain injury. The study is in Neurology. Of the T.B.I. cases, half were mild, involving a blow to the head with some subsequent symptoms but with little or no unconsciousness. The rest were moderate to severe, involving extended unconsciousness or long-term symptoms. After controlling for age, race, income and many medical and psychiatric diseases, they found that compared with those who had had no T.B.I., those with a mild T.B.I. had a 56 percent increased risk for Parkinson’s disease; those with moderate to severe T.B.I. had an 83 percent increased risk. “We don’t have brain biopsies, so we don’t know what the underlying biology is,” said the lead author, Dr. Raquel C. Gardner, an assistant professor of neurology at the University of California, San Francisco. “But in Parkinson’s you see abnormal protein accumulation, and there’s some evidence that T.B.I. is linked to deposits of these abnormal proteins.” In any case, she said, “This study provides the most definitive evidence that there is this association.” © 2018 The New York Times Company

Keyword: Brain Injury/Concussion; Parkinsons
Link ID: 24878 - Posted: 04.19.2018

By CEYLAN YEGINSU LONDON — Two decades after creating the clone Dolly the sheep and paving the way for new research into Parkinson’s, Dr. Ian Wilmut revealed on Wednesday that he has the disease himself. The 73-year-old professor, who lives in Scotland, announced on World Parkinson’s Day that he learned four months ago that he had the disease, and that he would participate in a major research program to test new types of treatments intended to slow the disease’s progression. “Initiatives of this kind are very effective not only because they bring more people together, but because they will include people with different experience and expertise,” Dr. Wilmut said in a statement. He was referring to the new Dundee-Edinburgh Parkinson’s Research Initiative, which aims to investigate the causes of the disease and to translate scientific discoveries into new therapies. “It was from such a rich seedbed that Dolly developed, and we can hope for similar benefits in this project,” he added. In 1996, Dr. Wilmut and a team of scientists at the Roslin Institute in Edinburgh cloned an adult sheep, resulting in the birth of Dolly. The achievement shocked researchers who had said it could not be done. But Dolly’s birth proved that cells from anywhere in the body could behave like a newly fertilized egg, an idea that transformed scientific thinking and encouraged researchers to find techniques to reprogram adult cells. The new research led to the discovery of induced pluripotent stem cells, or iPSCs, which hold great promise as a therapy for Parkinson’s because of their potential to repair damaged tissues, according to the Dundee-Edinburgh Parkinson’s Research Initiative. © 2018 The New York Times Company

Keyword: Parkinsons
Link ID: 24863 - Posted: 04.13.2018

By Matthew Hutson As artificial intelligence (AI) allows machines to become more like humans, will they experience similar psychological quirks such as hallucinations or depression? And might this be a good thing? Last month, New York University in New York City hosted a symposium called Canonical Computations in Brains and Machines, where neuroscientists and AI experts discussed overlaps in the way humans and machines think. Zachary Mainen, a neuroscientist at the Champalimaud Centre for the Unknown, a neuroscience and cancer research institute in Lisbon, speculated that we might expect an intelligent machine to suffer some of the same mental problems people do. Q: Why do you think AIs might get depressed and hallucinate? A: I’m drawing on the field of computational psychiatry, which assumes we can learn about a patient who’s depressed or hallucinating from studying AI algorithms like reinforcement learning. If you reverse the arrow, why wouldn’t an AI be subject to the sort of things that go wrong with patients? Q: Might the mechanism be the same as it is in humans? A: Depression and hallucinations appear to depend on a chemical in the brain called serotonin. It may be that serotonin is just a biological quirk. But if serotonin is helping solve a more general problem for intelligent systems, then machines might implement a similar function, and if serotonin goes wrong in humans, the equivalent in a machine could also go wrong. © 2018 American Association for the Advancement of Science

Keyword: Robotics; Intelligence
Link ID: 24843 - Posted: 04.10.2018

BCIs have deep roots. In the 18th century Luigi Galvani discovered the role of electricity in nerve activity when he found that applying voltage could cause a dead frog’s legs to twitch. In the 1920s Hans Berger used electroencephalography to record human brain waves. In the 1960s José Delgado theatrically used a brain implant to stop a charging bull in its tracks. One of the field’s father figures is still hard at work in the lab. Eberhard Fetz was a post-doctoral researcher at the University of Washington in Seattle when he decided to test whether a monkey could control the needle of a meter using only its mind. A paper based on that research, published in 1969, showed that it could. Dr Fetz tracked down the movement of the needle to the firing rate of a single neuron in the monkey’s brain. The animal learned to control the activity of that single cell within two minutes, and was also able to switch to control a different neuron. Dr Fetz disclaims any great insights in setting up the experiment. “I was just curious, and did not make the association with potential uses of robotic arms or the like,” he says. But the effect of his paper was profound. It showed both that volitional control of a BCI was possible, and that the brain was capable of learning how to operate one without any help. Some 48 years later, Dr Fetz is still at the University of Washington, still fizzing with energy and still enthralled by the brain’s plasticity. He is particularly interested in the possibility of artificially strengthening connections between cells, and perhaps forging entirely new ones.

Keyword: Robotics
Link ID: 24839 - Posted: 04.09.2018