R. Stanley Williams For the first time, my colleagues and I have built a single electronic device that is capable of copying the functions of neuron cells in a brain. We then connected 20 of them together to perform a complicated calculation. This work shows that it is scientifically possible to make an advanced computer that does not rely on transistors to calculate and that uses much less electrical power than today’s data centers. Our research, which I began in 2004, was motivated by two questions. Can we build a single electronic element – the equivalent of a transistor or switch – that performs most of the known functions of neurons in a brain? If so, can we use it as a building block to build useful computers? Neurons are very finely tuned, and so are electronic elements that emulate them. I co-authored a research paper in 2013 that laid out in principle what needed to be done. It took my colleague Suhas Kumar and others five years of careful exploration to get exactly the right material composition and structure to produce the necessary property predicted from theory. Kumar then went a major step further and built a circuit with 20 of these elements connected to one another through a network of devices that can be programmed to have particular capacitances, or abilities to store electric charge. He then mapped a mathematical problem to the capacitances in the network, which allowed him to use the device to find the solution to a small version of a problem that is important in a wide range of modern analytics. © 2010–2020, The Conversation US, Inc.

Keyword: Learning & Memory; Robotics
Link ID: 27512 - Posted: 10.07.2020

Ian Sample Science editor Doctors believe they are closer to a treatment for multiple sclerosis after discovering a drug that repairs the coatings around nerves that are damaged by the disease. A clinical trial of the cancer drug bexarotene showed that it repaired the protective myelin sheaths that MS destroys. The loss of myelin causes a range of neurological problems including balance, vision and muscle disorders, and ultimately, disability. While bexarotene cannot be used as a treatment, because the side-effects are too serious, doctors behind the trial said the results showed “remyelination” was possible in humans, suggesting other drugs or drug combinations will halt MS. Advertisement “It’s disappointing that this is not the drug we’ll use, but it’s exciting that repair is achievable and it gives us great hope for another trial we hope to start this year,” said Prof Alasdair Coles, who led the research at the University of Cambridge. MS arises when the immune system mistakenly attacks the fatty myelin coating that wraps around nerves in the brain and spinal cord. Without the lipid-rich substance, signals travel more slowly along nerves, are disrupted, or fail to get through at all. About 100,000 people in the UK live with the condition. Funded by the MS Society, bexarotene was assessed in a phase 2a trial that used brain scans to monitor changes to damaged neurons in patients with relapsing MS. This is an early stage of the condition that precedes secondary progressive disease, where neurons die off and cause permanent disability. © 2020 Guardian News & Media Limited

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 27496 - Posted: 09.28.2020

By Gunjan Sinha Light therapy can help lift moods, heal wounds, and boost the immune system. Can it improve symptoms of Parkinson’s disease, too? A first-of-its-kind trial scheduled to launch this fall in France aims to find out. In seven patients, a fiber optic cable implanted in their brain will deliver pulses of near-infrared (NIR) light directly to the substantia nigra, a region deep in the brain that degenerates in Parkinson’s disease. The team, led by neurosurgeon Alim- Louis Benabid of the Clinatec Institute—a partnership between several government-funded research institutes and industry—hopes the light will protect cells there from dying. The study is one of several set to explore how Parkinson’s patients might benefit from light. “I am so excited,” says neuropsychologist Dawn Bowers of the University of Florida College of Medicine, who is recruiting patients for a trial in which NIR will be beamed into the skull instead of delivered with an implant. Small tests in people with Parkinson’s and animal models of the disease have already suggested benefits, but some mainstream Parkinson’s researchers are skeptical. No one has shown exactly how light might protect the key neurons—or why it should have any effect at all on cells buried deep in the brain that never see the light of day. Much or all of the encouraging hints seen so far in people may be the result of the placebo effect, skeptics say. Because there are no biomarkers that correlate well with changes in Parkinson’s symptoms, “we are reliant on observing behavior,” says neurobiologist David Sulzer of Columbia University Irving Medical Center, an editor of the journal npj Parkinson’s Disease. “It’s not easy to guard against placebo effects.” © 2020 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 27482 - Posted: 09.19.2020

Ken Solt & Oluwaseun Akeju The state of dissociation is commonly described as feeling detached from reality or having an ‘out of body’ experience. This altered state of consciousness is often reported by people who have psychiatric disorders arising from devastating trauma or abuse. It is also evoked by a class of anaesthetic drug, and can occur in epilepsy. The neurological basis of dissociation has been a mystery, but writing in Nature, Vesuna et al.1 describe a localized brain rhythm that underlies this state. Their findings will have far-reaching implications for neuroscience. The authors first recorded brain-wide neuronal activity in mice using a technique called widefield calcium imaging. They studied changes in these brain rhythms in response to a range of drugs that have sedative, anaesthetic or hallucinogenic properties, including three that induce dissociation — ketamine, phencyclidine (PCP) and dizocilpine (MK801). Only the dissociative drugs produced robust oscillations in neuronal activity in a brain region called the retrosplenial cortex. This region is essential for various cognitive functions, including episodic memory and navigation2. The oscillations occurred at a low frequency, of about 1–3 hertz. By contrast, non-dissociative drugs such as the anaesthetic propofol and the hallucinogen lysergic acid diethylamide (LSD) did not trigger this rhythmic retrosplenial activity. Vesuna et al. examined the active cells in more detail using a high-resolution approach called two-photon imaging. This analysis revealed that the oscillations were restricted to cells in layer 5 of the retrosplenial cortex. The authors then recorded neuronal activity across multiple brain regions. Normally, other parts of the cortex and subcortex are functionally connected to neuronal activity in the retrosplenial cortex; however, ketamine caused a disconnect, such that many of these brain regions no longer communicated with the retrosplenial cortex. © 2020 Springer Nature Limited

Keyword: Drug Abuse; Consciousness
Link ID: 27481 - Posted: 09.19.2020

Jon Hamilton Scientists used light to control the firing of specific cells to artificially create a rhythm in the brain that acted like the drug ketamine enjoynz/Getty Images Out-of-body experiences are all about rhythm, a team reported Wednesday in the journal Nature. In mice and one person, scientists were able to reproduce the altered state often associated with ketamine by inducing certain brain cells to fire together in a slow, rhythmic fashion. "There was a rhythm that appeared, and it was an oscillation that appeared only when the patient was dissociating," says Dr. Karl Deisseroth, a psychiatrist and neuroscientist at Stanford University. Dissociation is a brain state in which a person feels separated from their own thoughts, feelings and body. It is common in people who have some mental illnesses or who have experienced a traumatic event. It can also be induced by certain drugs, including ketamine and PCP (angel dust). The study linking dissociation to brain rhythms represents "a big leap forward in understanding how these drugs produce this unique state," says Dr. Ken Solt, an anesthesiologist at Harvard Medical School and Massachusetts General Hospital. Solt is the co-author of an article that accompanied the study but was not involved in the research. The finding also could be a step toward finding non-drug methods to control states of consciousness, Solt says. Deisseroth's lab made the discovery while studying the brains of mice that had been given ketamine or other drugs that cause dissociation. The team was using technology that allowed them to monitor the activity of cells throughout the brain. © 2020 npr

Keyword: Drug Abuse; Consciousness
Link ID: 27480 - Posted: 09.19.2020

By Tanya Lewis During Musk’s demonstration, he strolled near a pen containing several pigs, some of which had Neuralink implants. One animal, named Gertrude, had hers for two months. The device’s electrodes were situated in a part of Gertrude’s cortex that connected to neurons in her snout. And for the purposes of the demo, her brain signals were converted to audible bleeps that became more frequent as she sniffed around the pen and enjoyed some tasty treats. Musk also showed off a pig whose implant had been successfully removed to show that the surgery was reversible. Some of the other displayed pigs had multiple implants. Neuralink implantable device Neuralink implantable device, v0.9. Credit: Neuralink Neuralink, which was founded by Musk and a team of engineers and scientists in 2016, unveiled an earlier, wired version of its implant technology in 2019. It had several modules: the electrodes were connected to a USB port in the skull, which was intended to be wired to an external battery and a radio transmitter that were located behind the ear. The latest version consists of a single integrated implant that fits in a hole in the skull and relays data through the skin via a Bluetooth radio. The wireless design makes it seem much more practical for human use but limits the bandwidth of data that can be sent, compared with state-of-the-art brain-computer interfaces. The company’s goal, Musk said in the demo, is to “solve important spine and brain problems with a seamlessly implanted device”—a far cry from his previously stated, much more fantastic aim of allowing humans to merge with artificial intelligence. This time Musk seemed more circumspect about the device’s applications. As before, he insisted the demonstration was purely intended as a recruiting event to attract potential staff. Neuralink’s efforts build on decades of work from researchers in the field of brain-computer interfaces. Although technically impressive, this wireless brain implant is not the first to be tested in pigs or other large mammals.] © 2020 Scientific American,

Keyword: Robotics; Movement Disorders
Link ID: 27457 - Posted: 09.07.2020

Rory Cellan-Jones He is the most charismatic figure in technology with some amazing achievements to his name, from making electric cars desirable to developing rockets that can return to earth and be reused. But dare to suggest that anything Elon Musk does is not groundbreaking or visionary and you can expect a backlash from the great man and his army of passionate fans. That is what happened when a British academic criticised Musk's demo on Friday of his Neuralink project - and the retaliation he faced was largely my fault. Neuralink is a hugely ambitious plan to link the human brain to a computer. It might eventually allow people with conditions such as Parkinson's disease to control their physical movements or manipulate machines via the power of thought. There are plenty of scientists already at work in this field. But Musk has far greater ambitions than most, talking of developing "superhuman cognition" - enhancing the human brain in part to combat the threat he sees from artificial intelligence. Friday night's demo involved a pig called Gertrude fitted with what the tech tycoon described as a "Fitbit in your skull". A tiny device recorded the animal's neural activity and sent it wirelessly to a screen. A series of beeps happened every time her snout was touched, indicating activity in the part of her brain seeking out food. "I think this is incredibly profound", commented Musk. Some neuroscience experts were not quite as impressed. The UK's Science Media Centre, which does a good job of trying to make complex scientific stories accessible, put out a press release quoting Prof Andrew Jackson, professor of neural interfaces at Newcastle University. "I don't think there was anything revolutionary in the presentation," he said. "But they are working through the engineering challenges of placing multiple electrodes into the brain. "In terms of their technology, 1,024 channels is not that impressive these days, but the electronics to relay them wirelessly is state-of-the-art, and the robotic implantation is nice. "The biggest challenge is what you do with all this brain data. The demonstrations were actually quite underwhelming in this regard, and didn't show anything that hasn't been done before." He went on to question why Neuralink's work was not being published in peer-reviewed papers. I took his words and his summary of the demo - "this is solid engineering but mediocre neuroscience" - and posted a tweet. © 2020 BBC.

Keyword: Brain imaging
Link ID: 27443 - Posted: 09.02.2020

by Nicholette Zeliadt An experimental drug prevents seizures and death in a mouse model of Dravet syndrome, a severe form of epilepsy that is related to autism, researchers reported 18 October 2019. The drug works by silencing a DNA segment called a ‘poison exon’ and is expected to enter clinical trials next year. If it works, it offers hope for treating not just Dravet, but other forms of autism as well: Another team has identified a poison exon in SYNGAP1, an autism gene that also causes epilepsy. Poison exons seem to impede the production of certain crucial proteins; blocking these segments would restore normal levels of the proteins. “The beauty of the technology,” says Gemma Carvill, assistant professor of neurology and pharmacology at Northwestern University in Chicago, Illinois, “is that “any gene that has a poison exon is potentially a target.” Several teams presented unpublished work on poison exons in a standing-room-only session at the 2019 American Society of Human Genetics meeting in Houston, Texas. People with Dravet often have autism, and most die in childhood2. The syndrome typically stems from mutations in a gene called SCN1A, which encodes an essential sodium channel in neurons. Only about 25 percent of mice with mutations in SCN1A live beyond 30 days of age. The new drug consists of short strands of ‘antisense’ RNA that restore normal levels of the channel, said Lori Isom of the University of Michigan, who presented the work. And all but 1 of 33 mice that received a single injection of the drug at 2 days of age remained alive 88 days later. © 2020 Simons Foundation

Keyword: Epilepsy; Autism
Link ID: 27437 - Posted: 08.29.2020

By Simon Makin New research could let scientists co-opt biology's basic building block—the cell—to construct materials and structures within organisms. A study, published in March in Science and led by Stanford University psychiatrist and bioengineer Karl Deisseroth, shows how to make specific cells produce electricity-carrying (or blocking) polymers on their surfaces. The work could someday allow researchers to build large-scale structures within the body or improve brain interfaces for prosthetic limbs. In the medium term, the technique may be useful in bioelectric medicine, which involves delivering therapeutic electrical pulses. Researchers in this area have long been interested in incorporating polymers that conduct or inhibit electricity without damaging surrounding tissues. Stimulating specific cells—to intervene in a seizure, for instance—is much more precise than flooding the whole organism with drugs, which can cause broad side effects. But current bioelectric methods, such as those using electrodes, still affect large numbers of cells indiscriminately. The new technique uses a virus to deliver genes to desired cell types, instructing them to produce an enzyme (Apex2) on their surface. The enzyme sparks a chemical reaction between precursor molecules and hydrogen peroxide, infused in the space between cells; this reaction causes the precursors to fuse into a polymer on the targeted cells. “What's new here is the intertwining of various emerging fields in one application,” says University of Florida biomedical engineer Kevin Otto, who was not involved in the research but co-authored an accompanying commentary in Science. “The use of conductive polymers assembled [inside living tissue] through synthetic biology, to enable cell-specific interfacing, is very novel.” © 2020 Scientific American

Keyword: Development of the Brain; Epigenetics
Link ID: 27411 - Posted: 08.11.2020

by Peter Hess / Infants with particular patterns of electrical activity in the brain go on to have high levels of autism traits as toddlers, a new study shows1. Specifically, babies who have unusually high or low synchrony between certain brain waves — as measured by electroencephalography (EEG) — at 3 months old tend to score high on a standardized scale of autism-linked behaviors when they are 18 months old. These levels of synchrony reflect underlying patterns of connectivity in the brain. The findings suggest that EEG could help clinicians identify autistic babies long before these children show behaviors flagged by standard diagnostic tests. The work “reinforces the concept and the truism that brain development is affected before autism diagnoses are made,” says lead researcher Shafali Spurling Jeste, associate professor of psychiatry and neurology at the University of California, Los Angeles. “We believe that we could work to start rewiring the brain if we intervene effectively and early enough. That message, quite simply, is a very important one.” The study involved ‘baby sibs,’ the younger siblings of autistic children. Baby sibs are 10 to 20 times more likely to have autism than the general population. Previous research showed similar patterns of altered connectivity in functional magnetic resonance imaging (MRI) data from infants who were later diagnosed with autism, but MRI is costly and prone to errors. EEG measurements, on the other hand, are relatively inexpensive and simple to perform, which makes them more practical for clinical use, says Charles Nelson, professor of pediatrics and neuroscience at Harvard University, who was not involved in the study. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27380 - Posted: 07.25.2020

Salvatore Domenic Morgera How the brain works remains a puzzle with only a few pieces in place. Of these, one big piece is actually a conjecture: that there’s a relationship between the physical structure of the brain and its functionality. The brain’s jobs include interpreting touch, visual and sound inputs, as well as speech, reasoning, emotions, learning, fine control of movement and many others. Neuroscientists presume that it’s the brain’s anatomy – with its hundreds of billions of nerve fibers – that make all of these functions possible. The brain’s “living wires” are connected in elaborate neurological networks that give rise to human beings’ amazing abilities. It would seem that if scientists can map the nerve fibers and their connections and record the timing of the impulses that flow through them for a higher function such as vision, they should be able to solve the question of how one sees, for instance. Researchers are getting better at mapping the brain using tractography – a technique that visually represents nerve fiber routes using 3D modeling. And they’re getting better at recording how information moves through the brain by using enhanced functional magnetic resonance imaging to measure blood flow. But in spite of these tools, no one seems much closer to figuring out how we really see. Neuroscience has only a rudimentary understanding of how it all fits together. To address this shortcoming, my team’s bioengineering research focuses on relationships between brain structure and function. The overall goal is to scientifically explain all the connections – both anatomical and wireless – that activate different brain regions during cognitive tasks. We’re working on complex models that better capture what scientists know of brain function. t © 2010–2020, The Conversation US, Inc.

Keyword: Brain imaging
Link ID: 27373 - Posted: 07.18.2020

By Lisa Sanders, M.D. The early-morning light wakened the middle-aged man early on a Saturday morning in 2003. He felt his 51-year-old wife move behind him and turned to see her whole body jerking erratically. He was a physician, a psychiatrist, and knew immediately that she was having a seizure. He grabbed his phone and dialed 911. His healthy, active wife had never had a seizure before. But this was only the most recent strange episode his wife had been through over the past 18 months. A year and a half earlier, the man returned to his suburban Pittsburgh home after a day of seeing patients and found his wife sitting in the kitchen, her hair soaking wet. He asked if she had just taken a shower. No, she answered vaguely, without offering anything more. Before he could ask her why she was so sweaty, their teenage son voiced his own observations. Earlier that day, the boy reported, “She wasn’t making any sense.” That wasn’t like her. Weeks later, his daughter reported that when she arrived home from school, she heard a banging sound in a room in the attic. She found her mother under a futon bed, trying to sit up and hitting her head on the wooden slats underneath. Her mother said she was looking for something, but she was obviously confused. The daughter helped her mother up and brought her some juice, which seemed to help. With both episodes, the children reported that their mother didn’t seem upset or distressed. The woman, who had trained as a psychiatrist before giving up her practice to stay with the kids, had no recollection of these odd events. The Problem Is Sugar Her husband persuaded her to see her primary-care doctor. Upon hearing about these strange spells, the physician said she suspected that her patient was having episodes of hypoglycemia. Very low blood sugar sends the body into a panicked mode of profuse sweating, shaking, weakness and, in severe cases, confusion. She referred her to a local endocrinologist. © 2020 The New York Times Company

Keyword: Epilepsy
Link ID: 27341 - Posted: 07.02.2020

by Peter Hess Early behavioral signs predict seizures in autistic children, according to a new study1. Previous work has shown that 5 to 46 percent of people with autism experience seizures. And autistic adults with epilepsy have, on average, less cognitive ability and weaker daily living skills than their autistic peers who do not have seizures2. The new study shows that people with autism who begin having seizures during childhood show small but significant behavioral differences before they ever experience a seizure, compared with those who do not develop epilepsy. They score lower than their peers on measures of quality of life and adaptive behaviors, which include communication, daily living skills, socialization and motor skills. They score higher on a measure of hyperactivity. The results suggest that seizures and certain behavioral issues in autism could have common origins, says co-lead investigator Jamie Capal, associate professor of pediatrics and neurology at the University of North Carolina at Chapel Hill. “I think it really does show us that in individuals with autism who eventually have epilepsy, there is some shared mechanism early on that we just haven’t been able to identify,” Capal says. Early signs: To investigate the relationship between childhood behaviors in autism and the development of seizures, the researchers analyzed data on 472 autistic children aged 2 to 15 from the Autism Treatment Network, a medical registry that includes 12 clinics in the United States and Canada. None of the children had experienced seizures before enrolling in the network, but 22 developed seizures two to six years after enrollment. © 2020 Simons Foundation

Keyword: Autism; Epilepsy
Link ID: 27294 - Posted: 06.09.2020

By Lisa Sanders, M.D. “I know what Danny has,” said the boy’s aunt to the boy’s mother, her sister-in-law. Her voice on the phone cracked with excitement. “I saw someone just like him on TV!” This was last fall, and Danny was 18. He had been a medical mystery since he was 7 months old. His mother recalled that she had just finished changing his diaper and picked him up when she heard him make a strange clicking noise, his mouth opening and closing oddly. And then his head flopped back as she held him. She hurried to the living room of their Queens home to show her husband, but by the time she got there, Danny was fine. Those sudden episodes of clicking and collapse happened again and again, eventually occurring more than 100 times a day. His first doctors thought these episodes could be tiny seizures. But none of the antiseizure medications they prescribed helped. Then, when Danny was 8, and almost too big for his mother to catch when he slow-motion slumped to the floor, his parents found a doctor who was willing to explore a different diagnosis and treatment. Could this be a rare disease known as cataplexy? In this disorder, patients have episodes of sudden weakness in the skeletal muscles of the body. In some, cataplexy may affect only the face or neck, causing the eyelids to droop or the head to fall forward. But in others, it can also affect the entire body. These episodes are often triggered by strong emotion, which was the case for Danny. Cataplexy is usually part of another rare disorder, narcolepsy, in which the normal control of sleep and wakefulness is somehow lost. Those with narcolepsy have sudden episodes of sleep that invade their waking hours and transient periods of wakefulness that disrupt their sleep. © 2020 The New York Times Company

Keyword: Sleep; Epilepsy
Link ID: 27290 - Posted: 06.08.2020

by Chloe Williams / A new flexible electrode array can detect the activity of neurons in a rat’s brain at high resolution for more than a year1. The device could be used to study how neuronal activity is altered in autism. Arrays usually have wires connected to each electrode to pick up its signal, but this design is bulky and works only in arrays consisting of 100 electrodes or fewer, limiting the array’s coverage and resolution. Devices with thousands of electrodes have integrated switches to consolidate signals into fewer wires. But these devices usually have a lifespan of only a few days. Their polymer-based coatings are often permeable to water or contain tiny defects that allow body fluids to seep into the device and current to leak out, damaging both the device and brain tissue. The new device combines electronic switches and a specialized protective coating so that scientists can record activity at the surface of the brain at high resolution over extended periods of time. The array, called Neural Matrix, consists of 1,008 surface electrodes laid out in 28 columns and 36 rows. Switches, or transistors, built into the array combine signals from all the electrodes in a column to a single output wire. The signals from each electrode in the column are recorded via the wire in a specific sequence, making it possible to separate them later. © 2020 Simons Foundation

Keyword: Brain imaging
Link ID: 27282 - Posted: 06.04.2020

By Robert Martone When a concert opens with a refrain from your favorite song, you are swept up in the music, happily tapping to the beat and swaying with the melody. All around you, people revel in the same familiar music. You can see that many of them are singing, the lights flashing to the rhythm, while other fans are clapping in time. Some wave their arms over their head, and others dance in place. The performers and audience seem to be moving as one, as synchronized to one another as the light show is to the beat. A new paper in the journal NeuroImage has shown that this synchrony can be seen in the brain activities of the audience and performer. And the greater the degree of synchrony, the study found, the more the audience enjoys the performance. This result offers insight into the nature of musical exchanges and demonstrates that the musical experience runs deep: we dance and feel the same emotions together, and our neurons fire together as well. In the study, a violinist performed brief excerpts from a dozen different compositions, which were videotaped and later played back to a listener. Researchers tracked changes in local brain activity by measuring levels of oxygenated blood. (More oxygen suggests greater activity, because the body works to keep active neurons supplied with it.) Musical performances caused increases in oxygenated blood flow to areas of the brain related to understanding patterns, interpersonal intentions and expression. Data for the musician, collected during a performance, was compared to those for the listener during playback. In all, there were 12 selections of familiar musical works, including “Edelweiss,” Franz Schubert’s “Ave Maria,” “Auld Lang Syne” and Ludwig van Beethoven’s “Ode to Joy.” The brain activities of 16 listeners were compared to that of a single violinist. © 2020 Scientific American,

Keyword: Hearing
Link ID: 27277 - Posted: 06.03.2020

Diana Kwon What if you could boost your brain’s processing capabilities simply by sticking electrodes onto your head and flipping a switch? Berkeley, California–based neurotechnology company Humm has developed a device that it claims serves that purpose. Their “bioelectric memory patch” is designed to enhance working memory—the type of short-term memory required to temporarily hold and process information—by noninvasively stimulating the brain. In recent years, neurotechnology companies have unveiled direct-to-consumer (DTC) brain stimulation devices that promise a range of benefits, including enhancing athletic performance, increasing concentration, and reducing depression. Humm’s memory patch, which resembles a large, rectangular Band-Aid, is one such product. Users can stick the device to their forehead and toggle a switch to activate it. Electrodes within the patch generate transcranial alternating current stimulation (tACS), a method of noninvasively zapping the brain with oscillating waves of electricity. The company recommends 15 minutes of stimulation to give users up to “90 minutes of boosted learning” immediately after using the device. The product is set for public release in 2021. Over the last year or so, Humm has generated much excitement among investors, consumers, and some members of the scientific community. In addition to raising several million dollars in venture capital funding, the company has drawn interest both from academic research labs and from the United States military. According to Humm cofounder and CEO Iain McIntyre, the US Air Force has ordered approximately 1,000 patches to use in a study at their training academy that is set to start later this year. © 1986–2020 The Scientist

Keyword: Learning & Memory
Link ID: 27269 - Posted: 05.29.2020

By Nicoletta Lanese, Scientists sent patterns of electricity coursing across people’s brains, coaxing their brains to see letters that weren’t there. The experiment worked in both sighted people and blind participants who had lost their sight in adulthood, according to the study, published today (May 14) in the journal Cell. Although this technology remains in its early days, implanted devices could potentially be used in the future to stimulate the brain and somewhat restore people’s vision. Known as visual prosthetics, the implants were placed on the visual cortex and then stimulated in a pattern to “trace” out shapes that the participants could then “see.” More advanced versions of these implants could work similarly to cochlear implants, which stimulate nerves of the inner ear with electrodes to help enhance the wearer’s hearing ability. “An early iteration [of such a device] could provide detection of the contours of shapes encountered,” study authors neuroscientist Michael Beauchamp and neurosurgeon Dr. Daniel Yoshor, both at the Baylor College of Medicine, told Live Science in an email. (Yoshor will start a new position at the Perelman School of Medicine at the University of Pennsylvania this summer.) “The ability to detect the form of a family member or to allow more independent navigation would be a wonderful advance for many blind patients.” The study authors crafted the letters by stimulating the brain with electrical currents, causing it to generate so-called phosphenes — tiny pinpricks of light that people sometimes perceive without any actual light entering their eyes. © 2020 Scientific American

Keyword: Vision; Robotics
Link ID: 27250 - Posted: 05.16.2020

Amber Dance A mouse finds itself in a box it’s never seen before. The walls are striped on one side, dotted on the other. The orange-like odor of acetophenone wafts from one end of the box, the spiced smell of carvone from the other. The mouse remembers that the orange smell is associated with something good. Although it may not recall the exact nature of the reward, the mouse heads toward the scent. Except this mouse has never smelled acetophenone in its life. Rather, the animal is responding to a false memory, implanted in its brain by neuroscientists at the Hospital for Sick Children in Toronto. Sheena Josselyn, a coauthor on a 2019 Nature Neuroscience study reporting the results of the project, says the goal was not to confuse the rodent, but for the scientists to confirm their understanding of mouse memory. “If we really understand memory, we should be able to trick the brain into remembering something that never happened at all,” she explains. By simultaneously activating the neurons that sense acetophenone and those associated with reward, the researchers created the “memory” that the orange-y scent heralded good things. Thanks to optogenetics, which uses a pulse of light to activate or deactivate neurons, Josselyn and other scientists are manipulating animal memories in all kinds of ways. Even before the Toronto team implanted false memories into mice, researchers were making rodents forget or recall an event with the flick of a molecular light switch. With every flash of light, they test their hypotheses about how these animals—and by extension, people—collect, store, and access past experiences. Scientists are also examining how memory formation and retrieval change with age, how those processes are altered in animal models of Alzheimer’s disease, and how accessing memories can influence an animal’s emotional state. © 1986–2020 The Scientist.

Keyword: Learning & Memory; Alzheimers
Link ID: 27228 - Posted: 05.02.2020

Ruth Williams Scientists have created a light-responsive opsin so sensitive that even when engineered into cells deep within tissue it can respond to an external light stimulus, according to a report in Neuron yesterday (April 30). Experiments in mice and macaques showed that shining blue light on the surface of the skull or brain was sufficient to activate opsin-expressing neurons six millimeters deep. “I was pretty blown away that this was even possible,” says Gregory Corder, who studies the neurological basis of pain and addiction at the University of Pennsylvania and who was not involved with the work. At that sort of depth, he continues, “essentially no part of the rodent brain is off-limits now for doing this non-invasive [technique]. . . . It’s pretty impressive.” “This development will help to extend the use of optogenetics in non-human primate models, and bring the techniques closer to clinical application in humans,” adds neurological disease expert Adriana Galvan of Yerkes National Primate Research Center in an email to The Scientist. Galvan was not a member of the research team. Optogenetics is a technique whereby excitable cells, such as neurons, can be controlled at will by light. To do this, cells are genetically engineered to produce ion channels called opsins that sit in the cells’ membranes and open in response to a certain wavelength of light. Switching on the light, then, floods the cells with ions, causing them to fire. Because light doesn’t penetrate tissue easily, to activate opsin-producing neurons deep in the brain of a living animal, researchers insert fiber optic cables. This is “highly invasive,” says Galvan, explaining that “the brain tissue can be damaged.” © 1986–2020 The Scientist.

Keyword: Brain imaging
Link ID: 27226 - Posted: 05.02.2020