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

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Rupert Neate The billionaire entrepreneur Elon Musk’s brain chip startup is preparing to launch clinical trials in humans. Musk, who co-founded Neuralink in 2016, has promised that the technology “will enable someone with paralysis to use a smartphone with their mind faster than someone using thumbs”. The Silicon Valley company, which has already successfully implanted artificial intelligence microchips in the brains of a macaque monkey named Pager and a pig named Gertrude, is now recruiting for a “clinical trial director” to run tests of the technology in humans. “As the clinical trial director, you’ll work closely with some of the most innovative doctors and top engineers, as well as working with Neuralink’s first clinical trial participants,” the advert for the role in Fremont, California, says. “You will lead and help build the team responsible for enabling Neuralink’s clinical research activities and developing the regulatory interactions that come with a fast-paced and ever-evolving environment.” Musk, the world’s richest person with an estimated $256bn fortune, said last month he was cautiously optimistic that the implants could allow tetraplegic people to walk. “We hope to have this in our first humans, which will be people that have severe spinal cord injuries like tetraplegics, quadriplegics, next year, pending FDA [Food and Drug Administration] approval,” he told the Wall Street Journal’s CEO Council summit. “I think we have a chance with Neuralink to restore full-body functionality to someone who has a spinal cord injury. Neuralink’s working well in monkeys, and we’re actually doing just a lot of testing and just confirming that it’s very safe and reliable and the Neuralink device can be removed safely.” © 2022 Guardian News & Media Limited

Keyword: Brain imaging; Robotics
Link ID: 28164 - Posted: 01.22.2022

By Gina Kolata For decades, researchers have suspected that people infected with an exceedingly common virus, Epstein-Barr, might be more likely to develop multiple sclerosis, a neurological illness that affects a million people in the United States. Now, a team of researchers reports what some say is the most compelling evidence yet of a strong link between the two diseases. The virus infects nearly everyone in their teen or young adult years, and very few go on to develop multiple sclerosis. The researchers also note that it is not the only known risk factor for people who develop the illness. But they say their data points to it being the clearest of them all. While it remains to be seen whether the finding will result in treatments or cures for multiple sclerosis, the study may further motivate research into therapies and vaccines for the condition. In their study, published Thursday in Science, the group examined data from 10 million people on active duty in the United States Armed Forces over two decades. The strength of their study, said its principal investigator, Dr. Alberto Ascherio, an epidemiologist at the Harvard T.H. Chan School of Public Health, is that they were able to follow people for years and ask whether infections with Epstein-Barr preceded multiple sclerosis. Among the service members in the study, 801 developed multiple sclerosis, a disabling disease that occurs when the immune system attacks the fatty insulation that protects nerves in the brain and spinal cord. Most who develop the disease are diagnosed between the ages of 20 and 50. The disease is rare, though — an individual’s chance of getting multiple sclerosis is half of one percent. At the same time, the virus in question, Epstein-Barr, is common, infecting nearly everyone in the population at some point. Although few are aware that they were infected, some develop mononucleosis. The virus remains in the body for life. © 2022 The New York Times Company

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28154 - Posted: 01.15.2022

by Anna Goshua A variety of traits, including developmental delay and intellectual disability, characterize people with mutations in the autism-linked gene MYT1L, according to a new study. The gene encodes a transcription factor important for cells that make myelin, which insulates nerve cells and is deficient in some forms of autism. The work, published 8 November in Human Genetics, represents the most detailed study of the traits associated with MYT1L mutations to date. “We wanted to gather more cases to bring a clearer clinical and molecular picture of the condition for lab scientists, clinicians and also for patients and families,” says study investigator Juliette Coursimault, a physician-researcher in the genetics department at Rouen University Hospital in France. She and her co-researchers described 62 people, whereas previous literature included only 12 cases. The new characterization will “benefit clinicians’ diagnosis and treatment strategies when a patient with MYT1L mutation arrives in their clinic,” says Brady Maher, a lead investigator at the Lieber Institute for Brain Development at Johns Hopkins University in Baltimore, Maryland, who was not part of the study. The researchers identified and reviewed data for 22 people with MYT1L mutations who had been described in the academic literature, and collected clinical and molecular data from an additional 40 people, aged 1 to 34 years old, with likely or confirmed pathogenic variants of MYT1L. They recruited the participants through Rouen University Hospital and data-sharing networks such as GeneMatcher, which connects clinicians and researchers. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28122 - Posted: 12.22.2021

by Anna Goshua Mice that lack one copy of TBX1, a gene in the autism-linked 22q11.2 chromosomal region, produce too little myelin — the fatty insulation that surrounds neurons — and perform poorly on tasks that measure cognitive speed, according to a new study. The work, published 5 November in Molecular Psychiatry, may offer insight into the mechanisms that underlie impaired cognitive function in some people with a 22q11.2 deletion, and possibly other copy number variants (CNVs). “The myelin changes could potentially emerge as a common neuronal deficit that mediates cognitive changes among many CNV cases,” says lead investigator Noboru Hiroi, professor of pharmacology at the University of Texas Health Science Center at San Antonio. Neuronal axons — the projections that conduct nerve impulses — are coated with myelin, which serves to speed up electrical transmission. The brains of autistic people and several mouse models of autism have disruptions in myelin, previous research has shown. These connecting fibers are the “highways of the brain,” says Valerie Bolivar, research scientist at the New York State Department of Health’s Wadsworth Center in Albany. “If the highway doesn’t work, you can’t get your goods from one place to another as fast.” TBX1 encodes a protein that regulates the expression of other genes during brain development. Deleting one copy of TBX1 leads to social and communication deficits in mice, according to previous studies by Hiroi’s team. © 2021 Simons Foundation

Keyword: Autism; Glia
Link ID: 28103 - Posted: 12.08.2021

By Kelly Servick For patients whose depression resists treatment with drugs and electroconvulsive therapy, surgically implanted wires that stimulate the brain might bring relief. But in recent years, two randomized, controlled trials of this approach, known as deep brain stimulation (DBS), were halted after underwhelming results in interim analyses. “It was like the air was let out of the room,” Sameer Sheth, a neurosurgeon at Baylor College of Medicine, says of those results. “It was a big let-down.” Now, researchers are testing more sophisticated, personalized DBS techniques they hope will yield stronger results. The tests to date have involved just one or a few patients, far from proof of effectiveness. But researchers hope they’ll inform larger studies that finally cement the effectiveness of DBS in depression. “With all these irons in the fire … we will hopefully build up enough understanding and evidence,” says Sheth, an author of a case study published this week. DBS is already approved in the United States to treat epilepsy, obsessive compulsive disorder, and movement disorders such as Parkinson’s disease. Could it also shift patterns of abnormal activity in neural circuits that may drive depression symptoms? Early studies without control groups yielded promising results, but two randomized, controlled trials, sponsored by the medical device companies Medtronic and St. Jude Medical, Inc. (which was later acquired by Abbott Laboratories) did not show significant benefits after several months of DBS, teams reported in 2015 and 2017. Long-term follow-up of participants has revived some optimism. For example, many people in the 30-participant Medtronic trial improved over 1 year or more—beyond the timeline of the initial study, says Stanford University psychiatrist Mahendra Bhati, a co-investigator. Last month, he and colleagues published a follow-up study of eight trial patients, most of whom continue to use their implant about 10 years later. About one-half have had at least a 50% improvement over their pretreatment score on a depression scale. © 2021 American Association for the Advancement of Science.

Keyword: Depression
Link ID: 28089 - Posted: 11.24.2021

Allison Whitten Every time a human or machine learns how to get better at a task, a trail of evidence is left behind. A sequence of physical changes — to cells in a brain or to numerical values in an algorithm — underlie the improved performance. But how the system figures out exactly what changes to make is no small feat. It’s called the credit assignment problem, in which a brain or artificial intelligence system must pinpoint which pieces in its pipeline are responsible for errors and then make the necessary changes. Put more simply: It’s a blame game to find who’s at fault. AI engineers solved the credit assignment problem for machines with a powerful algorithm called backpropagation, popularized in 1986 with the work of Geoffrey Hinton, David Rumelhart and Ronald Williams. It’s now the workhorse that powers learning in the most successful AI systems, known as deep neural networks, which have hidden layers of artificial “neurons” between their input and output layers. And now, in a paper published in Nature Neuroscience in May, scientists may finally have found an equivalent for living brains that could work in real time. A team of researchers led by Richard Naud of the University of Ottawa and Blake Richards of McGill University and the Mila AI Institute in Quebec revealed a new model of the brain’s learning algorithm that can mimic the backpropagation process. It appears so realistic that experimental neuroscientists have taken notice and are now interested in studying real neurons to find out whether the brain is actually doing it. Simons Foundation All Rights Reserved © 2021

Keyword: Learning & Memory
Link ID: 28044 - Posted: 10.20.2021

By Dave Itzkoff Selma Blair could only talk for a half-hour in our first session. That was as long as she trusted her brain and her body to cooperate — any longer and she feared that her focus might start to wander or her speech might begin to trail. “We’re being responsible in knowing that smaller moments will be clearer moments,” she said. For Blair no day is free from the effects of multiple sclerosis, the autoimmune disease that she learned she had in 2018 but that she believes began attacking her central nervous system many years earlier. This particular Friday in September had started out especially tough: She said she woke up in her Los Angeles home feeling “just bad as all get out,” but she found that talking with people helped alleviate her discomfort. Blair said she had had good conversations earlier in the day and that she had been looking forward to ours. So, if she needed to take a break during this interview, she said with a delighted cackle, “it just means you’re boring me.” An unparalleled lack of inhibition has always defined Blair’s best-known work. She is 49 now, with a résumé that includes seminal works of teensploitation (“Cruel Intentions”), comedy (“Legally Blonde”) and comic-book adventure (“Hellboy”). ImageBlair in one of her signature roles, as a fellow law student opposite Reese Witherspoon in “Legally Blonde.” That same unbridled bluntness persists in all her interactions, whether scripted or spontaneous, with cameras on or off, even when she is sharing her account of the time she went on “The Tonight Show” wearing a strappy top she accidentally put on sideways. It is a story she told me proudly, within five minutes of our introduction on a video call, while her fingers made a maelstrom of her close-cropped, bleached-blond hair. (By way of explaining this style choice, she burst into a brassy, Ethel Merman-esque voice and sang, “I want to be a shiksa.”) But Blair’s candor has come to mean something more in the three years since she went public about her M.S. diagnosis. Now, whether she is posting personal diaries on social media or appearing on a red carpet, she understands she is a representative with an opportunity to educate a wider audience about what she and others with M.S. are experiencing. © 2021 The New York Times Company

Keyword: Multiple Sclerosis
Link ID: 28030 - Posted: 10.13.2021

Allison Whitten Our mushy brains seem a far cry from the solid silicon chips in computer processors, but scientists have a long history of comparing the two. As Alan Turing put it in 1952: “We are not interested in the fact that the brain has the consistency of cold porridge.” In other words, the medium doesn’t matter, only the computational ability. Today, the most powerful artificial intelligence systems employ a type of machine learning called deep learning. Their algorithms learn by processing massive amounts of data through hidden layers of interconnected nodes, referred to as deep neural networks. As their name suggests, deep neural networks were inspired by the real neural networks in the brain, with the nodes modeled after real neurons — or, at least, after what neuroscientists knew about neurons back in the 1950s, when an influential neuron model called the perceptron was born. Since then, our understanding of the computational complexity of single neurons has dramatically expanded, so biological neurons are known to be more complex than artificial ones. But by how much? To find out, David Beniaguev, Idan Segev and Michael London, all at the Hebrew University of Jerusalem, trained an artificial deep neural network to mimic the computations of a simulated biological neuron. They showed that a deep neural network requires between five and eight layers of interconnected “neurons” to represent the complexity of one single biological neuron. All Rights Reserved © 2021

Keyword: Brain imaging; Vision
Link ID: 27978 - Posted: 09.04.2021

by Peter Hess Some mutations in SCN2A, a gene reliably linked to autism, change social behaviors in mice by dampening the electrical activity of their neurons, according to a new study. SCN2A encodes a sodium channel that helps neurons send electrical signals. So-called ‘gain-of-function’ mutations make the channel hyperactive and can lead to epilepsy, whereas ‘loss-of-function’ mutations diminish its activity and are typically associated with autism. The mice in the new study carry the latter type and, as a result, have fewer functioning sodium channels than usual. The animals also react to unfamiliar mice in an atypical way, mirroring social behaviors seen in autistic people with similar SCN2A mutations. “We’re in the position of really connecting a single mutation, or at least a defect in the channel, to the behavior,” says lead investigator Geoffrey Pitt, professor of medicine at Weill Cornell Medicine in New York. “The message that our paper shows is that loss-of-function mutations and decreased sodium current can lead to behaviors.” This study confirms previous work showing that autism-linked mutations in SCN2A dampen channel activity in neurons, and further connects the loss-of-function mutations to clear changes in behavior, says Kevin Bender, associate professor of neurology at the University of California San Francisco, who was not involved in the work. “The behavioral results were actually some of the most robust that I’ve seen in this field to date.” © 2021 Simons Foundation

Keyword: Autism
Link ID: 27968 - Posted: 08.28.2021

By Katie Free, Joel Goldberg When it comes to our senses, we frequently focus on the external—the crack of thunder, the glare of sunlight, the fragrance of flowers—that captured our attention in the first place. But our bodies also have a whole host of internal senses that tell our brains whether our hearts are beating at the right speed, for example, or whether our blood pressure is too high. These signals travel constantly via hormones and nerves, including a mysterious 100,000-fiber network called the vagus nerve. Now, new techniques are helping scientists map the thin, twisting branches of the vagus nerve—which connects the brain to the heart, intestines, and other internal organs—and make surprising discoveries about its role in memory and emotion. These findings have spawned investigations into treatments for everything from Alzheimer’s disease to post-traumatic stress disorder and have led to the approval of medical implants to help treat epilepsy and depression. When it comes to understanding the brain-mind connection, a gut check might not hurt. © 2021 American Association for the Advancement of Science.

Keyword: Epilepsy; Depression
Link ID: 27867 - Posted: 06.23.2021

By Christof Koch Consider the following experiences: • You're headed toward a storm that's a couple of miles away, and you've got to get across a hill. You ask yourself: “How am I going to get over that, through that?” • You see little white dots on a black background, as if looking up at the stars at night. Advertisement • You look down at yourself lying in bed from above but see only your legs and lower trunk. These may seem like idiosyncratic events drawn from the vast universe of perceptions, sensations, memories, thoughts and dreams that make up our daily stream of consciousness. In fact, each one was evoked by directly stimulating the brain with an electrode. As American poet Walt Whitman intuited in his poem “I Sing the Body Electric,” these anecdotes illustrate the intimate relationship between the body and its animating soul. The brain and the conscious mind are as inexorably linked as the two sides of a coin. Recent clinical studies have uncovered some of the laws and regularities of conscious activity, findings that have occasionally proved to be paradoxical. They show that brain areas involved in conscious perception have little to do with thinking, planning and other higher cognitive functions. Neuroengineers are now working to turn these insights into technologies to replace lost cognitive function and, in the more distant future, to enhance sensory, cognitive or memory capacities. For example, a recent brain-machine interface provides completely blind people with limited abilities to perceive light. These tools, however, also reveal the difficulties of fully restoring sight or hearing. They underline even more the snags that stand in the way of sci-fi-like enhancements that would enable access to the brain as if it were a computer storage drive. © 2021 Scientific American,

Keyword: Consciousness
Link ID: 27865 - Posted: 06.19.2021

By Laura Sanders Some big scientific discoveries aren’t actually discovered. They are borrowed. That’s what happened when scientists enlisted proteins from an unlikely lender: green algae. Cells of the algal species Chlamydomonas reinhardtii are decorated with proteins that can sense light. That ability, first noticed in 2002, quickly caught the attention of brain scientists. A light-sensing protein promised the power to control neurons — the brain’s nerve cells — by providing a way to turn them on and off, in exactly the right place and time. Nerve cells genetically engineered to produce the algal proteins become light-controlled puppets. A flash of light could induce a quiet neuron to fire off signals or force an active neuron to fall silent. “This molecule is the light sensor that we needed,” says vision neuroscientist Zhuo-Hua Pan, who had been searching for a way to control vision cells in mice’s retinas. The method enabled by these loaner proteins is now called optogenetics, for its combination of light (opto) and genes. In less than two decades, optogenetics has led to big insights into how memories are stored, what creates perceptions and what goes wrong in the brain during depression and addiction. Using light to drive the activity of certain nerve cells, scientists have toyed with mouse hallucinations: Mice have seen lines that aren’t there and have remembered a room they had never been inside. Scientists have used optogenetics to make mice fight, mate and eat, and even given blind mice sight. In a big first, optogenetics recently restored aspects of a blind man’s vision. © Society for Science & the Public 2000–2021.

Keyword: Brain imaging; Learning & Memory
Link ID: 27861 - Posted: 06.19.2021

By Virginia Hughes Late one evening last March, just before the coronavirus pandemic shut down the country, Mingzheng Wu, a graduate student at Northwestern University, plopped two male mice into a cage and watched as they explored their modest new digs: sniffing, digging, fighting a little. Sign up for Science Times: Get stories that capture the wonders of nature, the cosmos and the human body. With a few clicks on a nearby computer, Mr. Wu then switched on a blue light implanted in the front of each animal’s brain. That light activated a tiny piece of cortex, spurring neurons there to fire. Mr. Wu zapped the two mice at the same time and at the same rapid frequency — putting that portion of their brains quite literally in sync. Within a minute or two, any animus between the two creatures seemed to disappear, and they clung to each other like long-lost friends. “After a few minutes, we saw that those animals actually stayed together, and one animal was grooming the other,” said Mr. Wu, who works in the neurobiology lab of Yevgenia Kozorovitskiy. Mr. Wu and his colleagues then repeated the experiment, but zapped each animal’s cortex at frequencies different from the other’s. This time, the mice displayed far less of an urge to bond. The experiment, published this month in Nature Neuroscience, was made possible thanks to an impressive new wireless technology that allows scientists to observe — and manipulate — the brains of multiple animals as they interact with one another. “The fact that you can implant these miniaturized bits of hardware and turn neurons on and off by light, it’s just mind-blowingly cool,” said Thalia Wheatley, a social neuroscientist at Dartmouth College who was not involved in the work. © 2021 The New York Times Company

Keyword: Aggression; Sexual Behavior
Link ID: 27832 - Posted: 05.27.2021

Linda Geddes Science correspondent A blind man has had his sight partly restored after a form of gene therapy that uses pulses of light to control the activity of nerve cells – the first successful demonstration of so-called optogenetic therapy in humans. The 58-year-old man, from Brittany in northern France, was said to be “very excited” after regaining the ability to recognise, count, locate and touch different objects with the treated eye while wearing a pair of light-stimulating goggles, having lost his sight after being diagnosed with retinitis pigmentosa almost 40 years ago. The breakthrough marks an important step towards the more widespread use of optogenetics as a clinical treatment. It involves modifying nerve cells (neurons) so that they fire electrical signals when they’re exposed to certain wavelengths of light, equipping neuroscientists with the power to precisely control neuronal signalling within the brain and elsewhere. Christopher Petkov, a professor of comparative neuropsychology at Newcastle University medical school, said: “This is a tremendous development to restore vision using an innovative approach. The goal now is to see how well this might work in other patients with retinitis pigmentosa.” This group of rare, genetic disorders, which involves the loss of light-sensitive cells in the retina, affects more than 2 million people worldwide, and can lead to complete blindness. © 2021 Guardian News & Media Limited

Keyword: Vision
Link ID: 27831 - Posted: 05.27.2021

By Charles Q. Choi With the help of headsets and backpacks on mice, scientists are using light to switch nerve cells on and off in the rodents’ brains to probe the animals’ social behavior, a new study shows. These remote control experiments are revealing new insights on the neural circuitry underlying social interactions, supporting previous work suggesting minds in sync are more cooperative, researchers report online May 10 in Nature Neuroscience. The new devices rely on optogenetics, a technique in which researchers use bursts of light to activate or suppress the brain nerve cells, or neurons, often using tailored viruses to genetically modify cells so they respond to illumination (SN: 1/15/10). Scientists have used optogenetics to probe neural circuits in mice and other lab animals to yield insights on how they might work in humans (SN: 10/22/19). Optogenetic devices often feed light to neurons via fiber-optic cables, but such tethers can interfere with natural behaviors and social interactions. While scientists recently developed implantable wireless optogenetic devices, these depend on relatively simple remote controls or limited sets of preprogrammed instructions. These new fully implantable optogenetic arrays for mice and rats can enable more sophisticated research. Specifically, the researchers can adjust each device’s programming during the course of experiments, “so you can target what an animal does in a much more complex way,” says Genia Kozorovitskiy, a neurobiologist at Northwestern University in Evanston, Ill. © Society for Science & the Public 2000–2021.

Keyword: Brain imaging
Link ID: 27812 - Posted: 05.12.2021

Researchers are now able to wirelessly record the directly measured brain activity of patients living with Parkinson’s disease and to then use that information to adjust the stimulation delivered by an implanted device. Direct recording of deep and surface brain activity offers a unique look into the underlying causes of many brain disorders; however, technological challenges up to this point have limited direct human brain recordings to relatively short periods of time in controlled clinical settings. This project, published in the journal Nature Biotechnology, was funded by the National Institutes of Health’s Brain Research Through Advancing Innovative Neurotechnologies (BRAIN) Initiative. “This is really the first example of wirelessly recording deep and surface human brain activity for an extended period of time in the participants’ home environment,” said Kari Ashmont, Ph.D., project manager for the NIH BRAIN Initiative. “It is also the first demonstration of adaptive deep brain stimulation at home.” Deep brain stimulation (DBS) devices are approved by the U. S. Food and Drug Administration for the management of Parkinson’s disease symptoms by implanting a thin wire, or electrode, that sends electrical signals into the brain. In 2018, the laboratory of Philip Starr, M.D., Ph.D. at the University of California, San Francisco, developed an adaptive version of DBS that adapts its stimulation only when needed based on recorded brain activity. In this study, Dr. Starr and his colleagues made several additional improvements to the implanted technology.

Keyword: Brain imaging
Link ID: 27800 - Posted: 05.05.2021

By Christine Kenneally The first thing that Rita Leggett saw when she regained consciousness was a pair of piercing blue eyes peering curiously into hers. “I know you, don’t I?” she said. The man with the blue eyes replied, “Yes, you do.” But he didn’t say anything else, and for a while Leggett just wondered and stared. Then it came to her: “You’re my surgeon!” It was November, 2010, and Leggett had just undergone neurosurgery at the Royal Melbourne Hospital. She recalled a surge of loneliness as she waited alone in a hotel room the night before the operation and the fear she felt when she entered the operating room. She’d worried about the surgeon cutting off her waist-length hair. What am I doing in here? she’d thought. But just before the anesthetic took hold, she recalled, she had said to herself, “I deserve this.” Leggett was forty-nine years old and had suffered from epilepsy since she was born. During the operation, her surgeon, Andrew Morokoff, had placed an experimental device inside her skull, part of a brain-computer interface that, it was hoped, would be able to predict when she was about to have a seizure. The device, developed by a Seattle company called NeuroVista, had entered a trial stage known in medical research as “first in human.” A research team drawn from three prominent epilepsy centers based in Melbourne had selected fifteen patients to test the device. Leggett was Patient 14. © 2021 Condé Nast.

Keyword: Robotics; Epilepsy
Link ID: 27791 - Posted: 04.28.2021

By Kim Tingley The brain is an electrical organ. Everything that goes on in there is a result of millivolts zipping from one neuron to another in particular patterns. This raises the tantalizing possibility that, should we ever decode those patterns, we could electrically adjust them to treat neurological dysfunction — from Alzheimer’s to schizophrenia — or even optimize desirable qualities like intelligence and resilience. Of course, the brain is so complex, and so difficult to access, that this is much easier to imagine than to do. A pair of studies published in January in the journal Nature Medicine, however, demonstrate that electrical stimulation can address obsessive-compulsive urges and symptoms of depression with surprising speed and precision. Mapping participants’ brain activity when they experienced certain sensations allowed researchers to personalize the stimulation and modify moods and habits far more directly than is possible through therapy or medication. The results also showed the degree to which symptoms that we tend to categorize as a single disorder — depression, for example — may involve electrical processes that are unique to each person. In the first study, a team from the University of California, San Francisco, surgically implanted electrodes in the brain of a woman whose severe depression had proved resistant to other treatments. For 10 days, they delivered pulses through the electrodes to different areas of the brain at various frequencies and had the patient record her level of depression, anxiety and energy on an iPad. The impact of certain pulses was significant and nuanced. “Within a minute, she would say, ‘I feel like I’m reading a good book,’” says Katherine W. Scangos, a psychiatrist and the study’s lead author. The patient described the effect of another pulse as “less cobwebs and cotton.” © 2021 The New York Times Company

Keyword: Depression
Link ID: 27712 - Posted: 02.28.2021

By Leslie Nemo Ironically, this tangle of brain cells is helping scientists tease apart a larger problem: how to help people with Alzheimer’s disease. Matheus Victor, a researcher at the Massachusetts Institute of Technology, photographed these neurons after coaxing them to life in a petri dish in the hope that the rudimentary brain tissue will reveal why a new therapy might alleviate Alzheimer’s symptoms. In humans and mice, a healthy memory is associated with a high level of synced neurons that turn on and off simultaneously. Those with neurological conditions such as Alzheimer’s and Parkinson’s disease often have fewer brain cells blinking unanimously. A couple of years ago Victor’s lab leader Li-Huei Tsai and her team at M.I.T. found that when they surrounded mice genetically predisposed to Alzheimer’s with sound pulses beating 40 times a second, the rodents performed better on memory-related tasks. The animals also lost some amyloid plaques, protein deposits in the brain that are characteristic of the disease. The researchers had previously performed a similar study with light flickering at the same rate, and the mice were found to experience additional improvements when the sound and light pulses were combined. Astoundingly, the mouse neurons synced up to the 40-beats-per-second rhythm of the audio pulses, though the mechanism behind this result and the reason the shift improves symptoms remain a mystery. To help solve it, the researchers want to watch how brain tissue responds to the stimulants at the cellular level. The goal is to one day understand how this exposure treatment might work for people, so the team is growing human brain cells in the lab and engineering them to respond to sound and light without eyes and ears. “We are trying to mimic the sensory stimulation in mice but missing a lot of the hardware that makes it possible. So this is a bit of a hack,” Victor says. © 2021 Scientific American

Keyword: Alzheimers; Brain imaging
Link ID: 27690 - Posted: 02.15.2021

By Diana Kwon Obsessive-compulsive disorder (OCD) is marked by repetitive, anxiety-inducing thoughts, urges and compulsions, such as excessive cleaning, counting and checking. These behaviors are also prevalent in the general population: one study in a large sample of U.S. adults found more than a quarter had experienced obsessions or compulsions at some point in their life. Although most of these individuals do not develop full-blown OCD, such symptoms can still interfere with daily life. A new study, published on January 18 in Nature Medicine, hints that these behaviors may be alleviated by stimulating the brain with an electrical current—without the need to insert electrodes under the skull. Robert Reinhart, a neuroscientist at Boston University, and his group drew on two parallel lines of research for this study. First, evidence suggests that obsessive-compulsive behaviors may arise as a result of overlearning habits—leading to their excessive repetition—and abnormalities in brain circuits involved in learning from rewards. Separately, studies point to the importance of high-frequency rhythms in the so-called high-beta/low-gamma range (also referred to as simply beta-gamma) in decision-making and learning from positive feedback. Drawing on these prior observations, Shrey Grover, a doctoral student in Reinhart’s lab, hypothesized with others in the team that manipulating beta-gamma rhythms in the orbitofrontal cortex (OFC)—a key region in the reward network located in the front of the brain—might disrupt the ability to repetitively pursue rewarding choices. In doing so, the researchers thought, the intervention could reduce obsessive-compulsive behaviors associated with maladaptive habits. To test this hypothesis, Grover and his colleagues carried out a two-part study. The first segment was aimed at identifying whether the high-frequency brain activity influenced how well people were able to learn from rewards. The team recruited 60 volunteers and first used electroencephalography to pinpoint the unique frequencies of beta-gamma rhythms in the OFC that were active in a given individual while that person took part in a task that involved associating symbols with monetary wins or losses. Previous work had shown that applying stimulation based on the particular patterns of rhythms in a person’s brain may enhance the effectiveness of the procedure. © 2021 Scientific American

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 27657 - Posted: 01.20.2021