By Katherine Ellison “American Ninja Warrior” contestant Jimmy Choi was 27 when he was diagnosed with young-onset Parkinson’s disease after a routine medical exam. Today, Choi, 50, is an adviser to the Michael J. Fox Foundation for Parkinson’s Research who champions physical fitness and works to inspire others via public speaking and social media posts. More than 1 million Americans have Parkinson’s disease, a neurological illness that can cause tremors, loss of balance, confusion and depression. Choi spent the eight years after his diagnosis in denial as his symptoms grew worse. After a mortifying fall, however, his perspective changed, and he embraced exercise — in a big way. Since 2011, the Chicago-based former tech executive (he retired from full-time work in 2018, though he still works as a consultant) has run 16 marathons and earned three Guinness World records, the most recent in 2023 for consecutive double high five push-ups. He has also competed seven times on “American Ninja Warrior,” the reality-TV show in which contestants make their way past daunting obstacles, crossing unstable bridges, running up walls and leaping through the air, all while trying to avoid falling into a large pool of water. Last year Choi finished his seventh, and, he insists, last “Ninja” appearance. It’s set to air this spring. Q: What led to your diagnosis? A: It was a routine exam for health insurance, in 2003. A nurse noticed the way I was walking and said I should talk to my doctor. I had to see four neurologists before I got diagnosed, and for several years afterward, I lost my motivation. I started isolating from friends, gained a lot of weight and couldn’t walk without a cane.

Keyword: Parkinsons
Link ID: 29645 - Posted: 01.29.2025

By Angie Voyles Askham More than 150 years after the first known description of Huntington’s disease and 32 years after the causative gene, HTT, was identified, new evidence has emerged to explain how variants linked to the disease devastate the brain: The toxicity comes not from the initial variant itself but rather from its dynamic expansion past a set threshold in specific cells, according to a study published today in Cell. The results help explain why most people with Huntington’s disease don’t start to show symptoms—including muscle rigidity, irregular movements and severe psychological issues—until age 30 to 50, with the gradual loss of striatal projection neurons, also called medium spiny neurons, says co-lead researcher Steven McCarroll, professor of biomedical science and genetics at Harvard Medical School. “We hadn’t been thinking about mutations as dynamic things” that become toxic only later in life, he says. The HTT variants associated with Huntington’s disease all have extra repeats of the DNA triplet CAG. Typical people carry about 15 to 30 of these repeats, and those with the disease tend to have 40 or more. The disease-linked expansions, which are known to grow even larger over time, result in a gangly version of the Huntington’s protein that is thought to cause neurons to malfunction and degenerate. But the expansion does not appear to affect a cell’s biology until it exceeds 150 CAG copies, according to the new study. And the repeats accumulate quietly over the course of years, and at different rates for different cells. Striatal projection neurons with more than 150 repeats have severely dysregulated transcriptomes, McCarroll and his colleagues found by analyzing gene expression in postmortem tissue from people with Huntington’s disease. But other cell types in the striatum, including oligodendrocytes and interneurons, do not end up with as many repeats, nor do they undergo similar transcriptomic changes, the work shows. © 2025 Simons Foundation

Keyword: Huntingtons; Genes & Behavior
Link ID: 29636 - Posted: 01.22.2025

By Phie Jacobs For more than 30 years, scientists have known the genetic culprit behind Huntington disease, a devastating neurodegenerative disorder that causes cells deep in the brain to sicken and die. But they couldn’t account for why people who inherit the faulty gene variant take so long to develop symptoms, or why disease progression varies so widely from person to person. A study published today in Cell helps explain: In the brain cells that die off in Huntington, a repetitive stretch of a gene’s DNA gets longer and longer over a person’s life, and this accelerating expansion turns deadly to the cell—and ultimately to the person. The findings represent “a really remarkable insight,” says Leslie Thompson, a neuroscientist at the University of California, Irvine who wasn’t involved in the new research. “This study and some others are changing the way that we’re thinking about the disease.” People who develop Huntington inherit a flawed version of the HTT gene, which produces a protein called huntingtin. This gene contains an unusual stretch of DNA, where a sequence of three of its nucleotide bases—cytosine, adenine, and guanine, or CAG in genetic parlance—are repeated multiple times in a row. And although most people inherit versions of HTT with about 15 to 30 consecutive CAG repeats and never develop Huntington, those with 40 or more in the gene almost always have symptoms later in life, including psychological and cognitive problems and uncontrolled, jerking movements known as chorea. The genetic stutter produces an abnormally large, unstable version of the huntingtin protein, which forms clumps inside brain cells. The condition usually leads to early death, often from issues related to difficulty swallowing, injuries from falls, or suicide. The longer a person’s stretch of repeats, the earlier the disorder rears its head. Scientists originally thought the number of CAG repeats only increased as the HTT gene was passed down through generations; a child of a parent with Huntington might themselves develop the condition at an earlier age. But it turns out the length of this genetic “stutter” can change over a person’s life in at least some of their cells. A 2003 study analyzed brain samples donated by people who had died of Huntington and found shockingly large CAG expansions in a part of the brain known as the striatum.

Keyword: Huntingtons; Genes & Behavior
Link ID: 29634 - Posted: 01.18.2025

By Terence Monmaney The road switches back and forth again and again as it climbs into Montchavin, perched in the French Alps at 4,100 feet above sea level. The once-sleepy mountainside village, developed into a ski resort in the 1970s, is dotted with wooden chalet-style condo buildings and situated in the midst of a vast downhill complex known as Paradiski, one of the world’s largest. Well known to skiers and alpinistes, Montchavin also has grabbed the attention of medical researchers as the site of a highly unusual cluster of a devastating neurological disease, amyotrophic lateral sclerosis. ALS, brought about by the progressive loss of nerve function in the brain, spinal cord and motor neurons in the limbs and chest, leading to paralysis and death, is both rare and rather evenly distributed across the globe: It afflicts two to three new people out of 100,000 per year. Though Montchavin is flooded with visitors in winter and summer, the year-round resident population is only a couple hundred, and neighboring villages aren’t much bigger, so the odds are strongly against finding more than just a few ALS patients in the immediate area. Yet physicians have reported 14. The first of the village patients to arouse suspicion in Emmeline Lagrange, the neurologist who has led the investigation into the problem, was a woman in her late thirties, a ski instructor and ski lift ticket-checker originally from Poland who worked in the offseason at the local tourism office. It was 2009. A physician in Montchavin had referred the woman to Lagrange, who practices at Grenoble University Hospital, 84 miles southwest of the village. Lagrange diagnosed ALS and recalls phoning the Montchavin physician to explain the consequences: “The first thing she said was, ‘I certainly know what it is. It’s the fourth case in the village. My neighbor died of ALS 20 years ago and two friends of hers are still victims of the disease.’”

Keyword: ALS-Lou Gehrig's Disease ; Neurotoxins
Link ID: 29606 - Posted: 12.21.2024

By Fred Schwaller Scott Imbrie still remembers the first time that physicians switched on the electrodes sitting on the surface of his brain. He felt a tingling, poking sensation in his hand, like “reaching into an evergreen bush”, he says. “It was like I was decorating a Christmas tree.” Back in 1985, a car crash shattered three of Imbrie’s vertebrae and severed 70% of his spinal cord, leaving him with very limited sensation or mobility in parts of his body. Now, thanks to an implanted brain–computer interface (BCI), Imbrie can operate a robotic arm, and receive sensory information related to what that arm is doing. Imbrie spends four days a week, three hours at a time, testing, refining and tuning the device with a team of researchers at the University of Chicago in Illinois. Scientists have been trying to restore mobility for people with missing or paralysed limbs for decades. The aim, historically, was to give people the ability to control prosthetics with commands from the nervous system. But this motor-first approach produced bionic limbs that were much less helpful than hoped: devices were cumbersome and provided only rudimentary control of a hand or leg. What’s more, they just didn’t feel like they were part of the body and required too much concentration to use. Scientists gradually began to realize that restoring full mobility meant restoring the ability to sense touch and temperature, says Robert Gaunt, a bioengineer at the University of Pittsburgh in Pennsylvania. Gaunt says that this realization has led to a revolution in the field. A landmark study1 came in 2016, when a team led by Gaunt restored tactile sensations in a person with upper-limb paralysis using a computer chip implanted in a region of the brain that controls the hand. Gaunt then teamed up with his Pittsburgh colleague, bioengineer Jennifer Collinger, to integrate a robotic arm with the BCI, allowing the individual to feel and manipulate objects. © 2024 Springer Nature Limited

Keyword: Robotics; Pain & Touch
Link ID: 29557 - Posted: 11.13.2024

By Erin Garcia de Jesús The first detailed structure of an infectious prion that causes chronic wasting disease, or CWD, reveals features that could help guide vaccine development or explain why the illness hasn’t yet made the leap to people, researchers report October 24 in Acta Neuropathologica. One such feature is a 180-degree twist between two sections of the prion. In versions engineered to infect rodents in order to study the disease, that twist doesn’t exist. Like the prion illness Creutzfeldt-Jakob disease in people, CWD prions in deer, elk and moose transform a healthy brain protein called PrP into misshapen versions that clump together and cause symptoms such as listlessness, drastic weight loss and lack of fear. While no person has contracted the disease and studies in mice and primates suggest that the risk to humans is extremely low, CWD’s spread among animals that people eat has raised concerns that it one day could jump to people (SN: 6/10/24). Understanding how deer prions misfold could help reveal why CWD doesn’t easily spread to humans. But “prions are messy,” says Byron Caughey, a biochemist at the National Institutes of Health’s Rocky Mountain Laboratories in Hamilton, Mont. Because the proteins “are very sticky and they tend to cling together,” researchers have a tough time getting a clear picture of what diseased prions look like. Previous studies looking at other prions, including rodent-adapted versions originally from sheep, showed that the proteins stack together like plates. Using hundreds of thousands of electron microscopy images, Caughey and colleagues found that a natural prion from the brain tissue of a white-tailed deer stacks in a similar way, but with some potentially key differences. © Society for Science & the Public 2000–2024.

Keyword: Prions
Link ID: 29552 - Posted: 11.13.2024

By Simon Makin The word “bionic” conjures sci-fi visions of humans enhanced to superhuman levels. It’s true that engineering advances such as better motors and batteries, together with modern computing, mean that the required mechanical and electronic systems are no longer a barrier to advanced prostheses. But the field has struggled to integrate these powerful machines with the human body. That’s starting to change. A recent trial tested one new integration technique, which involves surgically reconstructing muscle pairs that give recipients a sense of the position and movement of a bionic limb. Signals from those muscles control robotic joints, so the prosthesis is fully under control of the user’s brain. The system enabled people with below-knee amputations to walk more naturally and better navigate slopes, stairs and obstacles, researchers reported in the July Nature Medicine. Engineers have typically viewed biology as a fixed limitation to be engineered around, says bioengineer Tyler Clites, who helped develop the technique several years ago while at MIT. “But if we look at the body as part of the system to be engineered, in parallel with the machine, the two will be able to interact better.” That view is driving a wave of techniques that reengineer the body to better integrate with the machine. Clites, now at UCLA, calls such techniques “anatomics,” to distinguish them from traditional bionics. “The issue we were tackling wasn’t an engineering problem,” he says. “The way the body had been manipulated during the amputation wasn’t leaving it in a position to be able to control the limbs we were creating.” In an anatomics approach, bones are exploited to provide stable anchors; nerves are rerouted to create control signals for robotic limbs or transmit sensory feedback; muscles are co-opted as biological amplifiers or grafted into place to provide more signal sources. © Society for Science & the Public 2000–2024.

Keyword: Robotics
Link ID: 29507 - Posted: 10.05.2024

By Pam Belluck When Shawn Connolly was diagnosed with Parkinson’s disease nine years ago, he was a 39-year-old daredevil on a skateboard, flipping and leaping from walls, benches and dumpsters through the streets of San Francisco. He appeared in videos and magazines, and had sponsorships from skateboard makers and shops. But gradually, he began to notice that “things weren’t really working right” with his body. He found that his right hand was cupping, and he began cradling his arm to hold it in place. His balance and alignment started to seem off. Over time, he developed a common Parkinson’s pattern, fluctuating between periods of rapid involuntary movements like “I’ve got ants in my pants” and periods of calcified slowness when, he said, “I could barely move.” A couple of years ago, Mr. Connolly volunteered for an experiment that summoned his daring and determination in a different way. He became a participant in a study exploring an innovative approach to deep brain stimulation. In the study, which was published Monday in the journal Nature Medicine, researchers transformed deep brain stimulation — an established treatment for Parkinson’s — into a personalized therapy that tailored the amount of electrical stimulation to each patient’s individual symptoms. The researchers found that for Mr. Connolly and the three other participants, the individualized approach, called adaptive deep brain stimulation, cut in half the time they experienced their most bothersome symptom. Mr. Connolly, now 48 and still skateboarding as much as his symptoms allow, said he noticed the difference “instantly.” He said the personalization gave him longer stretches of “feeling good and having that get-up-and-go.” © 2024 The New York Times Company

Keyword: Parkinsons
Link ID: 29447 - Posted: 08.21.2024

Julia Kollewe Oran Knowlson, a British teenager with a severe type of epilepsy called Lennox-Gastaut syndrome, became the first person in the world to trial a new brain implant last October, with phenomenal results – his daytime seizures were reduced by 80%. “It’s had a huge impact on his life and has prevented him from having the falls and injuring himself that he was having before,” says Martin Tisdall, a consultant paediatric neurosurgeon at Great Ormond Street Hospital (Gosh) in London, who implanted the device. “His mother was talking about how he’s had such a improvement in his quality of life, but also in his cognition: he’s more alert and more engaged.” Oran’s neurostimulator sits under the skull and sends constant electrical signals deep into his brain with the aim of blocking abnormal impulses that trigger seizures. The implant, called a Picostim and about the size of a mobile phone battery, is recharged via headphones and operates differently between day and night. The video player is currently playing an ad. You can skip the ad in 5 sec with a mouse or keyboard “The device has the ability to record from the brain, to measure brain activity, and that allows us to think about ways in which we could use that information to improve the efficacy of the stimulation that the kids are getting,” says Tisdall. “What we really want to do is to deliver this treatment on the NHS.” As part of a pilot, three more children with Lennox-Gastaut syndrome will be fitted with the implant in the coming weeks, followed by a full trial with 22 children early next year. If this goes well, the academic sponsors – Gosh and University College London – will apply for regulatory approval. Tim Denison – a professor of engineering science at Oxford University and co-founder and chief engineer of London-based Amber Therapeutics, which developed the implant with the university – hopes the device will be available on the NHS in four to five years’ time, and around the world. © 2024 Guardian News & Media Limite

Keyword: Robotics; Epilepsy
Link ID: 29442 - Posted: 08.19.2024

By Sara Talpos Nervous system disorders are among the leading causes of death and disability globally. Conditions such as paralysis and aphasia, which affects the ability to understand and produce language, can be devastating to patients and families. Significant investment has been put toward brain research, including the development of new technologies to treat some conditions, said Saskia Hendriks, a bioethicist at the U.S. National Institutes of Health. These technologies may very well improve lives, but they also raise a host of ethical issues. That’s in part because of the unique nature of the brain, said Hendriks. It’s “the seat of many functions that we think are really important to ourselves, like consciousness, thoughts, memories, emotions, perceptions, actions, perhaps identity.” Saskia Hendriks, a bioethicist at the U.S. National Institutes of Health, recently co-authored an essay on the emerging ethical questions in highly innovative brain research. In a June essay in The New England Journal of Medicine, Hendriks and a co-author, Christine Grady, outlined some of the thorny ethical questions related to brain research: What is the best way to protect the long-term interests of people who receive brain implants as part of a clinical trial? As technology gets better at decoding thoughts, how can researchers guard against violations of mental privacy? And what best way to prepare for the far-off possibility that consciousness may one day arise from work derived from human stem cells? Hendriks spoke about the essay in a Zoom interview. Our conversation has been edited for length and clarity.

Keyword: Robotics
Link ID: 29441 - Posted: 08.19.2024

Tijl Grootswagers Genevieve L Quek Manuel Varlet You are standing in the cereal aisle, weighing up whether to buy a healthy bran or a sugary chocolate-flavoured alternative. Your hand hovers momentarily before you make the final grab. But did you know that during those last few seconds, while you’re reaching out, your brain is still evaluating the pros and cons – influenced by everything from your last meal, the health star rating, the catchy jingle in the ad, and the colours of the letters on the box? Our recently published research shows our brains do not just think first and then act. Even while you are reaching for a product on a supermarket shelf, your brain is still evaluating whether you are making the right choice. Read news coverage based on evidence, not tweets Further, we found measuring hand movements offers an accurate window into the brain’s ongoing evaluation of the decision – you don’t have to hook people up to expensive brain scanners. What does this say about our decision-making? And what does it mean for consumers and the people marketing to them? There has been debate within neuroscience on whether a person’s movements to enact a decision can be modified once the brain’s “motor plan” has been made. Our research revealed not only that movements can be changed after a decision – “in flight” – but also the changes matched incoming information from a person’s senses. To study how our decisions unfold over time, we tracked people’s hand movements as they reached for different options shown in pictures – for example, in response to the question “is this picture a face or an object?” Put simply, reaching movements are shaped by ongoing thinking and decision-making. © 2010–2024, The Conversation US, Inc.

Keyword: Consciousness
Link ID: 29387 - Posted: 07.11.2024

By Miryam Naddaf Researchers have developed a four-dimensional model of spinal-cord injury in mice, which shows how nearly half a million cells in the spinal cord respond over time to injuries of varying severity. The model, known as a cell atlas, could help researchers to resolve outstanding questions and develop new treatments for people with spinal-cord injury (SCI). “If you know what every single cell on the spinal cord is doing in response to injury, you could use that knowledge to develop tailor-made and mechanism-based therapies,” says Mark Anderson, a neurobiologist at the Swiss Federal Institute of Technology in Geneva, Switzerland, who worked on the atlas. “Things don’t need to be a shot in the dark.” Anderson and his colleagues used machine-learning algorithms to build the atlas by mapping data from RNA sequencing and other cell-biology techniques. They described the work in a Nature paper published today1 and have made the entire atlas available through an online platform. The atlas is a valuable resource for testing hypotheses about SCI, says Binhai Zheng, who studies spinal-cord regeneration at the University of California, San Diego. “There are a lot of hidden treasures.” The researchers examined sections of the spinal cord, sampled from 52 injured and uninjured mice at 1, 4, 7, 14, 30 and 60 days after injury. Their analysis involved 18 experimental SCI conditions, including different types of injury and levels of severity. They used RNA-sequencing tools to explore how 482,825 cells responded to injury over time. © 2024 Springer Nature Limited

Keyword: Brain imaging; Brain Injury/Concussion
Link ID: 29368 - Posted: 06.26.2024

By Scott Sayare As a boy, Les Milne carried an air of triumph about him, and an air of sorrow. Les was a particularly promising and energetic young man, an all-Scottish swim champion, head boy at his academy in Dundee, a top student bound for medical school. But when he was young, his father died; his mother was institutionalized with a diagnosis of manic depression, and he and his younger brother were effectively left to fend for themselves. His high school girlfriend, Joy, was drawn to him as much by his sadness as his talents, by his yearning for her care. “We were very, very much in love,” Joy, now a flaxen-haired 72-year-old grandmother, told me recently. In a somewhat less conventional way, she also adored the way Les smelled, and this aroma of salt and musk, accented with a suggestion of leather from the carbolic soap he used at the pool, formed for her a lasting sense of who he was. “It was just him,” Joy said, a steadfast marker of his identity, no less distinctive than his face, his voice, his particular quality of mind. Listen to this article, read by Robert Petkoff Joy’s had always been an unusually sensitive nose, the inheritance, she believes, of her maternal line. Her grandmother was a “hyperosmic,” and she encouraged Joy, as a child, to make the most of her abilities, quizzing her on different varieties of rose, teaching her to distinguish the scent of the petals from the scent of the leaves from the scent of the pistils and stamens. Still, her grandmother did not think odor of any kind to be a polite topic of conversation, and however rich and enjoyable and dense with information the olfactory world might be, she urged her granddaughter to keep her experience of it to herself. Les only learned of Joy’s peculiar nose well after their relationship began, on a trip to the Scandinavian far north. Joy would not stop going on about the creamy odor of the tundra, or what she insisted was the aroma of the cold itself. Joy planned to go off to university in Paris or Rome. Faced with the prospect of tending to his mother alone, however, Les begged her to stay in Scotland. He trained as a doctor, she as a nurse; they married during his residency. He was soon the sort of capable young physician one might hope to meet, a practitioner of uncommon enthusiasm, and shortly after his 30th birthday, he was appointed consultant anesthesiologist at Macclesfield District General Hospital, outside Manchester, in England, the first in his graduating class to make consultant. © 2024 The New York Times Company

Keyword: Parkinsons; Chemical Senses (Smell & Taste)
Link ID: 29363 - Posted: 06.15.2024

By Lauren Leffer Noland Arbaugh has a computer chip embedded in his skull and an electrode array in his brain. But Arbaugh, the first user of the Neuralink brain-computer interface, or BCI, says he wouldn’t know the hardware was there if he didn’t remember going through with the surgery. “If I had lost my memory, and I woke up, and you told me there was something implanted in my brain, then I probably wouldn’t believe you,” says the 30-year-old Arizona resident, who has been paralyzed below the middle of his neck since a 2016 swimming accident. “I have no sensation of it—no way of telling it’s there unless someone goes and physically pushes on it.” The Neuralink chip may be physically unobtrusive, but Arbaugh says it’s had a big impact on his life, allowing him to “reconnect with the world.” He underwent robotic surgery in January to receive the N1 Implant, also called “the Link,” in Neuralink’s first approved human trial. BCIs have existed for decades. But because billionaire technologist Elon Musk owns Neuralink, the company has received outsize attention. It’s brought renewed public interest to a technology that could significantly improve the life of those living with quadriplegia, such as Arbaugh, as well as people with other disabilities or neurodegenerative diseases. BCIs record electrical activity in the brain and translate those data into output actions, such as opening and closing a robotic hand or clicking a computer mouse. They vary in their design, level of invasiveness and the resolution of the information they capture. Some detect neurons’ electrical activity with entirely external electroencephalogram (EEG) arrays placed over a subject’s head. Others use electrodes placed on the brain’s surface to track neural activity. Then there are intracortical devices, which use electrodes implanted directly into brain tissue, to get as close as possible to the targeted neurons. Neuralink’s implant falls into this category. © 2024 SCIENTIFIC AMERICAN,

Keyword: Robotics; Movement Disorders
Link ID: 29362 - Posted: 06.15.2024

By Erin Garcia de Jesús Chronic wasting disease has been spreading among deer in the United States, which has raised concerns that the fatal neurological illness might make the leap to people. But a recent study suggests that the disease has a tough path to take to get into humans. The culprit behind chronic wasting disease, or CWD, isn’t a virus or bacterium but a misfolded brain protein called a prion. A new study using miniature, lab-grown organs called organoids supports previous work, showing that CWD prions don’t infect human brain tissue. Brain organoids exposed to high doses of prions from white-tailed deer, mule deer and elk remained infection-free for the duration of the study, or 180 days, researchers report in the June 2024 Emerging Infectious Diseases. However, organoids exposed to human prions that cause a related condition, Creutzfeldt-Jakob disease, quickly became infected. The finding suggests that a substantial species barrier prevents CWD from making the jump from deer to humans. “This was a model that could really help tell us … whether or not it was a real risk,” says Bradley Groveman, a biologist at the National Institutes of Health’s Rocky Mountain Laboratories in Hamilton, Mont. But brain organoids aren’t a perfect mimic of the real thing and may lack features that would make them susceptible to infection. And new prion strains can appear, perhaps including some that might help deer prions lock onto healthy brain proteins in humans. © Society for Science & the Public 2000–2024.

Keyword: Prions
Link ID: 29355 - Posted: 06.11.2024

Leyland Cecco in Toronto A leading federal scientist in Canada has alleged he was barred from investigating a mystery brain illness in the province of New Brunswick and said he fears more than 200 people affected by the condition are experiencing unexplained neurological decline. The allegations, made in leaked emails to a colleague seen by the Guardian, have emerged two years after the eastern province closed its investigation into a possible “cluster” of cases. “All I will say is that my scientific opinion is that there is something real going on in [New Brunswick] that absolutely cannot be explained by the bias or personal agenda of an individual neurologist,” wrote Michael Coulthart, a prominent microbiologist. “A few cases might be best explained by the latter, but there are just too many (now over 200).” New Brunswick health officials warned in 2021 that more than 40 residents were suffering from a possible unknown neurological syndrome, with symptoms similar to those of the degenerative brain disorder Creutzfeldt-Jakob disease. Those symptoms were varied and dramatic: some patients started drooling and others felt as though bugs were crawling on their skin. A year later, however, an independent oversight committee created by the province determined that the group of patients had most likely been misdiagnosed and were suffering from known illnesses such as cancer and dementia. The committee and the New Brunswick government also cast doubt on the work of neurologist Alier Marrero, who was initially referred dozens of cases by baffled doctors in the region, and subsequently identified more cases. The doctor has since become a fierce advocate for patients he feels have been neglected by the province. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Depression
Link ID: 29342 - Posted: 06.04.2024

By Matthew Hutson ChatGPT and other AI tools are upending our digital lives, but our AI interactions are about to get physical. Humanoid robots trained with a particular type of AI to sense and react to their world could lend a hand in factories, space stations, nursing homes and beyond. Two recent papers in Science Robotics highlight how that type of AI — called reinforcement learning — could make such robots a reality. “We’ve seen really wonderful progress in AI in the digital world with tools like GPT,” says Ilija Radosavovic, a computer scientist at the University of California, Berkeley. “But I think that AI in the physical world has the potential to be even more transformational.” The state-of-the-art software that controls the movements of bipedal bots often uses what’s called model-based predictive control. It’s led to very sophisticated systems, such as the parkour-performing Atlas robot from Boston Dynamics. But these robot brains require a fair amount of human expertise to program, and they don’t adapt well to unfamiliar situations. Reinforcement learning, or RL, in which AI learns through trial and error to perform sequences of actions, may prove a better approach. “We wanted to see how far we can push reinforcement learning in real robots,” says Tuomas Haarnoja, a computer scientist at Google DeepMind and coauthor of one of the Science Robotics papers. Haarnoja and colleagues chose to develop software for a 20-inch-tall toy robot called OP3, made by the company Robotis. The team not only wanted to teach OP3 to walk but also to play one-on-one soccer. “Soccer is a nice environment to study general reinforcement learning,” says Guy Lever of Google DeepMind, a coauthor of the paper. It requires planning, agility, exploration, cooperation and competition. © Society for Science & the Public 2000–2024.

Keyword: Robotics
Link ID: 29328 - Posted: 05.29.2024

By Christina Jewett Just four months ago, Noland Arbaugh had a circle of bone removed from his skull and hair-thin sensor tentacles slipped into his brain. A computer about the size of a small stack of quarters was placed on top and the hole was sealed. Paralyzed below the neck, Mr. Arbaugh is the first patient to take part in the clinical trial of humans testing Elon Musk’s Neuralink device, and his early progress was greeted with excitement. Working with engineers, Mr. Arbaugh, 30, trained computer programs to translate the firing of neurons in his brain into the act of moving a cursor up, down and around. His command of the cursor was soon so agile that he could challenge his stepfather at Mario Kart and play an empire-building video game late into the night. But as weeks passed, about 85 percent of the device’s tendrils slipped out of his brain. Neuralink’s staff had to retool the system to allow him to regain command of the cursor. Though he needed to learn a new method to click on something, he can still skate the cursor across the screen. Neuralink advised him against a surgery to replace the threads, he said, adding that the situation had stabilized. The setback became public earlier this month. And although the diminished activity was initially difficult and disappointing, Mr. Arbaugh said it had been worth it for Neuralink to move forward in a tech-medical field aimed at helping people regain their speech, sight or movement. “I just want to bring everyone along this journey with me,” he said. “I want to show everyone how amazing this is. And it’s just been so rewarding. So I’m really excited to keep going.” From a small desert town in Arizona, Mr. Arbaugh has emerged as an enthusiastic spokesman for Neuralink, one of at least five companies leveraging decades of academic research to engineer a device that can help restore function in people with disabilities or degenerative diseases. © 2024 The New York Times Company

Keyword: Robotics
Link ID: 29320 - Posted: 05.23.2024

By Meghan Willcoxon In the summer of 1991, the neuroscientist Vittorio Gallese was studying how movement is represented in the brain when he noticed something odd. He and his research adviser, Giacomo Rizzolatti, at the University of Parma were tracking which neurons became active when monkeys interacted with certain objects. As the scientists had observed before, the same neurons fired when the monkeys either noticed the objects or picked them up. But then the neurons did something the researchers didn’t expect. Before the formal start of the experiment, Gallese grasped the objects to show them to a monkey. At that moment, the activity spiked in the same neurons that had fired when the monkey grasped the objects. It was the first time anyone had observed neurons encode information for both an action and another individual performing that action. Those neurons reminded the researchers of a mirror: Actions the monkeys observed were reflected in their brains through these peculiar motor cells. In 1992, Gallese and Rizzolatti first described the cells in the journal Experimental Brain Research and then in 1996 named them “mirror neurons” in Brain. The researchers knew they had found something interesting, but nothing could have prepared them for how the rest of the world would respond. Within 10 years of the discovery, the idea of a mirror neuron had become the rare neuroscience concept to capture the public imagination. From 2002 to 2009, scientists across disciplines joined science popularizers in sensationalizing these cells, attributing more properties to them to explain such complex human behaviors as empathy, altruism, learning, imitation, autism, and speech. Then, nearly as quickly as mirror neurons caught on, scientific doubts about their explanatory power crept in. Within a few years, these celebrity cells were filed away in the drawer of over-promised, under-delivered discoveries. © 2024 NautilusNext Inc.,

Keyword: Attention; Vision
Link ID: 29316 - Posted: 05.21.2024

Ian Sample Science editor A device that stimulates the spinal nerves with electrical pulses appears to boost how well people recover from major spinal cord injuries, doctors say. An international trial found that patients who had lost some or all use of their hands and arms after a spinal cord injury regained strength, control and sensation when the stimulation was applied during standard rehabilitation exercises. The improvements were small but were described by doctors and patients as life-changing because of the impact they had on the patients’ daily routines and quality of life. “It actually makes it easier for people to move, including people who have complete loss of movement in their hands and arms,” said Prof Chet Moritz, in the department of rehabilitation medicine at the University of Washington in Seattle. “The benefits accumulate gradually over time as we pair this spinal stimulation with intensive therapy of the hands and arms, such that there are benefits even when the stimulator is turned off.” Rather than being implanted, the Arc-Ex device is worn externally and uses electrodes that are placed on the skin near the section of the spinal cord responsible for controlling a particular movement or function. The researchers believe that electrical stimulation helps nerves that remain intact after the injury to send signals and ultimately partially restore some communication between the brain and paralysed body part. More than half of patients who suffer spinal cord injuries still have some intact nerves that cross the injury site. © 2024 Guardian News & Media Limited

Keyword: Robotics; Movement Disorders
Link ID: 29315 - Posted: 05.21.2024