Chapter 11. Motor Control and Plasticity
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By Pam Belluck In a step forward for the cutting-edge field of brain-computer interfaces, a patient with a paralyzing neurological disorder used a brain implant to converse in real time, even when she was simply thinking about what to say, a company said it would announce on Monday. The development, by the company Paradromics, marks the latest advance for these experimental devices, known as B.C.I.s — systems that involve implanting electrodes in the brain that read neurological signals and decode those signals through artificial intelligence. The 68-year-old Michigan woman, who has lost most of her speaking ability, was able to use the device to have spontaneous conversations via a computer-generated voice, including on the phone with her grandchildren. When she physically tried to speak, her brain generated signals that were read by the electrodes, transmitted through A.I. and displayed on the computer screen, which spoke the words aloud. The system could also produce speech when the woman imagined what to say without moving her speaking muscles. Because the Paradromics system is wireless and doesn’t require the patient to be connected by a cord to a computer, experts said, it offers a demonstration of how patients who have lost the ability to speak might be able to eventually use the technology in their daily lives, greatly improving their ability to communicate with family, friends and co-workers. The woman, the first patient in the Paradromics clinical trial, was implanted with the company’s Connexus B.C.I. system, which contains more than 400 electrodes, in June at University of Michigan Health. © 2026 The New York Times Company
Keyword: Robotics; Language
Link ID: 30414 - Posted: 09.16.2026
By Jennie Erin Smith The revolutionary brain-computer interfaces (BCIs) that help people with severe paralysis speak, type, move prosthetic limbs, and more are typically specialists, using sensors to pick up activity from select brain areas to perform a single function. Now, scientists have shown just one neural implant—in this case, a grid of minielectrodes surgically placed on the top part of the cortex—can do double duty, successfully “decoding” brain signals from paralyzed people as they attempt to speak as well as gesture with their upper bodies. The technology, described today in Nature Neuroscience, can create a computer-animated image of the user in real time, which can do things such as say hello while waving, or nod while saying yes. “The authors have taken an important step toward developing highly naturalistic systems to restore function for people with paralysis,” says neurologist Daniel Rubin of Massachusetts General Hospital, whose team developed a BCI that allows users to communicate by text as quickly as able-bodied people. The complexity of severe paralysis necessitates BCIs that can multitask, says neurosurgeon Edward Chang of the University of California (UC) San Francisco, who led the new study. People with amyotrophic lateral sclerosis (ALS) or brainstem stroke “have lost many functions,” he notes. “It’s rarely so simple that they just can’t talk or they just have a need to control a computer cursor.” Some existing BCIs can interpret different types of signals using implants for separate functions. A group of scientists at UC Davis, for example, recently published on the successful long-term use of a BCI system relying on that strategy to help a man with ALS both speak and manipulate a cursor. © 2026 American Association for the Advancement of Science.
Keyword: Robotics; Language
Link ID: 30413 - Posted: 09.16.2026
By Claudia Metzler-Baddeley About 8,000 people in the U.K. are living with Huntington’s disease, a devastating inherited condition that gradually affects movement, thinking and mood. Now, an advanced type of MRI scan could give researchers a way to estimate the cellular damage it causes in living people, which could eventually help show whether treatments are working. New research from my colleagues and I found that the technique can detect abnormalities in the brains of people living with Huntington’s that match those previously identified by examining brain tissue after death. Huntington’s disease is an inherited condition caused by a faulty gene. Its effects usually begin between the ages of 30 and 50. There is currently no cure, although new cell and gene therapies are being developed and tested. One of the main things that happens in Huntington’s is the loss of neuronal cells in the striatum, a part of the basal ganglia deep within the brain. These structures are important for controlling movement and other functions. As cells are lost, the brain tissue in these regions shrinks. We can see this shrinkage using conventional MRI. But a standard brain scan tells us relatively little about what is happening inside the tissue at a cellular level. That’s where our approach comes in. We used a technique called “soma and neurite density imaging”, or Sandi, to analyze diffusion MRI scans. Diffusion MRI detects how water moves through brain tissue. Because that movement is affected by the structures around the water, we can use it to make indirect estimates of properties such as the apparent size and density of cell bodies. This means we can get indirect estimates of the structures within the tissue itself. © 2026 SCIENTIFIC AMERICAN INC.
Keyword: Huntingtons; Brain imaging
Link ID: 30396 - Posted: 09.05.2026
Ushika Kidd Long-term exposure to road traffic noise is associated with a higher risk of Parkinson’s disease, the biggest study of its kind has found. Parkinson’s disease is a progressive disorder in which parts of the brain become damaged over time, affecting movement and balance. Existing research has found potential biological pathways that link noise exposure to Parkinson’s disease, largely due to stress responses and disrupted sleep. The researchers modelled noise exposure at the most and least exposed exterior of the residence of each participant and calculated the difference in noise levels. The magnitude of the effect was modest but consistent; at the most exposed facade, for every 11.5dB rise in noise level, the risk of Parkinson’s disease rose by 3% over the study period. Having a quiet part of the home may mitigate the association between exposure to road traffic noise and higher risk of Parkinson’s disease, according to the findings. The study, published in Jama Neurology, included 3.1 million Danish participants aged 40 and over, and followed them for 18 years. It was established using nationwide health register data, making it the largest study on road traffic noise and Parkinson’s disease. Previous research linked the rise in neurological disorders, including Parkinson’s disease, with exposure to environmental toxins. Environmental risk factors such as air pollution, microplastics and pesticides have become the main focus of prevention strategies. © 2026 Guardian News & Media Limited
Keyword: Parkinsons; Hearing
Link ID: 30339 - Posted: 07.25.2026
By Elie Dolgin Jeff Carroll was in his mid-twenties, fresh out of the U.S. Army, when a genetic test confirmed his worst fear: He was going to develop Huntington’s disease. He had watched his mother’s illness for years; the tremors first, small enough to explain away, then the involuntary movements that looked almost like dancing. The test revealed that the same mutation that caused her disease lived in him: a stretch of three DNA letters in a gene called HTT, repeated over and over again dozens of times. Carroll himself was not sick yet. He would not get sick for many years. But the countdown had begun. In fact, it had likely been running all his life, deep inside vulnerable neurons in his brain. There, the mutant HTT gene was slowly growing longer, its internal repeats piling up toward a threshold that, once crossed, would tip the cell into disarray. The first outward signs of Huntington’s often begin with mood changes and subtle cognitive effects. The hallmark jerky movements come later. Eventually, and relentlessly, patients lose the ability to speak, swallow or move. Most people die within a decade or two of symptom onset. Huntington’s disease is rare, affecting roughly 1 in 20,000 people worldwide. Yet because each child of an affected parent has a 50 percent chance of inheriting the mutation, the disease can haunt families for generations. It had already claimed Carroll’s grandmother and would take his mother at age 54. Without a therapy capable of altering its course, Carroll — along with three of his five siblings who also inherited the mutation — seemed fated to follow his ancestors into an early grave. Carroll decided the only rational response was to become one of the scientists seeking ways to beat the disease. He was midway through his undergraduate studies when he learned, in 2003, that he carried the mutation. He pressed on, earning a Ph.D. and completing postdoctoral training before establishing his own research group devoted to understanding and slowing the disease stalking him from within. © Society for Science & the Public 2000–2026.
Keyword: Huntingtons
Link ID: 30332 - Posted: 07.18.2026
Ian Sample Science editor A man who was paralysed from the chest down in a swimming accident six years ago has been able to feed himself and drink from a cup thanks to a brain implant that bypasses his spinal cord injury. Keith Thomas of Massapequa, New York, could not lift his arms off his wheelchair when he agreed to trial the technology in 2021, but after surgery to implant electrodes in his brain and many months of training, he was able to move the limbs again. Researchers fitted Thomas with a brain-computer interface that not only helped him move his arms and hands, but also sent signals back to his brain to recreate the sensation of touch. He has since been able to feel his sister’s hand and the fur on his pet dog. Remarkably, the technology appears to have partly rewired Thomas’s nervous system, helping to restore some hand functions and sensations that remain even when the system is switched off. “For me this is an incredible moment,” said Prof Chad Bouton, whose team developed the technology at the Feinstein Institutes for Medical Research, the research arm of the New York healthcare provider Northwell Health. “For years, we have been wanting to really tackle the restoration of movement and the sense of touch and bring those together and we’ve also wanted to create lasting effects,” Bouton added. “I think we’re going to continue to see progress and I think it’ll be applicable to the millions of folks around the world who really need this technology.” Thomas was 42 when he broke his neck diving into a swimming pool in July 2020. He blacked out and regained consciousness to see a helicopter on the front lawn. He was immediately taken to hospital. “The next day I couldn’t even move,” he said. The following October, he joined a three-year clinical trial of what the researchers called a “double neural bypass”. It uses electrodes implanted into Thomas’s brain to detect when he wants to move his arms. The signals are then routed to his arms and hands to move them. © 2026 Guardian News & Media Limited
Keyword: Robotics
Link ID: 30331 - Posted: 07.18.2026
By Jackie Rocheleau The cerebellum, the wizened “little brain” nestled in the base of the skull, may help keep us sharp as we age. Regions at the back of the cerebellum that resisted shrinkage with age were tied to better mental functioning, or cognition, even in people in the early stages of Alzheimer’s disease, researchers report June 10 in Nature Neuroscience. Though traditionally thought of as a movement control center, scientists now know the cerebellum is a key player in cognition. Researchers also know that parts of the cerebellum don’t age in unison, but the aging cerebellum is a relatively new area of research. In the new study, the team first analyzed brain scans and cognitive test scores from more than 700 U.S. adults whose data was collected as part of the Human Connectome Project, a brain mapping initiative. The test measured abilities including short-term memory, attention, language and visualizing 3-D objects. A clear trend emerged: The cerebellum tended to be smaller with increasing age, but the bigger the cerebellum, particularly in regions in the rear of the little brain, the higher the score on cognitive tests. The trend held even after adjusting for the different levels of education among participants, Princeton University neuroscientist Frederick d’Oleire Uquillas and colleagues report. The researchers found the same link in more than 35,000 adults in the U.K. Biobank, a biomedical database. The findings point to a larger cerebellum preserving cognition with greater age, says d’Oleire Uquillas. The researchers confirmed that scans of the larger cerebellums showed more brain tissue and connections between nerve cells, a © Society for Science & the Public 2000–2026.
Keyword: Alzheimers
Link ID: 30295 - Posted: 06.24.2026
Miryam Naddaf A brain implant is helping a man with paralysis to communicate with his family and friends and to use his personal computer at home. The brain–computer interface (BCI) has given 48-year-old study participant Casey Harrell, who was diagnosed with a type of motor neuron disease called amyotrophic lateral sclerosis six years ago, the ability to communicate with an average speed of 56 words per minute. It translates neural activity into text that appears on a computer screen and allows him to operate a computer, send text messages and e-mails and continue his job working in climate advocacy. It is “nothing short of revolutionary”, says Harrell, who is based in Oakland, California. “This has allowed me to keep working and earn money and insurance for my family. This is reconnecting me with friends and family who are too shy or too afraid to come over and not be able to understand me.” The study, published in Nature Medicine on 15 June1, analysed Harrell’s home use of the BCI for nearly two years and is “the most extensive data set and the longest-running speech communication of anyone” with such an implant, says co-author Sergey Stavisky, a neuroscientist at the University of California, Davis. Previous studies of participants testing BCIs at home showed that the devices had limited efficiency, and more-advanced devices have been tested only in the laboratory. “This is actually helping the patient in day-to-day life,” says Christian Herff, a computational neuroscientist at Maastricht University in the Netherlands. BCIs are “really becoming a medical device instead of a research tool”, he adds. Remarkable quality In 2023, Harrell had 256 microelectrodes implanted in his brain’s speech motor cortex. The electrodes were connected to electronic recording devices through titanium pedestals attached to his skull. He began to use the BCI device to decode his speech in the lab with the help of Stavisky and his colleagues. The researchers then trained Harrell and his care partners to operate the BCI system at home. After roughly 40 weeks, he began using the device independently; he is still using it today. The device also has a text-to-speech system that can read completed sentences aloud using a synthesized version of Harrell’s voice from before he was diagnosed. © 2026 Springer Nature Limited
Keyword: Robotics; Language
Link ID: 30284 - Posted: 06.17.2026
By Gina Kolata On my second visit with Nancy Wexler at her Manhattan apartment, she had a gift for me. It was a copy of her newly published memoir, “My Life, My Science: Pursuing a Cure for Huntington’s Disease.” It had been signed with a stamp of her signature — she isn’t able to sign it herself. Nor could she rise from her brown faux-leather recliner to greet me — she can’t get up unassisted. Speaking requires effort. She can manage at most a few badly slurred words or phrases or, with great difficulty, a short sentence. On that bright windy afternoon, Nancy and her sister, Alice Wexler, sat side by side in recliners, their backs to windows that offered a stunning view of the Hudson River far below. Alice lives in California, but she visits Nancy every other month. At age 80, Nancy Wexler has Huntington’s disease, a dreaded brain disease that destroys a person’s ability to control movements. There is no treatment. There is no cure. The disease is inherited: Nancy’s grandfather, three uncles and mother had it. Alice, however, does not: If a parent has Huntington’s, each child has a 50 percent chance of getting it. Their mother attempted suicide, a path that others with the disease have chosen, but ultimately died from Huntington’s. Nancy is not just any Huntington’s disease patient. For decades, she led a research effort in a remote area of Venezuela that found the gene responsible for Huntington’s. That work yielded a blood test that enable at-risk people to find out if they are destined to get the disease. In honor of this work, Nancy has garnered numerous accolades and prizes, including a Lasker award, among the most prestigious in science. She devoted her life to understanding what it’s like to be at risk for Huntington’s disease, what it’s like to have it. © 2026 The New York Times Company
Keyword: Huntingtons
Link ID: 30276 - Posted: 06.13.2026
Jon Hamilton Scientists who've spent decades learning how the brain works say they're now ready to start fixing it when it breaks. That's the premise of the Brain Health accelerator, a collaborative effort launched by the Allen Institute in Seattle, which has become a major player in brain research. The initiative includes plans to develop new genetic therapies — a term that includes gene editing as well as traditional gene therapy — for diseases including Alzheimer's, Parkinson's, ALS, and Huntington's. "The latest genetic treatments allow scientists to control the activity of particular genes," says Ed Lein, who directs the institute's brain health programs. "That opens up the possibility for very specific precision therapies for brain disorders." The accelerator is an outgrowth of the BRAIN Initiative, an ambitious research program unveiled by President Obama in 2013. The goal of this public-private partnership was to create tools that would allow scientists to see the brain's inner workings, and, eventually, to develop treatments. But the effort has progressed far faster than many scientists expected. "I am shocked at how far we've come in the last 10, 12 years," says John Ngai, a senior investigator at the National Institutes of Health who directs the BRAIN Initiative. "It's just been beyond my wildest imagination — and I've been accused of having a pretty good imagination." © 2026 npr
Keyword: Parkinsons; Alzheimers
Link ID: 30267 - Posted: 06.03.2026
By Laura Sanders This is a two-part series on Parkinson’s, detailing the daily struggles with the disease, new treatment programs and how patients’ lives have been impacted by emerging therapies. You can read the first part here. The night before he had brain surgery to treat his Parkinson’s disease symptoms, Robert Goings couldn’t sleep. “He was pacing all night,” says his wife, Diana. That’s because it hurt to stop moving. Normally, Goings’ restless movements, stiffness and muscle cramps were eased by medicine. But doctors wanted his symptoms unmasked for the procedure, which meant he was feeling them full blast. “My legs would cramp up, my arms, you know, everything would cramp up without the medication,” Goings says. The next morning, last November 5, Goings, who at age 68 had been living with increasingly disruptive symptoms for years, slid into an MRI machine at Oregon Health and Science University, or OHSU, in Portland. While Goings was inside the MRI tube, doctors aimed 1,024 ultrasound beams at several spots deep in his brain, burning the problematic tissue there. Afterward, Goings was wheeled to a recovery room. “He held out his hand — dead still,” Diana says. She remembers thinking, “Oh my God, I don’t believe this. It’s gone. Absolutely gone.” In opting for this treatment, called high-intensity focused ultrasound, Goings has joined a small but growing number of people choosing to control their Parkinson’s symptoms with permanent lesions in their brain. Already, an estimated 50 to 60 people have undergone the surgery at OHSU, where the treatment calendar is booked up months in advance. © Society for Science & the Public 2000–2026.
Keyword: Parkinsons
Link ID: 30258 - Posted: 05.27.2026
By Meghan Rosen Neurologist David Standaert can often tell if someone has Parkinson’s disease in a matter of minutes. Maybe their hand trembles and one of their arms doesn’t swing as much as the other when they walk. Maybe their voice sounds softer than usual, and they have a stillness to their body and a masklike look on their face, with little expressivity or blinking. “I always tell patients, ‘It’s not any one thing that tells me you have Parkinson’s. It’s all of these things together,’ ” he says. But Standaert’s is a rare skill. A movement disorder specialist at the University of Alabama at Birmingham, he has been diagnosing people with the disease for decades. He’s one of fewer than 1,000 doctors in the United States trained to spot and treat the sometimes-subtle signs of Parkinson’s. That’s a problem because more than 1 million people in the country have the disease, and the number is climbing as the population ages. “There are nowhere near enough movement disorder specialists to go diagnosing all these people,” Standaert says. A lack of specialists is just one of the problems that plagues Parkinson’s diagnosis, which has proved difficult in part because the disease is so complicated. Over time, and for reasons scientists don’t fully understand, particular nerve cells deep in the brain become damaged and die. For patients, this can manifest as tremors and a constellation of other symptoms that start mild and progressively worsen. Eventually, as muscles stiffen and swallowing becomes difficult, people may become bedridden, in need of round-the-clock care. But Parkinson’s disease varies tremendously, Standaert says. Which symptoms arise, how severe they are and how quickly they progress differ from person to person. “I have seen tens of thousands of patients with Parkinson’s disease, and no two are the same,” he says. © Society for Science & the Public 2000–2026.
Keyword: Parkinsons
Link ID: 30253 - Posted: 05.23.2026
By Pam Belluck Time was running out for Amanda Sifford, she and her doctors could tell. A.L.S., the paralyzing neurological disorder, was stealing her ability to breathe. On a breathing test, her lung function was only at 48 percent of capacity, a sharp drop from 86 percent five months earlier. “I couldn’t take 10 steps and be able to breathe,” she said. “I could no longer step up on a curb.” Ms. Sifford, 58, a school psychologist in Cape Coral, Fla., has lost 14 family members, including her father and grandfather, to a rare genetic form of A.L.S., also known as amyotrophic lateral sclerosis or Lou Gehrig’s disease. Her symptoms had been developing gradually, but her breathing suddenly nose-dived. “It was very scary,” said Dr. Nathan Carberry, one of her neurologists at the University of Miami Health System. “I worried that we were looking at months of life left.” “Was I thinking about dying?” said Ms. Sifford, pausing to collect herself. “I had my affairs in order.” It was May 2023, and the Food and Drug Administration had just approved the first therapy for a genetic form of A.L.S., even though clinical trial results had not yet proven the drug would be effective. The drug, tofersen, made by Biogen and marketed as Qalsody, targets the form of A.L.S. that Ms. Sifford inherited, so Dr. Carberry and Dr. Michael Benatar, the executive director of University of Miami A.L.S. Center, scrambled to establish a clinic to administer it. She began receiving tofersen monthly, through infusions into her spinal canal. © 2026 The New York Times Company
Keyword: ALS-Lou Gehrig's Disease
Link ID: 30245 - Posted: 05.16.2026
Liam Drew Three hearts; blue blood; no skeleton; arms like tongues. These are just some of the alien features of octopuses, squid and cuttlefish — members of the cephalopod family. The outlandish list continues. Cephalopod skin can taste chemicals, sense light and change colour and texture rapidly. In many species, the sucker-covered arms can even regenerate. These invertebrates have evolved independently from the vertebrate lineage for more than 600 million years. Their last common ancestor was probably a worm-like creature with a rudimentary nervous system and eye-like patches of light-sensitive cells. Despite this evolutionary gulf, vertebrates and these highly specialized molluscs share strange similarities. Their eyes, for example. “It’s eerie how similar they ended up,” says Cristopher Niell, a neuroscientist at the University of Oregon in Eugene. “The convergent evolution of the eye still blows my mind.” Now, one similarity is spurring a boom in cephalopod neuroscience. Around 400 million years ago, cuttlefish, squid and octopuses diverged from the only other living cephalopods — the nautiluses. They then lost their protective shells and evolved brains that are uniquely large among invertebrates. These brains bestow the soft-bodied cephalopods with high intelligence. Cuttlefish, squid and octopuses have excellent memories, use tools and are adept problem-solvers; they have a concept of time and are capable of delayed gratification. Cephalopods are the only non-vertebrate animals that have big, smart brains, says Cliff Ragsdale, a comparative neuroscientist at the University of Chicago in Illinois. And that presents a unique opportunity. Neuroscientists have gained a wealth of knowledge about how vertebrate brains work, but are increasingly looking to cephalopods for insights into ways to build large, high-functioning nervous systems. © 2026 Springer Nature Limited
Keyword: Evolution; Intelligence
Link ID: 30231 - Posted: 05.02.2026
Ian Sample Science editor Changes to microbes that live in the gut can identify people at greater risk of Parkinson’s disease long before symptoms develop, according to work that also raises hopes for new therapies. Researchers discovered signature changes in the gut microbiome that are more pronounced in people with a genetic risk for Parkinson’s and even more stark in those diagnosed with the disease. The signature could help doctors spot patients at risk of Parkinson’s years before they display clear symptoms and suggests that healthier diets and treatments that reshape the microbiome might prevent or delay the disease. Prof Anthony Schapira, the head of clinical and movement neurosciences at University College London and lead investigator on the study, said it was the first time a microbial signature in Parkinson’s patients had been seen in people with a genetic susceptibility but had yet to develop symptoms. The signature appears to become stronger as the disease progresses. “These same changes can be found in a small proportion of the general population that may put them at increased risk,” Schapira said. Cases of Parkinson’s have doubled in the past 25 years, with more than 8.5 million people globally now living with the condition. The disease causes progressive brain damage, leading to tremors, slow movement and stiff and inflexible muscles. Patients often experience depression, anxiety, sleep and memory problems, and difficulty with balance. © 2026 Guardian News & Media Limited
Keyword: Parkinsons
Link ID: 30209 - Posted: 04.22.2026
By Siddhant Pusdekar Deer mice, common across North America, come in two varieties: One lives in prairies, whereas the other inhabits forests. The life of the forest mouse requires greater dexterity—a skill it possesses thanks to its higher number of corticospinal tract axons, according to a January preprint. The existence of “genetically tractable subspecies of deer mice with different behavioral niches” made the discovery possible, says Eiman Azim, associate professor of molecular neurobiology at the Salk Institute for Biological Studies, who wasn’t involved in the study. It enabled the researchers to link genetically driven changes in corticospinal abundance and morphology to dexterity. The new work reveals one way dexterous skill may emerge, while also suggesting neuroscience should investigate “behaviors that evolved for the natural niches” to discover fresh insights, says Ariel Levine, a senior investigator at the U.S. National Institute of Neurological Disorders and Stroke, who wasn’t involved in the study. Dexterity in primates coevolved with direct connections between layer 5 cortical neurons and motor neurons in the spinal cord, Levine says. In rodents, cats and less dexterous monkeys, however, corticospinal neurons connect to motor neurons via interneurons. Direct cortical-motor neuron connections exist in juvenile mice, but they are pruned during development, a 2017 paper showed. Artificially stopping the pruning process created adult lab mice with greater skill at gathering food pellets.
Keyword: Evolution; Development of the Brain
Link ID: 30196 - Posted: 04.11.2026
Lynne Peeples In 2021, dermatologist David Ozog was on holiday with his family in the Bahamas, when his 18-year-old son had a massive stroke. The teenager was airlifted to Florida, and then to Chicago for surgery. As his son was lying partially paralysed in a hospital bed, Ozog got a call from a colleague who had an unconventional suggestion. The colleague, a dermatologist at Harvard Medical School in Boston, Massachusetts, told Ozog about research he was conducting with the US Department of Defense. Early results hinted that red and near-infrared light applied to the head might protect neural tissue after brain injury. He urged Ozog to consider trying it on his son. Ozog stayed up until 4 a.m. that night reading scientific papers and, ultimately, ordering several panels made of red and near-infrared light-emitting diodes (LEDs). “I started sneaking them into the hospital,” says Ozog, who works at Henry Ford Health in Grand Rapids, Michigan. Today, his son is walking and back in university. Ozog cannot prove that light therapy made a difference, but he thinks that it helped. He has since become a convert to an idea that, at the time, was considered fringe. “I thought the same thing,” he says, “How could shining this thing on you possibly have any biologic effect?” But what was at the margins of medicine just a few years ago is now edging towards the mainstream. Red-light devices are increasingly appearing in dermatology offices, wellness centres, locker rooms and homes. According to some projections, the global market will surpass US$1 billion by 2030, propelled by a surge of companies promising benefits for everything from ageing skin to attention deficit hyperactivity disorder (ADHD) — claims echoed widely across social media. Experts warn that there is considerable hype about red-light therapy. But a growing body of legitimate science has been exploring the benefits for several conditions. Clinical studies have reported improvements in peripheral neuropathy1, retinal degeneration2 and certain neurological disorders3. For some indications, expert groups now recommend red-light regimens1. Researchers are also uncovering how red and near-infrared light might exert these effects. Mitochondria — the power plants of the cell — are emerging as a central piece of the puzzle. © 2026 Springer Nature Limited
Keyword: Stroke; Parkinsons
Link ID: 30182 - Posted: 03.28.2026
by Pam Belluck Tango is the national dance of Argentina, known for its passion, precision and heart. In a hospital in Buenos Aires, it has another purpose: as a therapy for patients with Parkinson’s disease. Once a week, about a dozen patients come to Ramos Mejía Hospital to dance — a session that uses the movements of tango to help address issues of balance, stiffness and coordination. The goal is to give them approaches to movement that they can use in their daily lives, as well as a social and emotional boost from moving to music. The program began about 15 years ago, inspired by a patient who had danced tango since childhood and found it offered strategies that improved her mobility and gait problems, said Dr. Nélida Garretto, a neurologist who helped spearhead the sessions. Dr. Tomoko Arakaki, another neurologist leading the program, said Parkinson’s patients can struggle with the stop-and-start motions of walking and can benefit from practicing the “slow, short steps” and pauses of tango. Dr. Garretto said that because tango involves “multitasking with motor stimuli, visual stimuli and auditory stimuli,” it can help patients execute the series of small movements in everyday activities. First, warm-up exercises, usually in a circle, “try to tune everyone in, to prepare the body, to awaken the body,” said Manuel Firmani, a professional tango dancer leading the workshops. Some are done standing, some seated, depending on “the state people are in,” he said. After exercises focusing on posture, balance and other skills, dancing begins. Each patient is paired with a partner who doesn’t have Parkinson’s, often friends, relatives or volunteers. © 2026 The New York Times Company
Keyword: Parkinsons
Link ID: 30173 - Posted: 03.25.2026
Mariana Lenharo Exercise pumps up your muscles — but it might also be pumping up your neurons. According to a study published today in Neuron1, repeated exercise sessions on a treadmill strengthen the wiring in a mouse’s brain, making certain neurons quicker to activate. This ‘rewiring’ was essential for mice in the study to gradually improve their running endurance. The work reveals that the brain — in mice and, presumably, in humans — is actively involved in the development of endurance, the ability to get better at a physical activity with repeated practice, says Nicholas Betley, a neuroscientist at the University of Pennsylvania in Philadelphia, and a co-author of the paper. “You go for a run, and your lungs expand, your heart gets pumping better, your muscles break down and rebuild. All this great stuff happens, and the next time, it gets easier,” Betley says. “I didn’t expect that the brain was coordinating all of that.” Betley and his colleagues were curious about what happens in the brain as people get stronger through exercise. They decided to focus on the ventromedial hypothalamus, a brain region that regulates appetite and blood sugar. The team then zeroed in on a group of neurons in that region that produce a protein called steroidogenic factor 1 (SF1), which is known to play a part in regulating metabolism2. A previous study3 found that the deletion of the gene that codes for SF1 impairs endurance in mice. © 2026 Springer Nature Limited
Keyword: Obesity; Learning & Memory
Link ID: 30120 - Posted: 02.14.2026
Jon Hamilton Parkinson's disease does more than cause tremor and trouble walking. It can also affect sleep, smell, digestion and even thinking. That may be because the disease disrupts communication in a brain network that links the body and mind, a team reports in the journal Nature. "It almost feels like a tunnel is jammed, so no traffic can go normally," says Hesheng Liu, a brain scientist at Changping Laboratory and Peking University in Beijing and an author of the study. The finding fits nicely with growing evidence that Parkinson's is a network disorder, rather than one limited to brain areas that control specific movements, says Peter Strick, a professor and chair of neurobiology at the University of Pittsburgh who was not involved in the study. Other degenerative brain diseases affect other brain networks in different ways. Alzheimer's, for example, tends to reduce connectivity in the default mode network, which supports memory and sense of self. ALS (amyotrophic lateral sclerosis) primarily damages the motor system network, which controls movement. Understanding the network affected by Parkinson's, which affects about 1 million people in the United States, could change the way doctors treat the disease. A mystery solved? People with Parkinson's often have symptoms that vary in ways that are hard to explain. For example, someone who usually is unable to stand may suddenly leap when faced with an emergency. And Parkinson's patients who can still walk may freeze if they try to carry on a conversation. © 2026 npr
Keyword: Parkinsons
Link ID: 30116 - Posted: 02.11.2026


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