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

By Corinna da Fonseca-Wollheim The placid chords of a Debussy prelude splashed through a darkened auditorium during a recital by the pianist Nicolas Namoradze at the University of California, San Francisco, on a November evening. A translucent image of Namoradze’s brain appeared above him on a screen: Electrical currents of different wavelengths, associated with varying levels of alertness, registered as colorful activity coursing through the model like storm fronts on a weather map. With each chord, clouds of green and blue bloomed, then faded as the sound receded. As the recital progressed with works by Bach, Beethoven and Scriabin, the image of the gently rotating brain showed a complex choreography of signals that sometimes ping-ponged between different areas or flickered simultaneously across the organ’s hemispheres. As a visual spectacle accompanying Namoradze’s pellucid playing, it was mesmerizing: an X-ray, seemingly, of virtuosity at work. But to the scientists in the audience, attendees at a conference on the neuroscience of music and dance, it was more than entertainment. It was evidence of a breakthrough in experiment design — one that opens up possibilities in an area that has long eluded scientific study: how music activates the brain, not in listeners, but in performers. It was also a reminder of the value artists can bring to scientific inquiry as active participants shaping studies of their craft. The neuroscientist Theodore Zanto, a member of the Neuroscape lab at U.C.S.F. that created the “Glass Brain” animations, said in an interview the next day that he was surprised — and moved — by the result. “It’s probably the cleanest real-time representation of what’s happening inside the brain during a piano performance,” he said. © 2026 The New York Times Company

Keyword: Hearing; Brain imaging
Link ID: 30115 - Posted: 02.11.2026

By Natalia Mesa A region of the cerebellum shows language specificity akin to that of cortical language regions, indicating that it might be part of the broader language network, according to a new brain-imaging study. “This is the first time we see an area outside of the core left-hemisphere language areas that behaves so similarly to those core areas,” says study investigator Ev Fedorenko, associate professor of brain and cognitive sciences at the Massachusetts Institute of Technology. Initially thought to coordinate only movement, the cerebellum also contributes to cognitive processes, such as social reward, abstract reasoning and working memory, according to studies from the past decade. But despite the fact that people with cerebellar lesions have subtle language struggles, the region’s contributions to that skill have been ignored until recently, Fedorenko says. With this new work, “I think it becomes harder to dismiss language responses as somehow artifactual.” Fedorenko and her team analyzed nearly 1,700 whole-brain functional MRI experiments conducted over the course of 15 years. They originally collected and analyzed those scans to identify language-selective regions of the neocortex, but they reanalyzed many of them to determine the cerebellum’s role in linguistic processing. Four cerebellar regions activated robustly when participants performed language-related tasks, such as reading passages of text or listening to someone else reading the passages aloud, in line with previous work. But only one region responded exclusively to these language-related tasks; it did not activate during a variety of nonlinguistic tasks—including movement, arithmetic tasks and a spatial working memory task—or when participants listened to music or watched videos of faces and bodies. The findings were published last month in Neuron. © 2026 Simons Foundation

Keyword: Language
Link ID: 30110 - Posted: 02.07.2026

By Laura Sanders The brain’s “little brain” may hold big promise for people with language trouble. Tucked into the base of the brain, the fist-sized cerebellum is most known for its role in movement, posture and coordination. A new study maps the language system in this out-of-the-way place. These results, published January 22 in Neuron, uncover a spot in the cerebellum that shows strong and selective activity for language. The new study is “excellent,” says neurologist and cerebellum researcher Jeremy Schmahmann of Massachusetts General Hospital and Harvard Medical School in Boston. His work and that of others have shown that the cerebellum contributes to language and thinking more generally. The new research scrutinized the cerebellum in detail, “confirming and extending previous observations and contributing to our understanding” of the cerebellum’s activity, he says. Neuroscientist Colton Casto combed through about 15 years of brain scanning data collected by study coauthor Evelina Fedorenko, a cognitive neuroscientist at MIT, and her colleagues. Putting the data all together, the scans of 846 people showed brain activity in four spots in the right side of the cerebellum as people read or listened to a story. Three of these spots were also active when people did other things, such as working out a math problem, or listening to music or watching a movie without words. But one spot was more discerning, says Casto, of MIT and Harvard University. This region didn’t respond to nonverbal movies or math. It also ignored orchestral or jazz music, which, like language, relies on syntax and patterns and sound. Instead, this spot is attuned specifically to words. “You have to be reading or listening to language to fully recruit this region,” Casto says. © Society for Science & the Public 2000–2026.

Keyword: Language
Link ID: 30091 - Posted: 01.24.2026

Allison Aubrey If you feel a lift after exercise, you're in good company. Movement can boost mood, and according to the results of a new study, it can also help relieve symptoms of depression. As part of a review of evidence by the Cochrane collaboration — an independent network of researchers — scientists evaluated 73 randomized controlled trials that included about 5,000 people with depression, many of whom also tried antidepressant medication. "We found that exercise was as effective as pharmacological treatments or psychological therapies as well," says Andrew Clegg, a professor at the University of Lancashire in the U.K. The findings are not a surprise to psychiatrist Dr. Stephen Mateka, medical director of psychiatry at Inspira Health. "This new Cochrane review reinforces the evidence that exercise is one of the most evidence-based tools for improving mood," says Mateka. He explains how it mirrors some of the effects of medication. "Exercise can help improve neurotransmitter function, like serotonin as well as dopamine and endorphins. So there is certainly overlap between exercise and how antidepressants offer relief," Mateka says. And there's another powerful effect too. Exercise can trigger the release of brain growth factors, explains Dr. Nicholas Fabiano of the University of Ottawa. He says depression can decrease neuroplasticity, making it harder for the brain to adapt and change. "The brain in depression is thought to be less plastic. So there's less what we call neurotrophic factors, or BDNF," Fabiano explains. He calls it the Miracle-Gro for the brain. "And we know that exercise can also boost it. So I think exercise is a fundamental pillar we really need to counsel patients on," he says. © 2026 npr

Keyword: Depression
Link ID: 30077 - Posted: 01.14.2026

By Caroline Hopkins Legaspi In a study published Monday in JAMA Neurology, researchers linked obstructive sleep apnea, a condition that causes temporary pauses in breathing during sleep, with Parkinson’s disease. Parkinson’s disease is a progressive nervous system disorder that causes tremors, stiffness, and difficulty speaking, moving and swallowing. It is the second-most common neurodegenerative disease in the United States, after Alzheimer’s disease, with 90,000 people diagnosed each year. There is no cure for Parkinson’s disease, said Dr. Lee Neilson, a neurologist at Oregon Health & Science University who led the study. But the researchers did find that treating sleep apnea with a continuous positive airway pressure (or CPAP) machine was associated with a reduced likelihood of developing Parkinson’s. So identifying those at highest risk for the neurological condition — and intervening early, Dr. Neilson said, “might make the biggest impact.” The researchers analyzed medical records from more than 11 million U.S. veterans treated through the Department of Veterans Affairs between 1999 and 2022. The group was predominantly male with an average age of 60, representing those at highest risk for sleep apnea, experts said. The researchers found that about 14 percent of the participants had been diagnosed with sleep apnea between 1999 and 2022, according to their medical records. When the researchers looked at their health six years after those diagnoses, they found that the veterans with sleep apnea were nearly twice as likely to have developed Parkinson’s disease compared with those who had not been diagnosed with sleep apnea. This held even after controlling for other factors that could influence the development of sleep apnea or Parkinson’s disease, including high body mass index and conditions like diabetes, high blood pressure, traumatic brain injuries and depression. © 2025 The New York Times Company

Keyword: Sleep; Parkinsons
Link ID: 30029 - Posted: 11.26.2025

Liam Drew Paradromics, a neurotechnology developer, announced today that the US Food and Drug Administration (FDA) has approved a first long-term clinical trial of its brain–computer interface (BCI). Early next year, the company — one of the closet rivals to Elon Musk’s neurotechnology firm Neuralink — will implant its device in two volunteers who were left unable to speak owing to neurological diseases and injuries. It has two goals: to ensure the device is safe; and to restore a person’s ability to communicate with real-time speech. “We’re very excited about bringing this new hardware into a trial,” says Matt Angle, chief executive of Paradromics, which is based in Austin, Texas. Paradromics’ BCI has an active area of roughly 7.5 millimetres in diameter of thin, stiff, platinum-iridium electrodes that penetrate the surface of the cerebral cortex to record from individual neurons around 1.5 mm deep. This is then connected by wire to a power source and wireless transceiver implanted in an individual’s chest. Initially, the two volunteers will each have one electrode array implanted in the area of the motor cortex that controls the lips, tongue and larynx, Angle says. Neural activity will then be recorded from this region as the study participants imagine speaking sentences that are presented to them. Following previous work by researchers who are now collaborating with Paradromics1, the system learns what patterns of neural activity correspond to each intended speech sound. When participants imagine speaking these neural patterns will be converted into text on a screen for participants to approve, or into a real-time voice output based on old recordings of participants’ own voices. This is the first BCI clinical trial to formally target synthetic-voice generation. “Arguably, the greatest quality of life change you can deliver right now with BCI is communication,” Angle says. © 2025 Springer Nature Limited

Keyword: Robotics
Link ID: 30019 - Posted: 11.22.2025