By Dennis Normile For several decades, evidence has accumulated that animals turn to medicinal plants to relieve their ailments. Chimpanzees (and some other species) swallow leaves to mechanically clear the gut of parasites. Chimps also rely on the ingested pith of an African relative of the daisy, Vernonia amygdalina, to rid themselves of intestinal worms. Dolphins rub against antibacterial corals and sponges to treat skin infections. And recently, a male Sumatran orangutan was observed chewing the leaves of Fibraurea tinctoria, a South Asian plant with antibacterial and anti-inflammatory properties, and dabbing the juice onto a wound. These instances of animals playing doctor with therapeutic plants have typically been identified one by one. Today, in PLOS ONE, a multinational team proposes adding 17 samples from 13 plant species to the chimpanzee pharmacopia. “The paper provides important new findings about self-medication behavior in wild chimpanzees,” a topic that’s still relatively unknown, says Isabelle Laumer, a cognitive biologist at the Max Planck Institute of Animal Behavior and lead author on the orangutan self-medication paper who was not involved in the new chimp research. Observers with the team behind today's paper spent 4 months with each of two chimp communities habituated to human observers in Uganda’s Budongo Forest. The researchers supplemented their own observations with historical data. From the 170 chimps in the two communities, the observers zeroed in on 51 individuals suffering bacterial infections and inflammation as indicated by abnormal urine composition, diarrhea, traces of parasites, or apparent wounds. For 10 hours a day they followed the sick chimps through the forest, noting which plants they ate and when, and watching in particular to see whether the animals went out of their way to find and consume plants not part of their usual diet. In one example, researchers observed an individual suffering from diarrhea very briefly venture outside the group’s safe home territory to eat a small amount of dead wood from Alstonia boonei, a tree in the dogbane family. Chimps rarely eat dead wood, which is not nutritious for them, the team says.

Keyword: Evolution
Link ID: 29364 - Posted: 06.24.2024

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 Esther Landhuis Last month, researchers discovered cells in the brainstem that regulate inflammation throughout the body. In response to an injury, these nerve cells not only sense inflammatory molecules, but also dial their circulating levels up and down to keep infections from harming healthy tissues. The discovery adds control of the immune system to the brainstem’s core functions — a list that also includes monitoring heart rate, breathing and aspects of taste — and suggests new potential targets for treating inflammatory disorders like arthritis and inflammatory bowel disease. During an intense workout or high-stakes exam, your brain can sense the spike in your heart rate and help restore a normal rhythm. Likewise, the brain can help stabilize your blood pressure by triggering chemical signals that widen or constrict blood vessels. Such feats often go unnoticed, but they illustrate a fundamental concept of physiology known as homeostasis — the capacity of organisms to keep their internal systems working smoothly and stably amid shifting circumstances. Now, in a paper published on May 1 in Nature, researchers describe how homeostatic control extends even to the sprawl of cells and tissues that comprise our immune system. The team applied a clever genetic approach in mice to identify cells in the brainstem that adjust immune reactions to pathogens and other outside triggers. These neurons operate like a “volume controller” that keeps the animals’ inflammatory responses within a physiological range, said paper author Hao Jin, a neuroimmunologist at the National Institute of Allergy and Infectious Diseases. © 2024 Simons Foundation.

Keyword: Miscellaneous
Link ID: 29361 - Posted: 06.15.2024

By Shaena Montanari Five years ago, while working to develop a tool to label neurons active during seizures in mice, Quynh Anh Nguyen noticed something she had not seen before. “There was a particular region in the brain that seemed to light up really prominently,” she says. Nguyen, assistant professor of pharmacology at Vanderbilt University, had induced seizures in the animals by injecting kainic acid into the hippocampus—a common strategy to model temporal lobe epilepsy. The condition often involves hyperactivity in the anterior and middle regions of the hippocampus, but Nguyen’s mice also showed the activation in a tiny posterior part of the hippocampus that she was not familiar with. Nguyen brought the data to her then-supervisor Ivan Soltesz, professor of neurosciences and neurosurgery at Stanford University. Together they realized that these neurons were in an area called the fasciola cinereum—a subregion of the hippocampus so understudied, Soltesz says, that when Nguyen first asked him what it was, he had “no idea.” Despite the subregion’s obscurity, it looks to be an important and previously overlooked contributor to epilepsy in people who do not respond to anti-seizure medications or tissue ablation in the hippocampus, Nguyen and her colleagues say. Fasciola cinereum neurons were active during seizures in six people with drug-resistant epilepsy, the team reported in April. © 2024 Simons Foundation

Keyword: Epilepsy
Link ID: 29360 - Posted: 06.15.2024

By Susan Dominus About a year ago, a friend of mine started evading my invitations to grab a drink. It was only when we caught up for a walk that she explained she wasn’t putting me off for any personal reason — it was just that she had stopped drinking. She wasn’t a heavy drinker — she had a glass of wine with dinner, the occasional Aperol spritz — but she’d been hearing on podcasts and reading in the news that even a small amount of alcohol was much worse for her health than had previously been understood. Listen to this article, read by Kirsten Potter My friend was picking up on a swing in the public-health messaging around alcohol. For many years, she might have felt that she was making a healthy choice in having a glass of wine or a beer with dinner. Right around the time when she came of legal age to drink, the early 1990s, some prominent researchers were promoting, and the media helped popularize, the idea that moderate drinking — for women, a drink a night; for men, two — was linked to greater longevity. The cause of that association was not clear, but red wine, researchers theorized, might have anti-inflammatory properties that extended life and protected cardiovascular health. Major health organizations and some doctors always warned that alcohol consumption was linked to higher cancer risk, but the dominant message moderate drinkers heard was one of not just reassurance but encouragement. More recently, though, research has piled up debunking the idea that moderate drinking is good for you. Last year, a major meta-analysis that re-examined 107 studies over 40 years came to the conclusion that no amount of alcohol improves health; and in 2022, a well-designed study found that consuming even a small amount brought some risk to heart health. That same year, Nature published research stating that consuming as little as one or two drinks a day (even less for women) was associated with shrinkage in the brain — a phenomenon normally associated with aging. © 2024 The New York Times Company

Keyword: Drug Abuse
Link ID: 29359 - Posted: 06.15.2024

By Max Kozlov A crucial brain signal linked to long-term memory falters in rats when they are deprived of sleep — which might help to explain why poor sleep disrupts memory formation1. Even a night of normal slumber after a poor night’s sleep isn’t enough to fix the brain signal. These results, published today in Nature, suggest that there is a “critical window for memory processing”, says Loren Frank, a neuroscientist at the University of California, San Francisco, who was not involved with the study. “Once you’ve lost it, you’ve lost it.” In time, these findings could lead to targeted treatments to improve memory, says study co-author Kamran Diba, a computational neuroscientist at the University of Michigan Medical School in Ann Arbor. Neurons in the brain seldom act alone; they are highly interconnected and often fire together in a rhythmic or repetitive pattern. One such pattern is the sharp-wave ripple, in which a large group of neurons fire with extreme synchrony, then a second large group of neurons does the same and so on, one after the other at a particular tempo. These ripples occur in a brain area called the hippocampus, which is key to memory formation. The patterns are thought to facilitate communication with the neocortex, where long-term memories are later stored. One clue to their function is that some of these ripples are accelerated re-runs of brain-activity patterns that occurred during past events. For example, when an animal visits a particular spot in its cage, a specific group of neurons in the hippocampus fires in unison, creating a neural representation of that location. Later, these same neurons might participate in sharp-wave ripples — as if they were rapidly replaying snippets of that experience. © 2024 Springer Nature Limited

Keyword: Learning & Memory; Sleep
Link ID: 29358 - Posted: 06.13.2024

Jon Hamilton A flexible film bristling with tiny sensors could make surgery safer for patients with a brain tumor or severe epilepsy. The experimental film, which looks like Saran wrap, rests on the brain’s surface and detects the electrical activity of nerve cells below. It’s designed to help surgeons remove diseased tissue while preserving important functions like language and memory. “This will enable us to do a better job,” says Dr. Ahmed Raslan, a neurosurgeon at Oregon Health and Science University who helped develop the film. The technology is similar in concept to sensor grids already used in brain surgery. But the resolution is 100 times higher, says Shadi Dayeh, an engineer at the University of California, San Diego, who is leading the development effort. In addition to aiding surgery, the film should offer researchers a much clearer view of the neural activity responsible for functions including movement, speech, sensation, and even thought. “We have these complex circuits in our brains,” says John Ngai, who directs the BRAIN Initiative at the National Institutes of Health, which has funded much of the film’s development. “This will give us a better understanding of how they work.” Mapping an ailing brain The film is intended to improve a process called functional brain mapping, which is often used when a person needs surgery to remove a brain tumor or tissue causing severe epileptic seizures. © 2024 npr

Keyword: Brain imaging; Epilepsy
Link ID: 29357 - Posted: 06.13.2024

By Olivia Gieger Three pioneers in face-perception research have won the 2024 Kavli Prize in Neuroscience. Nancy Kanwisher, professor of cognitive neuroscience at the Massachusetts Institute of Technology; Winrich Freiwald, professor of neurosciences and behavior at Rockefeller University; and Doris Tsao, professor of neurobiology at the University of California, Berkeley, will share the $1 million Kavli Prize for their discoveries of the regions—in both the human and monkey brains—responsible for identifying and recognizing faces. “This is work that’s very classic and very elegant, not only in face-processing and face-recognition work, but the impact it’s had on how we think about brain organization in general is huge,” says Alexander Cohen, assistant professor of neurology at Harvard Medical School, who studies face recognition in autistic people. The Norwegian Academy of Science and Letters awards the prize every two years. Kanwisher says she long suspected that something special happens in the brain when we look at faces, because people with prosopagnosia—the inability to recognize faces—maintain the ability to recognize nearly all other objects. What’s more, it is harder to recognize an upside-down face than most other inverted objects, studies have shown. To get to the root of face processing, Kanwisher spent hours as a young researcher lying still in an MRI machine as images of faces and objects flashed before her. A spot in the bottom right of the cerebral cortex lit up when she and others looked at faces, according to functional MRI (fMRI) scans, she and her colleagues reported in a seminal 1997 paper. They called the region the fusiform face area. © 2024 Simons Foundation

Keyword: Attention
Link ID: 29356 - Posted: 06.13.2024

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

By Gina Kolata and Pam Belluck A committee of independent advisers to the Food and Drug Administration voted unanimously on Monday that the benefits outweigh the risks of the newest experimental drug for Alzheimer’s disease. Alzheimer’s afflicts more than six million Americans. It has no cure, and there is no treatment or lifestyle modification that can restore memory loss or reverse cognitive decline. The drug, made by Eli Lilly, is donanemab. It modestly slowed cognitive decline in patients in the early stages of the disease but also had significant safety risks, including swelling and bleeding in the brain. The committee concluded, though, that the consequences of Alzheimer’s are so dire that even a modest benefit can be worthwhile. The F.D.A. usually follows the advice of the agency’s advisory committees but not always. The drug is based on a long-held hypothesis that Alzheimer’s disease begins when rough hard balls of amyloid, a protein, pile up in patients’ brains, followed by a cascade of reactions leading to the death of neurons. The idea is to treat Alzheimer’s by attacking amyloid, clearing it from the brain. Two similar amyloid-fighting drugs were approved recently: Leqembi, made by Eisai and Biogen, was approved last year. That drug’s risks and modest benefits are similar to those of donanemab. Aduhelm, made by Biogen, is the other drug and was approved in 2021 but was discontinued because there was insufficient evidence that it could benefit patients. Donanemab was expected to be approved earlier this year, but in March, the F.D.A. decided that, instead, it would require donanemab to undergo the scrutiny of an independent advisory committee, a surprise to Eli Lilly. © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29354 - Posted: 06.11.2024

By Virginia Morell Leaping over waves or body surfing side by side, dolphins are a fun-loving bunch. But their frolicking—and that of species from hyenas to humans—has long baffled evolutionary biologists. Why expend so much energy on play? A new study offers an intriguing explanation: Juvenile male dolphins use play to acquire the skills required for fathering calves, researchers report today in the Proceedings of the National Academy of Sciences. Most significantly, the scientists found the most playful males go on to have more calves as adults. The study is likely to spur further research into play behavior in additional species, other scientists say. “It’s exciting research, and it solves an evolutionary puzzle,” says Jennifer Smith, a behavioral ecologist at the University of Wisconsin–Eau Claire. “This is the first study to link play behavior in the wild to reproductive success.” Since 1982, scientists have observed some 200 male Indo-Pacific bottlenose dolphins (Tursiops aduncus) in the exceptionally clear waters of Shark Bay in Australia. About 20 years ago, the researchers noticed that young males, 4 to 12 years old, often played together as if they were herding a fertile female, flanking her on either side, while swimming in sync with each other and making popping vocalizations. This kind of “synchronicity is crucial for male reproduction,” says Kathryn Holmes, a behavioral biologist with the Shark Bay Dolphin Research project and lead author of the new study. The young dolphins’ behaviors were strikingly similar to those of the adults. “We wondered if this was ‘play practice’ for the adult behaviors,” Holmes says. So she and her colleagues closely tracked 28 juvenile males for 4 to 5 months over several years, recording their interactions and play behaviors. When socializing, the males “played almost continuously,” Holmes says. “They seemed to never tire of their games.” © 2024 American Association for the Advancement of Science.

Keyword: Sexual Behavior; Evolution
Link ID: 29353 - Posted: 06.11.2024

Elephants call out to each other using individual names that they invent for their fellow pachyderms, according to a new study. While dolphins and parrots have been observed addressing each other by mimicking the sound of others from their species, elephants are the first non-human animals known to use names that do not involve imitation, the researchers suggested. For the new study published on Monday, a team of international researchers used an artificial intelligence algorithm to analyse the calls of two wild herds of African savanna elephants in Kenya. The research “not only shows that elephants use specific vocalisations for each individual, but that they recognise and react to a call addressed to them while ignoring those addressed to others”, the lead study author, Michael Pardo, said. The video player is currently playing an ad. “This indicates that elephants can determine whether a call was intended for them just by hearing the call, even when out of its original context,” the behavioural ecologist at Colorado State University said in a statement. The researchers sifted through elephant “rumbles” recorded at Kenya’s Samburu national reserve and Amboseli national park between 1986 and 2022. Using a machine-learning algorithm, they identified 469 distinct calls, which included 101 elephants issuing a call and 117 receiving one. Elephants make a wide range of sounds, from loud trumpeting to rumbles so low they cannot be heard by the human ear. Names were not always used in the elephant calls. But when names were called out, it was often over a long distance, and when adults were addressing young elephants. Adults were also more likely to use names than calves, suggesting it could take years to learn this particular talent. The most common call was “a harmonically rich, low-frequency sound”, according to the study in the journal Nature Ecology & Evolution. © 2024 Guardian News & Media Limited

Keyword: Animal Communication; Language
Link ID: 29352 - Posted: 06.11.2024

By Janna Levin During traumatic periods and their aftermath, our brains can fall into habitual ways of thinking that may be helpful in the short run but become maladaptive years later. For the brain to readjust to new situations later in life, it needs to be restored to the malleable state it was in when the habits first formed. That is exactly what Gül Dölen, a neuroscientist and psychiatric researcher at the University of California, Berkeley, is working toward in her lab. What is her surprising tool? Psychedelics. JANNA LEVIN: Welcome to “The Joy of Why.” This is Janna Levin. On June 4th, an advisory panel for the Federal Drug Administration recommended against approving the use of the psychedelic drug MDMA as a treatment for post-traumatic stress disorder. Various concerns, some about safety, overshadowed the demonstrable value of the drug in the opinion of the panel. The path to approval for drug therapies is notoriously fraught with profound complexities, a high bar on proof in clinical trials, the medical injunction to “do no harm,” as well as social and political nuances. But, what’s the fundamental neuroscience behind the news story? Why are so many psychiatric researchers enthusiastic about the promise of psychedelics? We happened to take on this subject a few weeks ago with neuroscientist Gül Dölen. Here is that episode. New drug leads can come from practically anywhere. Penicillin’s discovery was spurred from mold spores that accidentally landed in a petri dish. Cancer treatments can be dredged from the bottom of the sea. And synthetic antibodies can now be engineered from scratch. But there’s a class of drugs that mainstream medicine has generally overlooked that could prove life-changing for many people facing addiction, depression, post-traumatic stress — if scientists embrace the potential power of psychedelics. © 2024 the Simons Foundation.

Keyword: Stress; Depression
Link ID: 29351 - Posted: 06.08.2024

By Ellen Barry Post-traumatic stress disorder diagnoses among college students more than doubled between 2017 and 2022, climbing most sharply as the coronavirus pandemic shut down campuses and upended young adults’ lives, according to new research published on Thursday. The prevalence of PTSD rose to 7.5 percent from 3.4 percent during that period, according to the findings. Researchers analyzed responses from more than 390,000 participants in the Healthy Minds Study, an annual web-based survey. “The magnitude of this rise is indeed shocking,” said Yusen Zhai, the paper’s lead author, who heads the community counseling clinic at the University of Alabama at Birmingham. His clinic had seen more young people struggling in the aftermath of traumatic events. So he expected an increase, but not such a large one. Dr. Zhai, an assistant professor in the Department of Human Studies, attributed the rise to “broader societal stressors” on college students, such as campus shootings, social unrest and the sudden loss of loved ones from the coronavirus. PTSD is a mental health disorder characterized by intrusive thoughts, flashbacks and heightened sensitivity to reminders of an event, continuing more than a month after it occurs. It is a relatively common disorder, with an estimated 5 percent of adults in the United States experiencing it in any given year, according to the most recent epidemiological survey conducted by the Department of Health and Human Services. Lifetime prevalence is 8 percent in women and 4 percent in men, the survey found. The new research also found a sharp rise in the prevalence of a similar condition, acute stress disorder, which is diagnosed less than a month after a trauma. Diagnoses rose to 0.7 percent among college students in 2022, up from 0.2 percent five years earlier. Use of mental health care increased nationally during the pandemic, as teletherapy made it far easier to see clinicians. Treatment for anxiety disorders increased most steeply, followed by PTSD, bipolar disorder and depression, according to economists who analyzed more than 1.5 million insurance claims for clinician visits between 2020 and 2022. © 2024 The New York Times Company

Keyword: Stress
Link ID: 29350 - Posted: 06.08.2024

Hannah Devlin Science correspondent A 10-minute brain scan could detect dementia several years before people develop noticeable symptoms, a study suggests. Scientists used a scan of “resting” brain activity to identify whether people would go on to develop dementia, with an estimated 80% accuracy up to nine years before people received a diagnosis. If the findings were confirmed in a larger cohort, the scan could become a routine procedure in memory clinics, scientists said. “We’ve known for a long time that the function of the brain starts to change many years before you get dementia symptoms,” said Prof Charles Marshall, who led the work at Queen Mary University of London. “This could help us to be more precise at identifying those changes using an MRI scan that you could do on any NHS scanner.” The research comes as a new generation of Alzheimer’s drugs are on the horizon. The UK’s Medicines and Healthcare products Regulatory Agency (MHRA) is assessing lecanemab, made by Eisai and Biogen, and donanemab, made by Eli Lilly, and both drugs are widely expected to be licensed this year. “Predicting who is going to get dementia in the future will be vital for developing treatments that can prevent the irreversible loss of brain cells that causes the symptoms of dementia,” Marshall said. The researchers used functional MRI (fMRI) scans from 1,100 UK Biobank volunteers to detect changes in the brain’s “default mode network” (DMN). The scan measures correlations in brain activity between different regions while the volunteer lies still, not doing any particular task. The network, which reflects how effectively different regions are communicating with each other, is known to be particularly vulnerable to Alzheimer’s disease. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Brain imaging
Link ID: 29349 - Posted: 06.08.2024

By Francine Russo Desperate for sleep, you go to a sleep clinic, where your head is fitted with electrodes to record your brain waves through various sleep stages. In the morning, you report that you barely slept at all. Yet according to the test—polysomnography, the gold standard for sleep measurement—you slept all night. You’re not the classic example of a person with insomnia who waits for sleep to come, maybe checks the clock, paces, reads and waits for morning. What you have has been called subjective insomnia, paradoxical insomnia or sleep misperception. Scientists have doggedly attacked this stubborn puzzle for decades without result—until now. Now they say that you have not been misrepresenting your sleep; they have been mismeasuring it. The most recent studies, using far more enhanced measurement, have found that many people with subjective insomnia show different brain activity from good sleepers—throughout the night. Neuroscientist Aurélie Stephan and colleagues at the Netherlands Institute for Neuroscience (NIN) realized that something unusual was going on after they asked people in their study to put onto their head a net of 256 electrodes rather than the typical six to 20 used in sleep clinics. In one series of experiments, the researchers woke sleepers about 26 times on average during the night. The participants were asked whether they’d been asleep or awake and what they’d been thinking about. The most remarkable finding, Stephan says, is that these people showed pockets of arousal in the form of fast brain waves during rapid eye movement (REM) sleep. REM is the stage in normal sleep when your brain should completely disconnect from the systems that keep you aware and vigilant, Stephan says. © 2024 SCIENTIFIC AMERICAN

Keyword: Sleep
Link ID: 29348 - Posted: 06.08.2024

Ian Sample Science editor Five children who were born deaf now have hearing in both ears after taking part in an “astounding” gene therapy trial that raises hopes for further treatments. The children were unable to hear because of inherited genetic mutations that disrupt the body’s ability to make a protein needed to ensure auditory signals pass seamlessly from the ear to the brain. Doctors at Fudan University in Shanghai treated the children, aged between one and 11, in both ears in the hope they would gain sufficient 3D hearing to take part in conversations and work out which direction sounds were coming from. Within weeks of receiving the therapy, the children had gained hearing, could locate the sources of sounds, and recognised speech in noisy environments. Two of the children were recorded dancing to music, the researchers reported in Nature Medicine. A child facing away from the camera towards a panel of auditory testing equipment with script in the top left corner Dr Zheng-Yi Chen, a scientist at Massachusetts Eye and Ear, a Harvard teaching hospital in Boston that co-led the trial, said the results were “astounding”, adding that researchers continued to see the children’s hearing ability “dramatically progress”. The therapy uses an inactive virus to smuggle working copies of the affected gene, Otof, into the inner ear. Once inside, cells in the ear use the new genetic material as a template to churn out working copies of the crucial protein, otoferlin. Video footage of the patients shows a two-year-old boy responding to his name three weeks after the treatment and dancing to music after 13 weeks, having shown no response to either before receiving the injections. © 2024 Guardian News & Media Limited

Keyword: Hearing; Genes & Behavior
Link ID: 29347 - Posted: 06.06.2024

By Gemma Conroy Researchers have developed biodegradable, wireless sensors that can monitor changes in the brain following a head injury or cancer treatment, without invasive surgery. In rats and pigs, the soft sensors performed just as well as conventional wired sensors for up to a month after being injected under the skull. The gel-based sensors measure key health markers, including temperature, pH and pressure. “It is quite likely this technology will be useful for people in medical settings,” says study co-author Yueying Yang, a biomedical engineer at Huazhong University of Science and Technology (HUST) in Wuhan, China. The findings were published today in Nature1. “It’s a very comprehensive study,” says Christopher Reiche, who develops implantable microdevices at the University of Utah in Salt Lake City. For years, scientists have been developing brain sensors that can be implanted inside the skull. But many of these devices rely on wires to transmit data to clinicians. The wires are difficult to insert and remove, and create openings in the skin for viruses and bacteria to enter the body. Wireless sensors offer a solution to this problem, but are thwarted by their limited communication range and relatively large size. Developing sensors that can access and monitor the brain is “extremely difficult”, says Omid Kavehei, a biomedical engineer who specializes in neurotechnology at the University of Sydney in Australia. To overcome these challenges, Yang and her colleagues created a set of 2-millimetre cube-shaped sensors out of hydrogel, a soft, flexible material that’s often used in tissue regeneration and drug delivery. The gel sensors change shape under different temperatures, pressures and pH conditions, and respond to vibrations caused by variations in blood flow in the brain. When the sensors are implanted under the skull and scanned with an ultrasound probe — a tool that is already used to image the human brain in clinics — these changes are detectable in the form of ultrasonic waves that pass through the skull. The tiny gel-cubes completely dissolve in saline solution after around four months, and begin to break down in the brain after five weeks. © 2024 Springer Nature Limited

Keyword: Brain Injury/Concussion; Brain imaging
Link ID: 29346 - Posted: 06.06.2024

By Betsy Mason To help pay for his undergraduate education, Elias Garcia-Pelegrin had an unusual summer job: cruise ship magician. “I was that guy who comes out at dinnertime and does random magic for you,” he says. But his latest magic gig is even more unusual: performing for Eurasian jays at Cambridge University’s Comparative Cognition Lab. Birds can be harder to fool than tourists. And to do magic for the jays, he had to learn to do sleight-of-hand tricks with a live, wriggling waxworm instead of the customary coin or ball. But performing in an aviary does have at least one advantage over performing on a cruise ship: The birds aren’t expecting to be entertained. “You don’t have to worry about impressing anybody, or tell a joke,” Garcia-Pelegrin says. “So you just do the magic.” In just the last few years, researchers have become interested in what they can learn about animal minds by studying what does and doesn’t fool them. “Magic effects can reveal blind spots in seeing and roadblocks in thinking,” says Nicky Clayton, who heads the Cambridge lab and, with Garcia-Pelegrin and others, cowrote an overview of the science of magic in the Annual Review of Psychology. What we visually perceive about the world is a product of how our brains interpret what our eyes see. Humans and other animals have evolved to handle the immense amount of visual information we’re exposed to by prioritizing some types of information, filtering out things that are usually less relevant and filling in gaps with assumptions. Many magic effects exploit these cognitive shortcuts in humans, and comparing how well these same tricks work on other species may reveal something about how their minds operate. Clayton and her colleagues have used magic tricks with both jays and monkeys to reveal differences in how these animals experience the world. Now they are hoping to expand to more species and inspire other researchers to try magic to explore big questions about complex mental abilities and how they evolved.

Keyword: Attention; Evolution
Link ID: 29345 - Posted: 06.06.2024