By David Grimm “Whooo’s a good boy?” “Whooo’s a pretty kitty?” When it comes to communicating with our pets, most of us can’t help but talk to them like babies. We pitch our voices high, extend our vowels, and ask short, repetitive questions. Dogs seem to like this. They’re far more likely to pay attention to us when we use this “caregiver speech,” research has shown. Now, scientists have found the same is true for cats, though only when their owner is talking. The work adds evidence that cats—like dogs—may bond with us in some of the same ways infants do. “It’s a fascinating study,” says Kristyn Vitale, an animal behaviorist and expert on cat cognition at Unity College, who was not involved with the work. “It further supports the idea that our cats are always listening to us.” Charlotte de Mouzon had a practical reason for getting into this line of research. An ethologist at Paris Nanterre University, she had previously been a cat behaviorist, consulting with owners on how to solve everything from litter box problems to aggressive behavior. “Sometimes people would ask me, ‘What’s the scientific evidence behind your approaches?’” she says. “I was frustrated that there were no studies being done on cat behavior in France.” So, she began a Ph.D. and was soon studying cat-human communication. As a first step, de Mouzon confirmed what most cat owners already know: We dip into “baby talk” when we address our feline friends–a habit de Mouzon is guilty of herself. “What’s up, my little ones?” she finds herself asking in a high-pitched voice when greeting her two kitties, Mila and Shere Khan. But do cats, like dogs, actually respond more to this “cat-directed speech”? To find out, de Mouzon recruited 16 cats and their owners—students at the Alfort National Veterinary School just outside of Paris. Because cats can be challenging to work with, de Mouzon studied them on feline-friendly turf, converting a common room in the students’ dormitory into a makeshift animal behavior lab filled with toys, a litter box, and places to hide.

Keyword: Animal Communication; Language
Link ID: 28525 - Posted: 10.26.2022

By Elisabeth Egan BEVERLY HILLS, Calif. — When I pictured Matthew Perry, the actor frequently known as Chandler Bing, I saw him on the tangerine couch at Central Perk or seated on one of the twin recliners in the apartment he shared with Joey Tribbiani. In September, after arriving at his 6,300-square-foot rental house and being ushered through a driveway gate by his sober companion, I sat across from Perry, who perched on a white couch in a white living room, a world away from “Friends,” the NBC sitcom that aired for 10 seasons and catapulted all six of its stars into fame, fortune and infinite memes. Instead of the foosball table where Chandler, Joey, Monica, Phoebe, Rachel and Ross gathered, nudging each other through the first chapters of adulthood, Perry, 53, had a red felt pool table that looked untouched. There was plenty of light in the house, but not a lot of warmth. I have watched every episode of “Friends” three times — in prime time, on VHS and on Netflix — but I’m not sure I would have recognized Perry if I’d seen him on the street. If he was an ebullient terrier in those 1990s-era Must See TV days — as memorable for his full-body comedy as he was for the inflection that made “Can you BE any more [insert adjective]” the new “Gag me with a spoon” — he now seemed more like an apprehensive bulldog, with the forehead furrows to match. As his former co-star Lisa Kudrow confesses in the foreword to his memoir, “Friends, Lovers and the Big Terrible Thing,” the first question people ask about “Friends” is often “How’s Matthew Perry doing?” Perry answers that question in the book, which Flatiron will publish on Nov. 1, by starkly chronicling his decades-long cage match with drinking and drug use. His addiction led to a medical odyssey in 2018 that included pneumonia, an exploded colon, a brief stint on life support, two weeks in a coma, nine months with a colostomy bag, more than a dozen stomach surgeries, and the realization that, by the time he was 49, he had spent more than half of his life in treatment centers or sober living facilities. © 2022 The New York Times Company

Keyword: Drug Abuse
Link ID: 28524 - Posted: 10.26.2022

WASHINGTON — A massive recall of millions of sleep apnea machines has stoked anger and frustration among patients, and U.S. officials are weighing unprecedented legal action to speed a replacement effort that is set to drag into next year. Sound-dampening foam in the pressurized breathing machines can break down over time, leading users to potentially inhale tiny black particles or hazardous chemicals while they sleep, manufacturer Philips warned in June 2021. Philips initially estimated it could repair or replace the units within a year. But with the recall expanding to more than 5 million devices worldwide, the Dutch company now says the effort will stretch into 2023. That's left many patients to choose between using a potentially harmful device or trying risky remedies, including removing the foam themselves, buying second-hand machines online or simply going without the therapy. The devices are called continuous positive airway pressure, or CPAP, machines. They force air through a mask to keep passageways open during sleep. Untreated sleep apnea can cause people to stop breathing hundreds of times per night, leading to dangerous drowsiness and increased heart attack risk. The problem is more common in men than women, with estimates ranging from 10% to 30% of adults affected. Most patients are better off using a recalled device because the risks of untreated sleep apnea still outweigh the potential harms of the disintegrating foam, physicians say. But doctors have been hard pressed to help patients find new machines, which generally cost between $500 and $1,000, and were already in short supply due to supply chain problems. © 2022 npr

Keyword: Sleep
Link ID: 28523 - Posted: 10.26.2022

by Carey Gillam and Aliya Uteuova For decades, Swiss chemical giant Syngenta has manufactured and marketed a widely used weed-killing chemical called paraquat, and for much of that time the company has been dealing with external concerns that long-term exposure to the chemical may be a cause of the incurable brain ailment known as Parkinson’s disease. Syngenta has repeatedly told customers and regulators that scientific research does not prove a connection between its weedkiller and the disease, insisting that the chemical does not readily cross the blood-brain barrier, and does not affect brain cells in ways that cause Parkinson’s. But a cache of internal corporate documents dating back to the 1950s reviewed by the Guardian suggests that the public narrative put forward by Syngenta and the corporate entities that preceded it has at times contradicted the company’s own research and knowledge. And though the documents reviewed do not show that Syngenta’s scientists and executives accepted and believed that paraquat can cause Parkinson’s, they do show a corporate focus on strategies to protect product sales, refute external scientific research and influence regulators. In one defensive tactic, the documents indicate that the company worked behind the scenes to try to keep a highly regarded scientist from sitting on an advisory panel for the US Environmental Protection Agency (EPA). The agency is the chief US regulator for paraquat and other pesticides. Company officials wanted to make sure the efforts could not be traced back to Syngenta, the documents show. And the documents show that insiders feared they could face legal liability for long-term, chronic effects of paraquat as long ago as 1975. One company scientist called the situation “a quite terrible problem” for which “some plan could be made … ”

Keyword: Parkinsons; Neurotoxins
Link ID: 28522 - Posted: 10.22.2022

Ewen Callaway Set on a rocky outcrop in southern Siberia, Chagyrskaya Cave might not look like much. But for one family of Neanderthals, it was home. For the first time, researchers have identified a set of closely related Neanderthals: a father and his teenage daughter and two other, more-distant relatives. The discovery of the family — reported on 19 October in Nature1 — and seven other individuals (including a pair of possible cousins from another clan) in the same cave, along with two more from a nearby site, represents the largest ever cache of Neanderthal genomes. The findings also suggest that Neanderthal communities were small, and that females routinely left their families to join new groups. Gleaning insights into kinship and social structure is new territory for ancient-genome studies, which have typically focused on broader population history, says Krishna Veeramah, a population geneticist at Stonybrook University in New York. “The fact that we can do this with Neanderthals is incredible.” Buried treasure Set on the banks of the Charysh River in the foothills of the Altai mountains, Chagyrskaya is 100 kilometres west of Denisova Cave, an archaeological treasure trove in which humans, Neanderthals, Denisovans (and at least one Neanderthal–Denisovan hybrid) all lived intermittently over some 300,000 years2,3. Excavations of Chagyrskaya, however, have so far revealed only Neanderthal remains, dated to between 50,000 to 60,000 years ago, and characteristic stone tools. In 2020, a genome sequence from a female Neanderthal from Chagyrskaya suggested she belonged to population distinct from those that occupied Denisova Cave much earlier4. To study the cave’s inhabitants in greater depth, a team of researchers led by palaeogeneticist Laurits Skov and population geneticist Benjamin Peter at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, extracted DNA from 17 other ancient-human remains from Chagyrskaya, as well as several from a nearby cave, called Okladnikov. © 2022 Springer Nature Limited

Keyword: Evolution
Link ID: 28521 - Posted: 10.22.2022

By Fenit Nirappil A national shortage of Adderall has left patients who rely on the pills for attention-deficit/hyperactivity disorder scrambling to find alternative treatments and uncertain whether they will be able to refill their medication. The Food and Drug Administration announced the shortage last week, saying that one of the largest producers is experiencing “intermittent manufacturing delays” and that other makers cannot keep up with demand. Some patients say the announcement was a belated acknowledgment of a reality they have faced for months — pharmacies unable to fill their orders and anxiety about whether they will run out of a medication needed to manage their daily lives. Experts say it is often difficult for patients to access Adderall, a stimulant that is tightly regulated as a controlled substance because of high potential for abuse. Medication management generally requires monthly doctor visits. There have been other shortages in recent years. “This one is more sustained,” said Timothy Wilens, an ADHD expert and chief of child and adolescent psychiatry at Massachusetts General Hospital who said access issues stretch back to spring. “It’s putting pressure on patients, and it’s putting pressure on institutions that support the patients.” Erik Gude, a 28-year-old chef who lives in Atlanta, experiences regular challenges filling his Adderall prescription, whether it’s pharmacies not carrying generic versions or disputes with insurers. He has been off the medication for a month after his local pharmacy ran out.

Keyword: ADHD; Drug Abuse
Link ID: 28520 - Posted: 10.22.2022

Kate Siber Sharon Maxwell spent much of her life trying to make herself small. Her family put her on her first diet when she was 10. Early on Saturday mornings, she and her mother would drive through the empty suburban streets of Hammond, Ind., to attend Weight Watchers meetings. Maxwell did her best at that age to track her meals and log her points, but the scale wasn’t going down fast enough. So she decided to barely eat anything on Fridays and take laxatives that she found in the medicine cabinet. Food had long been a fraught subject in the Maxwell household. Her parents were also bigger-bodied and dieted frequently. They belonged to a fundamentalist Baptist megachurch where gluttony was seen as a sin. To eat at home was to navigate a labyrinth of rules and restrictions. Maxwell watched one time as her mother lost 74 pounds in six months by consuming little more than carrot juice (her skin temporarily turned orange). Sometimes her father, seized with a new diet idea, abruptly ransacked shelves in the kitchen, sweeping newly forbidden foods into the trash. Maxwell was constantly worried about eating too much. She started to eat alone and in secret. She took to chewing morsels and spitting them out. She hid food behind books, in her pockets, under mattresses and between clothes folded neatly in drawers. Through Maxwell’s teenage years and early 20s, eating became even more stressful. Her thoughts constantly orbited around food: what she was eating or not eating, the calories she was burning or not burning, the size of her body and, especially, what people thought of it. Her appearance was often a topic of public interest. When she went grocery shopping for her family, other customers commented on the items in her cart. “Honey, are you sure you want to eat that?” one person said. Other shoppers offered unsolicited advice about diets. Strangers congratulated her when her cart was filled with vegetables. As she grew older, people at the gym clapped and cheered for her while she worked out. “People would say: ‘Go! You can lose the weight!’” she says. While eating in public, other diners offered feedback — and still do to this day — on her choices, a few even asking if she wanted to join their gym. Some would call her names: Pig, Fatty. Sometimes people told her she was brave for wearing shorts, while others said she should cover up. She was always aware, whether she wanted to be or not, of how others viewed her body. © 2022 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 28519 - Posted: 10.19.2022

By Sandra G. Boodman For years Carter Caldwell had adamantly rejected doctors’ recommendations that he consider surgery to treat the frequent, uncontrolled seizures that were ravaging his brain. Caldwell, who had developed epilepsy when he was 28, regarded the operation that involved removing a portion of his brain as too big a risk — particularly because doctors weren’t sure what was causing the seizures and couldn’t pinpoint their location. Instead the Philadelphia business executive had organized his life to minimize certain foreseeable hazards: He lived downtown and didn’t drive. He didn’t push his toddler’s stroller. When taking the train he stood at the back of the platform — nowhere near the tracks in case he suddenly collapsed. His colleagues at work knew about his condition. But that calculus changed abruptly in November 2014. Caldwell, accompanied by his wife, Connie, and their 3-year-old son, was atop a hill at Pennsylvania’s Valley Forge National Historical Park posing for photos for a holiday card. Without warning he began an awkward shuffling walk that signified the onset of a seizure. Then he lost consciousness and fell head first down a rocky 15-foot embankment before landing at the edge of a stream. “Thankfully,” he said, “I didn’t roll into the stream.” He spent the next 2 1/2 weeks in a nearby hospital where a plastic surgeon performed multiple operations on his broken jawbone, lacerated cheek and shattered eye socket. “I remember him saying, ‘I can’t believe this happened in front of my family,’ ” recalled his longtime neurologist John R. Pollard, formerly associate director of the epilepsy center at the University of Pennsylvania. Pollard had warned Caldwell that his intractable seizures, which had proved resistant to numerous medications, placed him at risk for sudden death or serious injury. In September 2015 a successful operation unmasked the very unusual cause of Caldwell’s seizures, a culprit experts had long suspected but had been unable to definitively identify.

Keyword: Epilepsy; Emotions
Link ID: 28518 - Posted: 10.19.2022

By Jyoti Madhusoodanan Q: I recently started taking an S.S.R.I. antidepressant, but I have been confused about whether it’s safe to drink alcohol. Some internet sources say it’s fine, others say to avoid drinking completely. Help! For many health care providers who treat anxiety and depression, the concern about whether it’s safe — or even advised — to drink alcohol while taking an antidepressant is a common one. “Patients tell me all the time, ‘I’m going to be drinking with friends tonight, so I skipped a dose,’” said Dr. Sarah Ramsay Andrews, a psychiatrist at the Johns Hopkins University School of Medicine. But skipping a dose is never a good idea, said Dr. Jody Glance, an addiction medicine specialist at the University of Pittsburgh Medical Center Western Behavioral Health — even if you’re going out for cocktails with friends. “When people stop taking their medicines for a day or two, they often don’t resume, and that can lead to a relapse of anxiety or depression.” Besides, she added, how safe it is to drink while on antidepressants depends on the kind of antidepressant you’re taking — and for most people taking selective serotonin reuptake inhibitors (or S.S.R.I.s), an occasional drink likely won’t do much harm. There are, however, caveats to keep in mind. S.S.R.I. medications — which include citalopram (Celexa), sertraline (Zoloft) and escitalopram (Lexapro) — are the most commonly prescribed class of antidepressants. They are typically used to help treat depression, and can also be effective for other conditions like anxiety, obsessive compulsive disorder, certain phobias and even premenstrual dysphoric disorder. They work by increasing the levels of the brain chemical serotonin — which is thought to influence your mood and emotions, among other things — by blocking its removal after it carries messages in the brain. But unlike many other medications used to treat mood disorders — like the anxiety medication alprazolam (Xanax) or the tricyclic antidepressant amitriptyline (Elavil) — S.S.R.I.s are less likely to interact with alcohol than other kinds of drugs, Dr. Glance said. © 2022 The New York Times Company

Keyword: Depression; Drug Abuse
Link ID: 28517 - Posted: 10.19.2022

Nicola Davis Science correspondent Playing sounds while you slumber might help to strengthen some memories while weakening others, research suggests, with experts noting the approach might one day help people living with traumatic recollections. Previous work has shown that when a sound is played as a person learns an association between two words, the memory of that word association is boosted if the same sound is played while the individual sleeps. Now researchers have found fresh evidence the approach could also be used to weaken such memories. “We can an actually induce forgetting of specific material whilst people are asleep,” said Dr Aidan Horner, co-author of the study from the University of York. Advertisement Writing in the journal Learning & Memory, Horner and colleagues report how 29 participants were shown pairs of words on a computer screen, one of which was an object word, such as bicycle, while the other was either a place word, such as office, or a person, such as David Beckham. The process was repeated for 60 different object words, and in the course of the process both possible pairings were shown, resulting in 120 associations. As the pairs flashed up, participants heard the object word being spoken out loud. The team tested the participants on a subset of the associations, presenting them with one of the words and asking them to select a paired word from a list of six options. Participants then spent a night in the team’s sleep laboratory. Once they had entered a particular sleep state – as judged by electrodes placed on their heads – they were played audio of 30 of the object words. The team tested participants on the word associations the next day. The results reveal participants’ ability to recall the first word they had learned to pair with an object word was boosted if audio of the latter was played as they slept, compared with if it was not played. However, their ability to recall the second word they learned to associate with the same object decreased relative to the audio-free scenario. © 2022 Guardian News & Media Limited

Keyword: Sleep; Learning & Memory
Link ID: 28516 - Posted: 10.19.2022

McKenzie Prillaman A twist on functional magnetic resonance imaging (fMRI) offers a multi-fold improvement in its time sensitivity, better enabling it to unveil the fine-scale dynamics underlying mental processes. Researchers published the results on 13 October in Science1. Can brain scans reveal behaviour? Bombshell study says not yet A standard fMRI technique measures brain activity indirectly, by tracking increases in blood flow in regions where neurons are suddenly consuming more oxygen. This signal, however, can lag behind neuronal activity by 1 second, which dampens time sensitivity — the speedy cells take mere milliseconds to send messages to one another. Jang-Yeon Park, an MRI physicist at Sungkyunkwan University in Suwon, South Korea, set out to enhance fMRI’s temporal precision to track neuronal activity on the order of milliseconds. He and his colleagues accomplished this by changing the software of a high-intensity MRI scanner to acquire data every 5 milliseconds — about 8 times faster than what the standard technique can capture — and applying frequent, repetitive stimulation to animals they were testing. This suppressed the slower-paced blood oxygenation signal, making it possible to observe faster-paced brain activity. The researchers named their technique direct imaging of neuronal activity, or DIANA. In the study, an anaesthetized mouse inside an MRI scanner received a minor electric shock to its face every 200 milliseconds. Between shocks, the machine acquired data from one tiny region of the mouse’s brain every 5 milliseconds. It moved on to a new area after the next electric shock. After the software stitched everything together, the process produced a head-on image of one full slice of the brain, capturing neuronal activity over a 200-millisecond time period. (Spatial resolution was 0.22 millimetres, which is standard for high-intensity MRI.) During the scan, the facial stimulation activated a part of the brain that processes sensory inputs, causing the region to light up with a signal. The researchers found that this ‘DIANA response’ happened at the same time that neurons fired off signals, or ‘spiked’ — activity that was measured separately, using a surgically inserted probe. Furthermore, the team was able to trace the DIANA signal through a brain circuit as groups of neurons sequentially triggered each other. © 2022 Springer Nature Limited

Keyword: Brain imaging
Link ID: 28515 - Posted: 10.15.2022

By Lisa Sanders, M.D. “What just happened?” The 16-year-old girl’s voice was flat and tired. “I think you had a seizure,” her mother answered. Her daughter had asked to be taken to the pediatrician’s office because she hadn’t felt right for the past several weeks — not since she had what looked like a seizure at school. And now she’d had another. “You’re OK now,” the mother continued. “It’s good news because it means that maybe we finally figured out what’s going on.” To most people, that might have been a stretch — to call having a seizure good news. But for the past several years, the young woman had been plagued by headaches, episodes of dizziness and odd bouts of profound fatigue, and her mother embraced the possibility of a treatable disorder. The specialists she had taken her daughter to see attributed her collection of symptoms to the lingering effect of the many concussions she suffered playing sports. She had at least one concussion every year since she was in the fourth grade. Because of her frequent head injuries, her parents made her drop all her sports. Even when not on the playing field, the young woman continued to fall and hit her head. The headaches and other symptoms persisted long after each injury. She saw several specialists who agreed that she had what was called persistent post-concussive syndrome — symptoms caused either by a severe brain injury or, in her case, repeated mild injuries. She should get better with time and patience, the girl and her mother were told. And yet her head pounded and she retreated to her darkened room several times a week. She did everything her doctors suggested: She got plenty of sleep, rested when she was tired and tried to be patient. But she still got headaches, still got dizzy. She found it harder and harder to pay attention. For the past couple of years, it had even started to affect her grades. © 2022 The New York Times Company

Keyword: Epilepsy; Attention
Link ID: 28514 - Posted: 10.15.2022

Andrew Gregory Health editor Scientists have discovered that it may be possible to spot signs of dementia as early as nine years before patients receive an official diagnosis. The findings raise the possibility that, in the future, at-risk people could be screened to help select those who could benefit from interventions, or help identify patients suitable for clinical trials for new treatments. Researchers at Cambridge University published the study – funded by the Medical Research Council with support from the NIHR Cambridge Biomedical Research Centre – in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. Dr Richard Oakley, associate director of research at the Alzheimer’s Society, said the “important” findings suggested that “for some people who go on to develop Alzheimer’s disease, memory and thinking problems can begin up to nine years before they receive a diagnosis”. Advertisement He added: “This opens up the possibility of screening programmes in the future to help identify people at risk and who may benefit from interventions, and identify more people suitable for clinical trials for new dementia treatments, which are both so desperately needed.” The study’s first author, Nol Swaddiwudhipong, said: “When we looked back at patients’ histories, it became clear that they were showing some cognitive impairment several years before their symptoms became obvious enough to prompt a diagnosis. The impairments were often subtle, but across a number of aspects of cognition. “This is a step towards us being able to screen people who are at greatest risk – for example, people over 50 or those who have high blood pressure or do not do enough exercise – and intervene at an earlier stage to help them reduce their risk.” Man in bed with pillow over his head. © 2022 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 28513 - Posted: 10.15.2022

Allison Whitten Our understanding of the inner workings of the human brain has long been held back by the practical and ethical difficulty of observing human neurons develop, connect and interact. Today, in a new study published in Nature, neuroscientists at Stanford University led by Sergiu Paşca report that they have found a new way to study human neurons — by transplanting human brainlike tissue into rats that are just days old, when their brains have not yet fully formed. The researchers show that human neurons and other brain cells can grow and integrate themselves into the rat’s brain, becoming part of the functional neural circuitry that processes sensations and controls aspects of behaviors. Using this technique, scientists should be able to create new living models for a wide range of neurodevelopmental disorders, including at least some forms of autism spectrum disorder. The models would be just as practical for neuroscientific lab studies as current animal models are but would be better stand-ins for human disorders because they would consist of real human cells in functional neural circuits. They could be ideal targets for modern neuroscience tools that are too invasive to use in real human brains. “This approach is a step forward for the field and offers a new way to understand disorders of neuronal functioning,” said Madeline Lancaster, a neuroscientist at the MRC Laboratory of Molecular Biology in Cambridge, U.K., who was not involved in the work. The work also marks an exciting new chapter in the use of neural organoids. Nearly 15 years ago, biologists discovered that human stem cells could self-organize and grow into small spheres that held different types of cells and resembled brain tissue. These organoids opened a new window into the activities of brain cells, but the view has its limits. While neurons in a dish can connect to each other and communicate electrically, they can’t form truly functional circuits or attain the full growth and computational prowess of healthy neurons in their natural habitat, the brain. Pioneering work by various research groups proved years ago that human brain organoids could be inserted into the brains of adult rats and survive. But the new study shows for the first time that the burgeoning brain of a newborn rat will accept human neurons and allow them to mature, while also integrating them into local circuits capable of driving the rat’s behavior. All Rights Reserved © 2022

Keyword: Development of the Brain
Link ID: 28512 - Posted: 10.13.2022

Heidi Ledford Hundreds of thousands of human neurons growing in a dish coated with electrodes have been taught to play a version of the classic computer game Pong1. In doing so, the cells join a growing pantheon of Pong players, including pigs taught to manipulate joysticks with their snout2 and monkeys wired to control the game with their minds. (Google’s DeepMind artificial-intelligence (AI) algorithms mastered Pong many years ago3 and have moved on to more-sophisticated computer games such as StarCraft II4.) The gamer cells respond not to visual cues on a screen but to electrical signals from the electrodes in the dish. These electrodes both stimulate the cells and record changes in neuronal activity. Researchers then converted the stimulation signals and the cellular responses into a visual depiction of the game. The results are reported today in Neuron. The work is a proof of principle that neurons in a dish can learn and exhibit basic signs of intelligence, says lead author Brett Kagan, chief scientific officer at Cortical Labs in Melbourne, Australia. “In current textbooks, neurons are thought of predominantly in terms of their implication for human or animal biology,” he says. “They’re not thought about as an information processor, but a neuron is this amazing system that can process information in real time with very low power consumption.” Although the company calls its system DishBrain, the neurons are a far cry from an actual brain, Kagan says, and show no signs of consciousness. The definition of intelligence is also hotly debated; Kagan defines it as the ability to collate information and apply it in an adaptive behaviour in a given environment. Cortical Labs’ work follows on work by neuroengineer Steve Potter, now at the Georgia Institute of Technology in Atlanta, and his colleagues. In 2008, the team reported that neurons cultured from rats can exhibit learning and goal-directed behaviour5,6. Animated gif of 4 different microscopy images of different Dishbrain neural cells with different coloured fluorescent markers. © 2022 Springer Nature Limited

Keyword: Learning & Memory; Intelligence
Link ID: 28511 - Posted: 10.13.2022

By Diana Kwon A Scottish woman named Joy Milne made headlines in 2015 for an unusual talent: her ability to sniff out people afflicted with Parkinson’s disease, a progressive neurodegenerative illness that is estimated to affect nearly a million people in the U.S. alone. Since then a group of scientists in the U.K. has been working with Milne to pinpoint the molecules that give Parkinson’s its distinct olfactory signature. The team has now zeroed in on a set of molecules specific to the disease—and has created a simple skin-swab-based test to detect them. Milne, a 72-year-old retired nurse from Perth, Scotland, has hereditary hyperosmia, a condition that endows people with a hypersensitivity to smell. She discovered that she could sense Parkinson’s with her nose after noticing her late husband, Les, was emitting a musky odor that she had not detected before. Eventually, she linked this change in scent to Parkinson’s when he was diagnosed with the disease many years later. Les passed away in 2015. In 2012 Milne met Tilo Kunath, a neuroscientist at the University of Edinburgh in Scotland, at an event organized by the research and support charity Parkinson’s UK. Although skeptical at first, Kunath and his colleagues decided to put Milne’s claims to the test. They gave her 12 T-shirts, six from people with Parkinson’s and six from healthy individuals. She correctly identified the disease in all six cases—and the one T-shirt from a healthy person she categorized as having Parkinson’s belonged to someone who went on to be diagnosed with the disease less than a year later. Advertisement Subsequently, Kunath, along with chemist Perdita Barran of the University of Manchester in England and her colleagues, has been searching for the molecules responsible for the change in smell that Milne can detect. The researchers used mass spectrometry to identify types and quantities of molecules in a sample of sebum, an oily substance found on the skin’s surface. They discovered changes to fatty molecules known as lipids in people with Parkinson’s. © 2022 Scientific American

Keyword: Chemical Senses (Smell & Taste); Parkinsons
Link ID: 28510 - Posted: 10.13.2022

By Paula Span The world of hearing health will change on Oct. 17, when the Food and Drug Administration’s new regulations, announced in August, will make quality hearing aids an over-the-counter product. It just won’t transform as quickly or as dramatically, at least at first, as advocates, technology and consumer electronics companies and people with mild to moderate hearing loss have been hoping. “It finally, actually happened after all these years,” said Dr. Frank Lin, the director of the Johns Hopkins Cochlear Center for Hearing and Public Health and a longtime supporter of the regulations, which Congress authorized five years ago. “Ninety-plus percent of adults with hearing loss have needs that can be served by over-the-counter hearing aids,” he said. For decades, the sale of hearing aids was restricted to licensed audiologists and other professionals; that has kept prices high — prescription hearing aids can cost $4,000 to $5,000 — and access limited. In contrast, the regulations provide “a clear glide path for new companies to enter this field,” Dr. Lin said. But, he quickly added, “it may be the Wild West for the next few years.” Barbara Kelley, the executive director of the Hearing Loss Association of America, concurred: “It’s a new frontier, and it is confusing. We need time to see how the market settles out.” In an ideal scenario, a person would be able to walk into almost any pharmacy or big-box store and buy a sophisticated pair of hearing aids for a few hundred dollars, no prescription required. But the shift won’t materialize right away, experts say. In 2017, Congress granted the F.D.A. three years to develop standards for safe and effective over-the-counter hearing aids. The agency took five years instead, and the long delay and continued industry opposition made manufacturers skittish about investing, Dr. Lin said. © 2022 The New York Times Company

Keyword: Hearing
Link ID: 28509 - Posted: 10.13.2022

By Greg Miller If you’re lucky enough to live to 80, you’ll take up to a billion breaths in the course of your life, inhaling and exhaling enough air to fill about 50 Goodyear blimps or more. We take about 20,000 breaths a day, sucking in oxygen to fuel our cells and tissues, and ridding the body of carbon dioxide that builds up as a result of cellular metabolism. Breathing is so essential to life that people generally die within minutes if it stops. It’s a behavior so automatic that we tend to take it for granted. But breathing is a physiological marvel — both extremely reliable and incredibly flexible. Our breathing rate can change almost instantaneously in response to stress or arousal and even before an increase in physical activity. And breathing is so seamlessly coordinated with other behaviors like eating, talking, laughing and sighing that you may have never even noticed how your breathing changes to accommodate them. Breathing can also influence your state of mind, as evidenced by the controlled breathing practices of yoga and other ancient meditative traditions. In recent years, researchers have begun to unravel some of the underlying neural mechanisms of breathing and its many influences on body and mind. In the late 1980s, neuroscientists identified a network of neurons in the brainstem that sets the rhythm for respiration. That discovery has been a springboard for investigations into how the brain integrates breathing with other behaviors. At the same time, researchers have been finding evidence that breathing may influence activity across wide swaths of the brain, including ones with important roles in emotion and cognition. “Breathing has a lot of jobs,” says Jack L. Feldman, a neuroscientist at the University of California, Los Angeles, and coauthor of a recent article on the interplay of breathing and emotion in the Annual Review of Neuroscience. “It’s very complicated because we’re constantly changing our posture and our metabolism, and it has to be coordinated with all these other behaviors.” © 2022 Annual Reviews

Keyword: ADHD
Link ID: 28508 - Posted: 10.08.2022

Ian Sample Science editor It was while watching University Challenge that the doctor first suspected something wrong with Jeremy Paxman. Normally highly animated, the TV presenter was less effusive and exuberant than usual. He had acquired what specialists in the field call the “Parkinson’s mask”. Paxman was formally diagnosed with Parkinson’s disease in hospital after he collapsed while walking his dog and found himself in hospital. There, Paxman recalled in an ITV documentary, the doctor walked in and said: “I think you’ve got Parkinson’s”. For Paxman, at least, the news came out of the blue. Parkinson’s was first described in medical texts more than 200 years ago, yet there is still no cure. It’s a common condition, particularly in the over-50s. About 1 in 37 people in the UK will be diagnosed at some point in their life. Existing drugs aim to manage patients’ symptoms, rather than slow down or stop the condition’s progression. But scientists have made progress in understanding the neurodegenerative disorder. The hope now is that gamechanging therapies are finally on the horizon. Advertisement “Parkinson’s is a hugely complex condition and there’s probably no single cure,” says Katherine Fletcher, a research communications manager at Parkinson’s UK. “It’s the progressive loss of dopamine-producing cells in the brain. If you want to slow or stop the condition, you somehow need to protect those cells or maybe even regrow those cells in the brain. That is the ultimate goal.” Why brain cells die off in Parkinson’s is still unknown. The condition strikes a brain region called the substantia nigra, where neurons make a chemical called dopamine. The loss of these brain cells causes dopamine to plunge, and this drives most of the problems patient’s experience. It is not a fast decline: typically, patients only become aware of symptoms when about 80% of nerve cells in the substantia nigra have failed. © 2022 Guardian News & Media Limited or its affiliated companies.

Keyword: Parkinsons
Link ID: 28507 - Posted: 10.08.2022

By Laura Sanders In a football game on September 25, Miami Dolphins quarterback Tua Tagovailoa got the pass off but he got knocked down. Fans watched him shake his head and stumble to the ground as he tried to jog it off. After a medical check, he went back into the game against the Buffalo Bills with what his coach later said was a back injury. Four days later, in a game against the Cincinnati Bengals, Tagovailoa, 24, got hit again. This time, he left the field on a stretcher with what was later diagnosed as a concussion. Many observers suspect that the first hit — given Tagovailoa’s subsequent headshaking and wobbliness — left the athlete with a concussion, also called a mild traumatic brain injury. If those were indeed signs of a head injury, that first hit may have lined him up for an even worse brain injury just days later. “The science tells us that yes, a person who is still recovering from a concussion is at an elevated risk for sustaining another concussion,” says Kristen Dams-O’Connor, a neuropsychologist and director of the Brain Injury Research Center at the Icahn School of Medicine at Mount Sinai in New York City. As one example, a concussion roughly doubled the chance of a second one among young Swedish men, researchers reported in 2013 in the British Medical Journal. “This, I think, was avoidable,” Dams-O’Connor says of Tagovailoa’s brain injury in the game against the Bengals. After a hit to the head, when the soft brain hits the unyielding skull, the injury kicks off a cascade of changes. Some nerve cells become overactive, inflammation sets in, and blood flow is altered. These downstream events in the brain — and how they relate to concussion symptoms — can happen over hours and days, and are not easy to quickly measure, Dams-O’Connor says. © Society for Science & the Public 2000–2022.

Keyword: Brain Injury/Concussion
Link ID: 28506 - Posted: 10.08.2022