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

By Phil Jaekl One fine spring afternoon this year, as I was out running errands in the small Norwegian town where I live, a loud beep startled me into awareness. What had just been on my mind? After a moment’s pause, I realized something strange. I’d been thinking two things at the same time—rehearsing the combination of a new bike lock and contemplating whether I should wear the clunky white beeper that had just sounded into a bank. How, I wondered, could I have been saying two things simultaneously in my mind? Was I deceiving myself? Was this, mentally, normal? I silenced the beeper on my belt and pulled out my phone to make a voice memo of the bizarre experience before I walked into the bank; aesthetics be damned. I was in the midst of an experiment that involved keeping a log of my inner thoughts for Russ Hurlburt, a senior psychologist at the University of Las Vegas. For decades, Hurlburt has been motivated by one question: How, exactly, do we experience our own mental life? It’s a simple enough question. And, one might argue, an existentially important one. But it’s a surprisingly vexing query to try to answer. Once we turn our gaze inward, the subjective squishiness of our mental experience seems to defy objective scrutiny. For centuries, philosophers and psychologists have presumed our mental life is composed primarily of a single-stream inner monologue. I know that’s what I had assumed, and my training in cognitive neuroscience had never led me to suppose otherwise. Hurlburt, however, finds this armchair conclusion “dramatically wrong.”1 © 2022 NautilusThink Inc,

Keyword: Attention; Consciousness
Link ID: 28505 - Posted: 10.08.2022

Inside a Berlin neuroscience lab one day last year, Subject 1 sat on a chair with their arms up and their bare toes pointed down. Hiding behind them, with full access to the soles of their feet, was Subject 2, waiting with fingers curled. At a moment of their choosing, Subject 2 was instructed to take the open shot: Tickle the hell out of their partner. In order to capture the moment, a high-speed GoPro was pointed at Subject 1’s face and body. Another at their feet. A microphone hung nearby. As planned, Subject 1 couldn’t help but laugh. The fact that they couldn’t help it is what has drawn Michael Brecht, leader of the research group from Humboldt University, to the neuroscience of tickling and play. It’s funny, but it’s also deeply mysterious—and understudied. “It’s been a bit of a stepchild of scientific investigation,” Brecht says. After all, brain and behavior research typically skew toward gloom, topics like depression, pain, and fear. “But,” he says, “I think there are also more deep prejudices against play—it's something for children.” The prevailing wisdom holds that laughter is a social behavior among certain mammals. It’s a way of disarming others, easing social tensions, and bonding. Chimps do it. Dogs and dolphins too. Rats are the usual subjects in tickling studies. If you flip ’em over and go to town on their bellies, they’ll squeak at a pitch more than twice as high as the limit of human ears. But there are plenty of lingering mysteries about tickling, whether among rats or people. The biggest one of all: why we can’t tickle ourselves. “If you read the ancient Greeks, Aristotle was wondering about ticklishness. Also Socrates, Galileo Galilei, and Francis Bacon,” says Konstantina Kilteni, a cognitive neuroscientist who studies touch and tickling at Sweden’s Karolinska Institutet, and who is not involved in Brecht’s work. We don’t know why touch can be ticklish, nor what happens in the brain. We don’t know why some people—or some body parts—are more ticklish than others. “These questions are very old,” she continues, “and after almost 2,000 years, we still really don’t have the answer.” © 2022 Condé Nast.

Keyword: Attention; Emotions
Link ID: 28504 - Posted: 10.08.2022

By Erin Blakemore Empathy and generosity are two traits that arguably make the world go ‘round. But a study suggests that the willingness to help collapses when people get too little — or poor — sleep. To see how sleep affects how much humans help one another, researchers conducted three experiments designed to examine the issue from the individual to the societal scale. Their results are published in PLOS Biology. In the first experiment, researchers performed functional magnetic resonance imaging scans of the brain and asked questions to 24 adults after eight hours of sleep and after a night with no sleep. When they were well rested, the participants scored well on a helping behavior test. But after sleep deprivation, 78 percent had less of a desire to help others, even when it came to friends and family. The scans showed that areas of the brain associated with social cognition — our thought processes related to other people — were less active with sleep deprivation. The second experiment tracked 136 healthy adults over four nights and asked them questions about helping the following day. The effect held for them, too, and those who reported worse sleep quality scored worse on the tests. Just one hour of extra sleep each night can lead to better eating habits To test the effects on a societal level, the researchers then looked at a database of 3 million charitable donations given between 2001 and 2016. They found that immediately following the beginning of daylight saving time — a notorious sleep disrupter — donations dropped 10 percent. The effect wasn’t found in data from Hawaii or Arizona, however; neither observe DST. Nor did the shift back to standard time have such an association with donations.

Keyword: Sleep; Emotions
Link ID: 28503 - Posted: 10.08.2022

Jon Hamilton Drugs like magic mushrooms and LSD can act as powerful and long-lasting antidepressants. But they also tend to produce mind-bending side-effects that limit their use. Now, scientists report in the journal Nature that they have created drugs based on LSD that seem to relieve anxiety and depression – in mice – without inducing the usual hallucinations. "We found our compounds had essentially the same antidepressant activity as psychedelic drugs," says Dr. Bryan Roth, an author of the study and a professor of pharmacology at UNC Chapel Hill School of Medicine. But, he says, "they had no psychedelic drug-like actions at all." The discovery could eventually lead to medications for depression and anxiety that work better, work faster, have fewer side effects, and last longer. The success is just the latest involving tripless versions of psychedelic drugs. One previous effort created a hallucination-free variant of ibogaine, which is made from the root bark of a shrubby plant native to Central Africa known as the iboga tree. "It's very encouraging to see multiple groups approach this problem in different ways and come up with very similar solutions," says David E. Olson, a chemical neuroscientist at the University of California, Davis, who led the ibogaine project. The new drug comes from a large team of scientists who did not start out looking for an antidepressant. They had been building a virtual library of 75 million molecules that include an unusual structure found in a number of drugs, including the psychedelics psilocybin and LSD, a migraine drug (ergotamine), and cancer drugs including vincristine. The team decided to focus on molecules that affect the brain's serotonin system, which is involved in regulating a person's mood. But they still weren't looking for an antidepressant. Roth recalls that during one meeting, someone asked, "What are we looking for here anyway? And I said, well, if nothing else, we'll have the world's greatest psychedelic drugs." © 2022 npr

Keyword: Depression; Drug Abuse
Link ID: 28502 - Posted: 10.05.2022

By Dan Diamond A high-profile NFL injury has put the spotlight back on football’s persistent concussions, which are linked to head trauma and a variety of long-lasting symptoms, and can be worsened by rushing back to physical activity. Miami Dolphins quarterback Tua Tagovailoa, who appeared to suffer head trauma in a game Sunday afternoon that was later described as a back injury, was diagnosed with a concussion Thursday night following a tackle. After Tagovailoa’s head hit the turf, he remained on the ground and held his arms and fingers splayed in front of his face — which experts said evoked conditions known as “decorticate posturing” or “fencing response,” where brain damage triggers the involuntary reaction. “It’s a potentially life-threatening brain injury,” said Chris Nowinski, a neuroscientist and co-founder of the Concussion Legacy Foundation, a nonprofit group focused on concussion research and prevention, adding that he worried about Tagovailoa’s long-term prognosis, given that it can take months or years for an athlete to fully recover from repeated concussions. Nowinski said he was particularly concerned about situations where people suffer two concussions within a short period — a condition sometimes known as second impact syndrome — which can lead to brain swelling and other persistent problems. “That’s why we should at least be cautious with the easy stuff, like withholding players with a concussion from the game and letting their brain recover,” Nowinski said. The Dolphins said Tagovailoa had movement in all of his extremities and had been discharged Thursday night from University of Cincinnati Medical Center. The NFL’s top health official said in an interview on Friday that he was worried about Tagovailoa’s health, and pointed to a joint review the league and its players association was conducting into the Dolphins’ handling of the quarterback’s initial injury on Sunday.

Keyword: Brain Injury/Concussion
Link ID: 28501 - Posted: 10.05.2022

By Benjamin Mueller Svante Pääbo, a Swedish scientist who peered back into human history by retrieving genetic material from 40,000-year-old bones, producing a complete Neanderthal genome and launching the field of ancient DNA studies, was awarded the Nobel Prize in Physiology or Medicine on Monday. The prize recognized an improbable scientific career. Having once dreamed of becoming an Egyptologist, Dr. Pääbo devoted his early years of research to extracting genetic material from mummies, only for that research to run aground because the samples might have become contaminated by his and his colleagues’ own DNA. Within about two decades, in 2006, he had launched an unlikely effort to decipher a Neanderthal genome. He designed so-called clean rooms dedicated to handling ancient DNA, which protected his fossils from the genetic material of living humans. And dramatic advances in sequencing technology allowed him to decode the sort of badly damaged DNA found in ancient bones. “It was certainly considered to be impossible to recover DNA from 40,000-year-old bones,” said Dr. Nils-Göran Larsson, the chairman of the Nobel Committee for Physiology or Medicine and a professor of medical biochemistry at the Karolinska Institute in Stockholm. In 2010, Dr. Pääbo unveiled the Neanderthal genome. The publication opened a window into questions about what made early humans different from modern ones. It also helped scientists track genetic differences in modern humans and understand what role those differences play in disease, including Covid-19. In 2020, Dr. Pääbo and a colleague found that the coronavirus caused more severe symptoms in people who had inherited a stretch of Neanderthal DNA. Even some of Dr. Pääbo’s biggest admirers described the prize as unexpected. Analysts have long speculated that the scientists who sequenced the modern human genome were strong contenders for a Nobel Prize, not thinking that the scientist who sequenced Neanderthal DNA would get there first. But geneticists said that the two projects were interwoven: Rapid advances in sequencing technology that followed the beginning of the Human Genome Project in 1990, they said, helped Dr. Pääbo to interpret tiny quantities of Neanderthal DNA, damaged as they were from tens of thousands of years underground. © 2022 The New York Times Company

Keyword: Evolution; Genes & Behavior
Link ID: 28500 - Posted: 10.05.2022

By Claudia Lopez Lloreda If you look at parts of the circulatory system of whales and dolphins, you might think that you are looking at a Jackson Pollock painting, not blood vessels. These cetaceans have especially dense, complex networks of blood vessels mainly associated with the brain and spine, but scientists didn’t know why. A new analysis suggests that the networks protect cetaceans’ brains from the pulses of blood pressure that the animals endure while diving deep in the ocean, researchers report in the Sept. 23 Science. Whales and dolphins “have gone through these really amazing vascular adaptations to support their brain,” says Ashley Blawas, a marine scientist at the Duke University Marine Lab in Beaufort, N.C., who was not involved with the research. Called retia mirabilia, which means “wonderful nets,” the blood vessel networks are present in some other animals besides cetaceans, including giraffes and horses. But the networks aren’t found in other aquatic vertebrates that move differently from whales, such as seals. So scientists had suspected that the cetaceans’ retia mirabilia play a role in controlling blood pressure surges. When whales and dolphins dive, they move their tail up and down in an undulating manner, which creates surges in blood pressure. Land animals that experience similar surges, like galloping horses, are able to release some of this pressure by exhaling. But some cetaceans hold their breath to dive for long periods of time (SN: 9/23/20). Without a way to relieve that pressure, those blasts could tear blood vessels and harm other organs, including the brain. In the new study, biomechanics researcher Margo Lillie of the University of British Columbia in Vancouver and colleagues used data on the morphology of 11 cetacean species to create a computational model that can simulate the animals’ retia mirabilia. It revealed that the arteries and veins in this tangle of blood vessels are really close and may even sometimes be joined. As a result, the retia mirabilia could equalize the differences in blood pressure generated by diving, perhaps by redistributing the blood pulses from arteries to veins and vice versa. This way, the networks get rid of, or at least weaken, huge blood pressure surges that might otherwise reach and devastate the brain. © Society for Science & the Public 2000–2022.

Keyword: Brain imaging
Link ID: 28499 - Posted: 10.05.2022

Nicola Davis Science correspondent Whether it’s a tricky maths problem or an unexpected bill, daily life is full of stressful experiences. Now researchers have found that humans produce a different odour when under pressure – and dogs can sniff it out. While previous studies have suggested canines might pick up on human emotions, possibly through smell, questions remained over whether they could detect stress and if this could be done through scent. “This study has definitively proven that people, when they have a stress response, their odour profile changes,” said Clara Wilson, a PhD student at Queen’s University Belfast, and first author of the research. Wilson added the findings could prove useful when training service dogs, such as those that support people with post-raumatic stress disorder (PTSD). “They’re often trained to look at someone either crouching down on the floor, or starting to do self-injurious behaviours,” said Wilson.. The latest study, she said, offers another potential cue. “There is definitely a smell component, and that might be valuable in the training of these dogs in addition to all of the visual stuff,” said Wilson. Writing in the journal Plos One, Wilson and colleagues report how they first constructed a stand bearing three containers, each topped by a perforated lid. The researchers report they were able to train four dogs to indicate the container holding a particular breath and sweat sample, even when the line-up included unused gauze, samples from another person, or samples from the same person taken at a different time of day. © 2022 Guardian News & Media Limited

Keyword: Stress; Chemical Senses (Smell & Taste)
Link ID: 28498 - Posted: 10.01.2022

McKenzie Prillaman Some researchers are celebrating this week’s announcement that a drug candidate for Alzheimer’s disease slowed the rate of cognitive decline for people in a clinical trial by 27%. Others, however, remain hesitant, wanting to see data beyond what was disclosed in a 27 September press release. If the results stand up, the treatment — called lecanemab — would be the first of its kind to show a strong signal of cognitive benefit in a robust trial. “It’s such a win for our field,” says Liana Apostolova, a neurologist at the Indiana University School of Medicine in Indianapolis. The results are “quite promising”, says Caleb Alexander, an internal-medicine specialist and epidemiologist at the Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland, and an advisory committee member for the US Food and Drug Administration (FDA). But, he adds, “we’ll have to see what the full analysis of the trial suggests”. Alexander and others also note that, although the results indicate that lecanemab does provide some clinical benefit, the degree to which it does so is small. Developed by Eisai, a pharmaceutical company in Tokyo, and biotechnology firm Biogen in Cambridge, Massachusetts, lecanemab is a monoclonal antibody designed to clear clumps of protein from the brain that many think are a root cause of Alzheimer’s disease. This theory, known as the ‘amyloid hypothesis’, holds that the protein amyloid-β accumulates into toxic deposits as the disease progresses, ultimately causing dementia. Whether or not lecanemab confirms the amyloid hypothesis remains to be seen, researchers say. “I don’t think one study will prove a very long-standing controversial hypothesis,” says Brent Forester, director of the Geriatric Psychiatry Research Program at McLean Hospital in Belmont, Massachusetts, who helped to run the clinical trial for lecanemab. “But one positive study supports the hypothesis.” Amyloid is “associated with the problem, but it isn’t ‘the’ problem”, says George Perry, a neurobiologist at the University of Texas at San Antonio and a sceptic of the amyloid hypothesis. “If you modulate it, of course you can have some small benefit.” © 2022 Springer Nature Limited

Keyword: Alzheimers
Link ID: 28497 - Posted: 10.01.2022

Daniel Merino & Josjan Zijlmans As research into psychedelics and their medical uses makes a comeback, scientists are having to deal with the legacy – both scientific and social – of a 40-year nearly total freeze on psychedelics research. In this episode of “The Conversation Weekly” podcast, we speak with three experts about the early rise and fall of psychedelics in Western science and culture, how the mystical and often vague language of the ‘60s and '70s still pervades research today and what it’s like to actually run clinical trials using psilocybin. According to a poll done in the summer of 2022, nearly 30% of U.S. residents have tried at least one psychedelic drug in their lifetime. Whether from personal experience, hearing about the experiences of friends or widespread depictions in the media, many people will have either tried to describe a psychedelic trip or heard someone else describe one. The language commonly used in these descriptions is, for lack of a better word, often quite trippy. “A key function of the ego is to identify differentiation,” says Robin Carhart-Harris, a neurologist and psychologist at the University of California, San Francisco, and one of the world’s leading psychedelics researchers. “And when that function breaks down, it’s replaced with a sense of de-differentiation, a sense of unity, like everything is interconnected in a web of relationships. That’s not nothingness, it’s sort of everythingness.” Many psychedelics researchers use an approach called “the mystical framework” to assess psychedelic experiences. Researchers who use this framework give participants in psychedelics studies a survey as a way to define and categorize the experience. The survey asks participants to rate how strongly they felt certain phenomena during their trip, including feelings like the “certainty of encounter with ultimate reality (in the sense of being able to 'know’ and ‘see’ what is really real at some point during your experience).” © 2010–2022, The Conversation US, Inc.

Keyword: Depression; Drug Abuse
Link ID: 28496 - Posted: 10.01.2022

By Pam Belluck A new medication for A.L.S., the devastating neurological disorder that causes paralysis and death, will have a list price of $158,000 a year, its manufacturer disclosed Friday. The treatment, to be marketed as Relyvrio, is a combination of two existing drugs and will be available to patients in the United States in about four to six weeks, according to officials of the company, Amylyx Pharmaceuticals. Relyvrio was approved by the Food and Drug Administration on Thursday, even though the agency’s analysis concluded there was not yet sufficient evidence that the medication could help patients live longer or slow the rate at which they lose functions like muscle control, speaking or breathing without assistance. The F.D.A. decided to greenlight the drug instead of waiting until 2024 for results of a large clinical trial partly because the treatment is considered to be safe. The agency said that although the evidence of effectiveness was uncertain, “given the serious and life-threatening nature of A.L.S. and the substantial unmet need, this level of uncertainty is acceptable in this instance.” A.L.S., or amyotrophic lateral sclerosis — also called Lou Gehrig’s disease — often strikes patients in the prime of life and frequently causes death within two to five years. It is diagnosed in about 6,000 people worldwide each year, and Amylyx estimates that there are about 29,000 people living with the disease in the United States. Amylyx officials predicted that most patients would pay little or nothing for the treatment because the company expects insurers, both private and public, to cover it. Amylyx plans to provide it free to uninsured patients experiencing financial hardship. Still, the list price is much higher than that recommended by the Institute for Clinical and Economic Review, a nonprofit organization that evaluates the value of medicines. In a statement, the group’s chief medical officer, Dr. David Rind, said that while “there are clear benefits to patients with a rapidly fatal disease to have early access to a safe therapy,” his organization had concluded that “an annual price of $9,100 to $30,700 would be reasonable if the therapy actually works.” © 2022 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28495 - Posted: 10.01.2022

By Deborah Balthazar It’s a frustration many parents know all too well: You’ve finally lulled your crying baby to sleep, so you put them down in their crib … and the wailing begins again. Science may have a trick for you. Carrying a crying infant for about five minutes, then sitting for at least another five to eight minutes can calm and lull the baby to sleep long enough to allow a parent to put the child down without waking them, researchers report September 13 in Current Biology. Some of those same researchers previously showed that carrying a crying baby soothes the child and calms a racing heart rate (SN: 4/18/13). For the new study, the team looked at what it takes to get that crying baby to nod off and stay asleep. The researchers put heart rate monitors on 21 crying babies, ranging in age from newborns to 7 months old. The team also took videos of the infants, monitoring their moods as their mothers carried them around a room, sat holding them and laid them in a crib. That allowed the team to observe how the babies responded to different environments, whether they were crying, fussy, alert or drowsy, heartbeat by heartbeat. “We tested the physiology behind these things that tend to be kind of common knowledge, though it’s not really well understood why they work,” says Gianluca Esposito, a developmental psychologist at the University of Trento in Italy. The babies’ heart rates slowed and they stopped crying when their mothers picked them up and carried them around for five minutes. Some infants even fell asleep. But the researchers also noticed that the babies tended to respond to the movement of the parent, whether they were in deep sleep or not. For instance, a baby’s heart rate quickened if a parent turned quickly while walking or tried to put the baby down. © Society for Science & the Public 2000–2022.

Keyword: Sleep; Development of the Brain
Link ID: 28494 - Posted: 10.01.2022