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

Nicola Davis Science correspondent If the taste of kale makes you screw up your face, you are not alone: researchers have observed foetuses pull a crying expression when exposed to the greens in the womb. While previous studies have suggested our food preferences may begin before birth and can be influenced by the mother’s diet, the team says the new research is the first to look directly at the response of unborn babies to different flavours. “[Previously researchers] just looked at what happens after birth in terms of what do [offspring] prefer, but actually seeing facial expressions of the foetus when they are getting hit by the bitter or by the non-bitter taste, that is something which is completely new,” said Prof Nadja Reissland, from Durham University, co-author of the research. Writing in the journal Psychological Science, the team noted that aromas from the mother’s diet were present in the amniotic fluid. Taste buds can detect taste-related chemicals from 14 weeks’ gestation, and odour molecules can be sensed from 24 weeks’ gestation. To delve into whether foetuses differentiate specific flavours, the team looked at ultrasound scans from almost 70 pregnant women, aged 18 to 40 from the north-east of England, who were split into two groups. One group was asked to take a capsule of powdered kale 20 minutes before an ultrasound scan, and the other was asked to take a capsule of powdered carrot. Vegetable consumption by the mothers did not differ between the kale and carrot group. The team also examined scans from 30 women, taken from an archive, who were not given any capsules. All the women were asked to refrain from eating anything else in the hour before their scans. The team then carried out a frame-by-frame analysis of the frequency of a host of different facial movements of the foetuses, including combinations that resembled laughing or crying. Overall, the researchers examined 180 scans from 99 foetuses, scanned at either 32 weeks, 36 weeks, or at both time points. © 2022 Guardian News & Media Limited

Keyword: Development of the Brain; Chemical Senses (Smell & Taste)
Link ID: 28493 - Posted: 09.28.2022

By Tess Joosse “Bird brain” insults be damned. The noggins of our flying friends are packed with neurons, and recent studies have shown birds can develop complex tools and even discriminate between paintings by Claude Monet and Pablo Picasso. But is this avian acumen a recent development, evolutionarily speaking, or does it trace back tens of millions of years? A remarkably preserved fossil unearthed in Brazil may hold some answers. The 80-million-year-old bird skull contains impressions of advanced brain structures, suggesting early birds were bright like modern ones. The preserved braincase, from a now-extinct bird lineage, is “exceptional … a big step forward,” says Matteo Fabbri, an evolutionary biologist at the Field Museum of Natural History who was not involved with the work. “This is the first time we have really good information regarding the brain of [this] group.” Birds began to evolve about 165 million to 150 million years ago from dinosaurs. Some of the earliest—whose ancestors were carnivorous icons such as Velociraptor—were the famous feathered Archaeopteryx. Over time, avians branched into a group called the enantiornithines and close cousins who became modern birds. Ranging from the size of hummingbirds to turkeys, enantiornithines took to the skies in the Mesozoic era beginning 130 million years ago. The creatures eventually spanned the globe before going extinct 66 million years ago from the same asteroid impact that killed off the dinosaurs. Their position between Archaeopteryx and living birds gives them a “magical place on the dino-bird family tree,” says Daniel Field, a paleontologist at the University of Cambridge and co-author of the new study. To reconstruct the brains of ancient birds, researchers need fossils that preserve the hollow space where a brain would sit: the braincase. But no enantiornithine skeletons have preserved that space—until the new find. © 2022 American Association for the Advancement of Science.

Keyword: Evolution
Link ID: 28492 - Posted: 09.28.2022

Terriline Porelle is puzzling over two mysteries. The first is: what’s plaguing her? For the past two years, the formerly healthy, active, 34-year-old resident of Cocagne, N.B. has been experiencing many strange and alarming symptoms, including muscle twitches and blurred vision, auditory hallucinations, brain fog and loss of balance and co-ordination. The second mystery is why health authorities no longer seem interested in finding out why she’s ill. “It’s like nobody’s really looking to see what’s going on and it doesn’t make any sense,” she said. Ms. Porelle is one of 48 people who were initially identified between late 2020 and May, 2021, as being part of a cluster of patients in New Brunswick who all had a mysterious brain illness, which the province referred to as a “potential neurological syndrome of unknown cause.” Doctors and researchers puzzled over the cases for months. Then, in a February report, the province announced that there was no mystery illness, and that its investigation into the matter had concluded. An independent oversight committee had found that the 48 patients were likely suffering from various previously known diseases that had simply been misdiagnosed, the report said. But some of the patients and their families say their suffering remains very real – and that it’s made worse by the fact that they’re no closer to getting answers about what’s causing it. The province’s report said neurologists on the oversight committee had provided potential alternative diagnoses for 41 of the 48 patients, including Alzheimer’s disease and other types of dementia, post-concussion syndrome, chronic severe anxiety disorder and cancer. It recommended that patients contact their primary caregivers for referrals to further treatment, or that they seek help from a specialized clinic in Moncton called the Moncton Interdisciplinary Neurodegenerative Diseases (MIND) Clinic.

Keyword: Alzheimers
Link ID: 28491 - Posted: 09.28.2022

by Angie Voyles Askham / Brain connectivity patterns in people with autism and other neuropsychiatric conditions are more closely related to genetics than to phenotypic traits, according to two new studies. The findings highlight why a single brain biomarker for autism has remained elusive, the researchers say. The condition’s genetic heterogeneity has hampered the search for a shared brain signature: More than 100 genes have been identified as strongly linked to autism, and multiple copy number variations (CNVs) — deleted or duplicated stretches of genetic code — can increase a person’s likelihood of the condition. Autism also often overlaps with other conditions, such as schizophrenia and attention-deficit/hyperactivity disorder (ADHD), making autism-specific markers difficult to disentangle. Common variants tied to autism overlap strongly with those linked to schizophrenia and high IQ, for example, whereas rare autism-linked variants track with low IQ. According to the new papers, however, autism’s genetic heterogeneity corresponds to similarly disparate maps of ‘functional connectivity’ — a measure of which brain areas activate in sync while the brain is at rest. “What we’re seeing is that these groups of variants have specific functional connectivity signatures,” says lead investigator Sébastien Jacquemont, associate professor of pediatrics at the University of Montreal in Canada. The findings need to be replicated, says Aaron Alexander-Bloch, assistant professor of psychiatry at the University of Pennsylvania and the Children’s Hospital of Philadelphia, who was not involved in the work, but they point to the importance of subgrouping study participants based on their underlying genetics. © 2022 Simons Foundation

Keyword: Autism; Brain imaging
Link ID: 28490 - Posted: 09.28.2022

By Hedda Hassel Mørch The nature of consciousness seems to be unique among scientific puzzles. Not only do neuroscientists have no fundamental explanation for how it arises from physical states of the brain, we are not even sure whether we ever will. Astronomers wonder what dark matter is, geologists seek the origins of life, and biologists try to understand cancer—all difficult problems, of course, yet at least we have some idea of how to go about investigating them and rough conceptions of what their solutions could look like. Our first-person experience, on the other hand, lies beyond the traditional methods of science. Following the philosopher David Chalmers, we call it the hard problem of consciousness. But perhaps consciousness is not uniquely troublesome. Going back to Gottfried Leibniz and Immanuel Kant, philosophers of science have struggled with a lesser known, but equally hard, problem of matter. What is physical matter in and of itself, behind the mathematical structure described by physics? This problem, too, seems to lie beyond the traditional methods of science, because all we can observe is what matter does, not what it is in itself—the “software” of the universe but not its ultimate “hardware.” On the surface, these problems seem entirely separate. But a closer look reveals that they might be deeply connected. Consciousness is a multifaceted phenomenon, but subjective experience is its most puzzling aspect. Our brains do not merely seem to gather and process information. They do not merely undergo biochemical processes. Rather, they create a vivid series of feelings and experiences, such as seeing red, feeling hungry, or being baffled about philosophy. There is something that it’s like to be you, and no one else can ever know that as directly as you do. © 2022 NautilusThink Inc, All rights reserved.

Keyword: Consciousness
Link ID: 28489 - Posted: 09.24.2022

by Charles Q. Choi Infection during pregnancy may be associated with having an autistic child simply because mothers of autistic children are prone to infections, a new study finds. The results suggest that “common infections during pregnancy do not seem increase their children’s risk of autism,” says study investigator Martin Brynge, a psychiatrist and doctoral student of global public health at the Karolinska Institutet in Stockholm, Sweden. “Prevention of maternal infections would likely not affect the prevalence of autism in the population.” A great deal of previous research has linked maternal infection during pregnancy with autism and intellectual disability in children. Whether the former causes the latter, however, has remained uncertain. For instance, both autism and intellectual disability are linked with gene variants that may influence the immune system, so mothers of children with either condition may also just be more vulnerable to serious infections. The new study analyzed data from 549,967 children, including 267,995 girls, living in Stockholm County who were born between 1987 and 2010; about 34,000 of the children had been exposed to a maternal infection requiring specialized health care, according to data from Sweden’s National Patient Register and National Medical Birth Register. Of the exposed children, 3.3 percent have autism, compared with 2.5 percent of unexposed children — a 16 percent increase in the chance of autism. But maternal infection in the year before pregnancy was also linked with a 25 percent greater chance of autism. “Mothers who had an infection during pregnancy may not be comparable to those mothers without infections,” Brynge says. “There may be systematic differences at the group level.” © 2022 Simons Foundation

Keyword: Autism; Neuroimmunology
Link ID: 28488 - Posted: 09.24.2022

By Ed Yong On March 25, 2020, Hannah Davis was texting with two friends when she realized that she couldn’t understand one of their messages. In hindsight, that was the first sign that she had COVID-19. It was also her first experience with the phenomenon known as “brain fog,” and the moment when her old life contracted into her current one. She once worked in artificial intelligence and analyzed complex systems without hesitation, but now “runs into a mental wall” when faced with tasks as simple as filling out forms. Her memory, once vivid, feels frayed and fleeting. Former mundanities—buying food, making meals, cleaning up—can be agonizingly difficult. Her inner world—what she calls “the extras of thinking, like daydreaming, making plans, imagining”—is gone. The fog “is so encompassing,” she told me, “it affects every area of my life.” For more than 900 days, while other long-COVID symptoms have waxed and waned, her brain fog has never really lifted. Of long COVID’s many possible symptoms, brain fog “is by far one of the most disabling and destructive,” Emma Ladds, a primary-care specialist from the University of Oxford, told me. It’s also among the most misunderstood. It wasn’t even included in the list of possible COVID symptoms when the coronavirus pandemic first began. But 20 to 30 percent of patients report brain fog three months after their initial infection, as do 65 to 85 percent of the long-haulers who stay sick for much longer. It can afflict people who were never ill enough to need a ventilator—or any hospital care. And it can affect young people in the prime of their mental lives. Long-haulers with brain fog say that it’s like none of the things that people—including many medical professionals—jeeringly compare it to. It is more profound than the clouded thinking that accompanies hangovers, stress, or fatigue. For Davis, it has been distinct from and worse than her experience with ADHD. It is not psychosomatic, and involves real changes to the structure and chemistry of the brain. It is not a mood disorder: “If anyone is saying that this is due to depression and anxiety, they have no basis for that, and data suggest it might be the other direction,” Joanna Hellmuth, a neurologist at UC San Francisco, told me. (c) 2022 by The Atlantic Monthly Group. All Rights Reserved.

Keyword: Attention; Learning & Memory
Link ID: 28487 - Posted: 09.21.2022

By Darren Incorvaia Songbirds get a lot of love for their dulcet tones, but drummers may start to steal some of that spotlight. Woodpeckers, which don’t sing but do drum on trees, have brain regions that are similar to those of songbirds, researchers report September 20 in PLOS Biology. The finding is surprising because songbirds use these regions to learn their songs at an early age, yet it’s not clear if woodpeckers learn their drum beats (SN: 9/16/21). Whether woodpeckers do or not, the result suggests a shared evolutionary origin for both singing and drumming. The ability to learn vocalizations by listening to them, just like humans do when learning to speak, is a rare trait in the animal kingdom. Vocal learners, such as songbirds, hummingbirds and parrots, have independently evolved certain clusters of nerve cells called nuclei in their forebrains that control the ability. Animals that don’t learn vocally are thought to lack these brain features. While it’s commonly assumed that other birds don’t have these nuclei, “there’s thousands of birds in the world,” says Matthew Fuxjager, a biologist at Brown University in Providence, R.I. “While we say these brain regions only exist in these small groups of species, nobody’s really looked in a lot of these other taxa.” Fuxjager and his colleagues examined the noggins of several birds that don’t learn vocally to check if they really did lack these brain nuclei. Using molecular probes, the team checked the bird brains for activity of a gene called parvalbumin, a known marker of the vocal learning nuclei. Many of the birds, including penguins and flamingos, came up short, but there was one exception — male and female woodpeckers, which had three spots in their brains with high parvalbumin activity. © Society for Science & the Public 2000–2022.

Keyword: Animal Communication; Language
Link ID: 28486 - Posted: 09.21.2022