By Gina Kolata What if an uncontrollable urge to rapidly eat large amounts of food is rooted in an impaired brain circuit? If that were the case, people who live with binge eating disorder — a psychiatric diagnosis — might be no more at fault for overeating than a patient with Parkinson’s disease is for their tremors. That question led doctors to try a new treatment different from anything ever attempted to help people with this common but underreported eating disorder. At least 3 percent of the population has it, said Dr. Casey Halpern, a neurosurgeon at the University of Pennsylvania. He and his colleagues decided to try deep brain stimulation, a method routinely used to quell tremors in patients with Parkinson’s. It involves placing electrodes in the brain to regulate aberrant signals. The wires, connected to the electrodes, are placed under the scalp, where they are invisible and unobtrusive. For the binge eating treatment, the device only stimulates neurons when the device detects a signal to start a binge. The pilot study, funded by the National Institutes of Health and published earlier this year in the journal Nature Medicine, involves two women and will be expanded in a few months to include four more people living with binge eating disorder who regained the weight they lost after bariatric surgery. Before the treatment can be approved by the Food and Drug Administration, researchers will need to rigorously test the method in at least 100 people in multiple medical centers. Such a study would take several years to complete. The two women whose devices were implanted a year ago will be followed for up to three years. They had the option to have their devices removed after 12 months, but both wanted to keep them because they no longer felt irresistible urges to binge. One of them, Robyn Baldwin, 58, of Citrus Heights, Calif., described herself as a “chunko child” who had “always been big.” She tried a wide range of diets. Once, she consumed only protein shakes for a month. In 2003 she had bariatric surgery, which usually involves altering the digestive system so that the stomach is smaller and food is more difficult to digest. It has enabled many people to lose weight when other methods failed. But for Ms. Baldwin, the weight she lost came back. © 2022 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 28545 - Posted: 11.09.2022

by David Dobbs For 40 years, Leo Kanner and Hans Asperger have dominated virtually every story about the ‘pioneers of autism research.’ These two men published in 1943 and 1944, respectively, what were long accepted as the first descriptions of, as Kanner’s seminal paper claimed, ”children whose condition differs … markedly and uniquely from anything reported so far.” Both papers are absorbing, touching and authoritative. Both describe young people whose challenges defied the known diagnoses of the time but clearly fall into what we now call autism. And both offered a new diagnostic category for such people. Kanner’s 1943 paper, ”Autistic Disturbances of Affective Contact,” drew almost immediate attention. Within a year, he renamed the condition these children shared, dubbing it ‘early infantile autism,’ which soon became known as ‘autism’ or ‘Kanner’s syndrome.’ His articulation of the condition, based on observations of 11 children he and his associates treated in his Baltimore, Maryland, clinic, remained the standard well into the 1980s and involved three elements: Autism was a condition marked by: (1) emergence early in childhood, (2) deficits in communication and social interaction, and (3) restricted or repetitive behaviors and a desire for sameness. Even today, these three elements anchor the official diagnostic criteria in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, as well as the widely used International Classification of Diseases and Related Health Problems. Asperger’s 1944 paper, which presented case studies on four children he and his colleagues had seen in his clinic in Vienna, Austria, made its impact far more slowly. In fact, because Asperger published in German (and in a German journal in the middle of a war that had essentially halted transatlantic scholarly exchange), the paper went largely unnoticed outside Europe for decades. Asperger’s descriptions resembled Kanner’s in many ways, although he outlined a wider apparent range of intelligence and capabilities than Kanner did, with some of his study participants reaching prominence in their fields. Asperger coined the diagnostic term ‘autistic psychopathy.’ © 2022 Simons Foundation

Keyword: Autism
Link ID: 28544 - Posted: 11.09.2022

By Ken Belson AMSTERDAM — For the first time since 2016, one of the most influential groups guiding doctors, trainers and sports leagues on concussions met last month to decide, among other things, if it was time to recognize the causal relationship between repeated head hits and the degenerative brain disease known as C.T.E. Despite mounting evidence and a highly regarded U.S. government agency recently acknowledging the link, the group all but decided it was not. Leaders of the International Consensus Conference on Concussion in Sport, meeting in Amsterdam, signaled that it would continue its long practice of casting doubt on the connection between the ravages of head trauma and sports. C.T.E., or chronic traumatic encephalopathy, was first identified in boxers in 1928 and burst into prominence in 2005, when scientists published their posthumous diagnosis of the disease in the N.F.L. Hall of Fame center Mike Webster, creating an existential crisis for sports such as football and rugby that involve players hitting their heads thousands of times a year. Scientists have spent the past decade analyzing hundreds of brains from athletes and military veterans, and the variable evident in nearly every case of C.T.E. has been their exposure to repeated head trauma. Researchers have also established what they call a dose response between the severity of the C.T.E. and the number of years playing collision sports. After playing down an association between head injuries and brain damage for years, the N.F.L. in 2016 acknowledged that there was a link between football and degenerative brain disorders such as C.T.E. Just days before the conference in Amsterdam, the National Institutes of Health, the biggest funder of brain research in the United States, said that C.T.E. “is caused in part by repeated traumatic brain injuries.” But in one of the final sessions of the three-day conference, one of the leaders of the conference, a neuropsychologist who has received $1.5 million in research funding from the N.F.L., dismissed the work of scientists who have documented C.T.E. in hundreds of athletes and soldiers because he said their studies thus far did not account for other health variables, including heart disease, diabetes and substance abuse. © 2022 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 28543 - Posted: 11.09.2022

By Katherine Ellison News organizations were quick to trumpet the recent findings of a small study suggesting that “magic mushrooms” could be part of a breakthrough treatment for alcoholism. It’s no wonder. Every year, alcohol abuse kills more than 140,000 Americans and affects millions more, with a steep increase in deaths in recent years, according to data published by the Centers for Disease Control and Prevention on Nov. 4. But excitement about the psilocybin study also raises a question: Why aren’t there more medical treatments for such an obviously devastating problem? “There is a desperate need for new medications, and there are many good avenues that we’re pursuing,” said Dorit Ron, a neurology professor at the University of California at San Francisco Medical Center, who has been studying potential treatments that include rapamycin, a drug designed to help transplant patients tolerate new organs. But getting promising new medications into the hands of doctors and their patients has proved difficult, said George Koob, director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), adding “it doesn’t go for lack of trying.” Lack of awareness by doctors, funding decisions by the pharmaceutical industry and the stigma surrounding alcoholism have all held up progress, he said. Can pills help? Ron and other researchers say medication can play a vital role in combating alcohol use disorder, the medical condition commonly known as alcoholism. But fewer than 2 percent of people with an alcohol addiction take medication for the condition, national surveys show, compared with 13.4 percent of those dealing with opioid addiction.

Keyword: Drug Abuse
Link ID: 28542 - Posted: 11.09.2022

Hannah Devlin Science correspondent Scientists claim to have found the first direct evidence that people with depression have a reduced capacity for releasing serotonin in the brain. The findings from a brain-imaging study reignite a debate within psychiatry over the so-called serotonin hypothesis of depression and challenge the conclusions of an influential review published in July that found “no clear evidence” that low serotonin levels are responsible. The latest work, led by scientists at Imperial College London, suggested that people with depression have a decreased serotonin response. “This is the first direct evidence that the release of serotonin is blunted in the brains of people with depression,” said Prof Oliver Howes, a consultant psychiatrist based at Imperial College and King’s College London, and a co-author. “People have been debating this question for 60 years, but it’s all been based on indirect measures. So this is a really important step.” The serotonin hypothesis arose from evidence from postmortem brains and blood samples that suggested a serotonin deficit could be involved in depression. The theory provides a plausible biological mechanism for how the main class of antidepressant drugs, selective serotonin reuptake inhibitors (SSRIs), are effective, and is why the brain chemical is sometimes referred to as a “happy hormone”. However, there is not yet conclusive evidence that serotonin abnormalities are the underlying cause of depression and resolving this question is seen as crucial to providing better treatments. The latest paper adds weight to the view that serotonin plays a role and demonstrates a new brain imaging technique that could pave the way to a better understanding of why SSRI drugs fail to help an estimated 10% to 30% of patients. “It’s the closest anyone has been able to get so far,” said Howes. “It’s hard to measure these transmitters in the brains of living people. We can’t put a pipette in there and take a sample. This is the closest we’re likely to come.” © 2022 Guardian News & Media Limited o

Keyword: Depression
Link ID: 28541 - Posted: 11.05.2022

By Leo Sands Psilocybin, the active hallucinogen found in psychedelic mushrooms — also known as “magic mushrooms” — can effectively alleviate a severe bout of depression when administered in a single dose and combined with talk therapy, a new clinical study found. Adults with depression who were administered a single 25-miligram dose of psilocybin were more likely to experience significant improvements in their mental health — both immediately and for up to three months — than others who were randomly assigned smaller doses of the same drug, said the peer-reviewed study, which was published Wednesday in the New England Journal of Medicine. “There’s something about the psychedelic experience that leads to a rapid resolution of depression symptoms,” said James Rucker, a consultant psychiatrist at King’s College London who worked on the trial. “We don’t really know what that is at the moment, but it’s very different to standard antidepressants.” The trial’s findings could be an encouraging sign for the 16 million Americans estimated each year by the Centers for Disease Control and Prevention to have depression, many of whom struggle to find treatments that work for them. Its authors hope the study — which was relatively small, with just 79 participants receiving the 25 mg dose — will pave the way for eventual regulatory approval of psilocybin by the Food and Drug Administration for use as a drug against depression. The new study randomly assigned 233 adults with depression three doses of psilocybin — 25 mg, 10 mg and 1 mg — across 22 sites in 10 countries. The authors found that the group given the largest dose recorded the most significant improvements in their depression, both immediately and for several weeks after.

Keyword: Depression; Drug Abuse
Link ID: 28540 - Posted: 11.05.2022

By Aimee Cunningham The death rate from alcohol use rose sharply in the United States in the first year of the pandemic. From 2019 to 2020, the rate of alcohol-induced deaths climbed 26 percent, from 10.4 per 100,000 people to 13.1 per 100,000, researchers report in a National Center for Health Statistics data brief published November 4. The rate of alcohol-induced deaths has generally increased yearly for the last two decades, but the annual uptick tended to be 7 percent or less. Deaths from alcoholic liver disease, which includes hepatitis and cirrhosis, were the most common driver of the increased rate. Deaths from mental and behavioral disorders due to alcohol use — mortality from dependence syndrome or withdrawal, for example — were the second most frequent contributor. The death rate from alcohol use jumped 26 percent overall from 2019 to 2020, a marked increase from previous years. Other researchers have reported that adults were drinking more frequently, and more heavily, early in the pandemic compared with the year before. There is also evidence of an increase in cases of alcoholic liver disease. A study at Johns Hopkins Hospital in Baltimore reported that 2.3 times as many patients with severe alcoholic liver disease and with recent unhealthy drinking were referred to their liver transplant center from July to December of 2020 compared with those months in 2019. © Society for Science & the Public 2000–2022.

Keyword: Drug Abuse; Stress
Link ID: 28539 - Posted: 11.05.2022

Vanessa Rom When put to the test, bees have proved over and over again that they've got a lot more to offer than pollinating, making honey and being fiercely loyal to a queen. The industrious insects can count and alter their behavior when things seem difficult, and now some scientists say there's proof they also like to play. A study recently published in Animal Behavior suggests that bumblebees, when given the chance, like to fool around with toys. Researchers from Queen Mary University of London conducted an experiment in which they set up a container that allowed bees to travel from their nest to a feeding area. But along the way, the bees could opt to pass through a separate section with a smattering of small wooden balls. Over 18 days, the scientists watched as the bees "went out of their way to roll wooden balls repeatedly, despite no apparent incentive to do so." The finding suggests that like humans, insects also interact with inanimate objects as a form of play. Also similar to people, younger bees seemed to be more playful than adult bees. In this experiment from researchers at Queen Mary University of London, bumblebees, especially young ones, appeared to show they liked to cling to wooden balls twice their size and roll them around just for the fun of it. "This research provides a strong indication that insect minds are far more sophisticated than we might imagine," Lars Chittka, a professor of sensory and behavioral ecology at Queen Mary University of London, who led the study, said in a statement. Earlier studies have shown that the black and yellow bugs are willing to learn new tricks in exchange for food or other rewards, so in this case Chittka and his team set out to create conditions that would eliminate external variables. They made sure that the bees had acclimated to their new home and that their environment was stress free. © 2022 npr

Keyword: Emotions; Evolution
Link ID: 28538 - Posted: 11.05.2022

By Veronique Greenwood Anyone who’s had a shady oyster or a mushroom soup that didn’t sit well remembers the ominous queasiness heralding impending bad times. Bacteria release toxins that start the body’s process of speedily evacuating the contents of the stomach. It’s a protective mechanism of sorts — getting rid of the invaders en masse is probably helpful in the long term, even if it’s unpleasant in the short. But it has remained something of a mystery how the brain gets the alarm signal, then sends another one to tell the stomach to initiate a technicolor yawn. Your next bout of food poisoning isn’t the only reason to understand this particular neural pathway. Figuring out how to counter it could be helpful for people who develop nausea caused by chemotherapy medication and other drugs. As if fighting cancer isn’t painful and scary enough, patients are often so turned off by food that keeping their weight up becomes a major struggle. In a new study, researchers report that both bacteria and chemotherapy drugs appear to trigger the same molecular pathways in the gut. The findings, which were based on experiments with mice and published Tuesday in the journal Cell, showed that a bacterial toxin and a chemo medication both set in motion a cascade of similar neural messages that cause queasiness. Choosing mice for the study was unusual. Mice, it turns out, can’t puke — a little foible that typically makes it difficult to use them to study nausea. Researchers have used cats and dogs in the past, but the biology of mice in general is so much better understood, with much better tools available to scientists to do so. Cao Peng, a professor at Tsinghua University in Beijing, and his colleagues wondered whether mice might still be capable of feeling ill in the way people do after ingesting a chemo drug or a bad salad — or close enough, anyway, that researchers could use the creatures to understand the origins of the sensation. © 2022 The New York Times Company

Keyword: Obesity; Stress
Link ID: 28537 - Posted: 11.02.2022

By Elena Renken The brain’s lifeline, its network of blood vessels, is like a tree, says Mathieu Pernot, deputy director of the Physics for Medicine Paris Lab. The trunk begins in the neck with the carotid arteries, a pair of broad channels that then split into branches that climb into the various lobes of the brain. These channels fork endlessly into a web of tiny vessels that form a kind of canopy. The narrowest of these vessels are only wide enough for a single red blood cell to pass through, and in one important sense these vessels are akin to the tree’s leaves. “When you want to look at pathology, usually you don’t see the sickness in the tree, but in the leaves,” Pernot says. (You can identify Dutch Elm Disease when the tree’s leaves yellow and wilt.) Just like leaves, the tiniest blood vessels in the brain often register changes in neuron and synapse activity first, including illness, such as new growth in a cancerous brain tumor.1, 2 But only in the past decade or so have we developed the technology to detect these microscopic changes in blood flow: It’s called ultrafast ultrasound. Standard ultrasound is already popular in clinical imaging given that it is minimally invasive, low-cost, portable, and can generate images in real time.3 But until now, it has rarely been used to image the brain. That’s partly because the skull gets in the way—bone tends to scatter ultrasound waves—and the technology is too slow to detect blood flow in the smaller arteries that support most brain function. Neurologists have mostly used it in niche applications: to examine newborns, whose skulls have gaps between the bone plates, or to guide surgeons in some brain surgeries, where part of the skull is typically removed. Neuroscience researchers have also used it to study functional differences between the two hemispheres of the brain, based on imaging of the major cerebral arteries, by positioning the device over the temporal bone window, the thinnest area of the skull. © 2022 NautilusThink Inc,

Keyword: Brain imaging; Hearing
Link ID: 28536 - Posted: 11.02.2022

Jon Hamilton Computer games designed to boost self-esteem appear to prolong the antidepressant benefits of the mind-bending anesthetic ketamine. A recent study of 154 people found that those who played games featuring smiling faces and positive messages remained free of depression up to three months after a ketamine infusion, a team reports in the American Journal of Psychiatry. People who got ketamine alone tended to relapse after a week or two. The results are important because "we need new approaches that help people get feeling better faster and help them stay feeling better," says Rebecca Price, an author of the study and an associate professor of psychiatry and psychology at the University of Pittsburgh. Established drugs like Prozac and Zoloft can take weeks to ease depression, and don't work for every patient. Ketamine can offer immediate relief, but the effects often fade after a few days or weeks. "And then returning for infusions over and over to keep that relief going can end up being really burdensome and costly," Price says, "and just isn't accessible to all patients." So Price and a team of researchers wanted to find a way to make ketamine's antidepressant effects last longer. They decided to focus on a common symptom of depression: low self-esteem and self-loathing. The team drew on research suggesting that ketamine temporarily causes certain brain areas to enter a state in which they form lots of new connections. During this period, the brain seems to be more receptive to learning and change. "So we tried to use that window of opportunity just after ketamine to strengthen associations specifically between the idea of me, myself, and positive information and attributes," Price says. © 2022 npr

Keyword: Depression; Drug Abuse
Link ID: 28535 - Posted: 11.02.2022

Jon Hamilton An idea that has propelled Alzheimer's research for more than 30 years is approaching its day of reckoning. Scientists are launching a study designed to make or break the hypothesis that Alzheimer's is caused by a sticky substance called beta-amyloid. The study will give an experimental anti-amyloid drug to people as young as 18 who have gene mutations that often cause Alzheimer's to appear in their 30s or 40s. The study comes after several experimental drugs have failed to prevent declines in memory and thinking even though they succeeded in removing amyloid from the brains of patients in the early stages of Alzheimer's. Those failures have eroded support for the idea that amyloid is responsible for a cascade of events that eventually lead to the death of brain cells. "Many of us think of that as the ultimate test of the amyloid hypothesis," says Dr. Randall Bateman, a professor of neurology at Washington University School of Medicine in St. Louis."If that doesn't work, nothing will work." The new experiment, called the DIAN-TU primary Prevention Trial, is scheduled to begin enrolling patients by the end of the year. The amyloid hypothesis can be traced to Dr. Alois Alzheimer, a pathologist who first described the disease that would bear his name in 1906. Alzheimer was working at a psychiatric clinic in Munich, where he had the chance to conduct an autopsy on a woman who died at 50 after experiencing memory loss, disorientation, and hallucinations. He observed that the woman's brain had an "unusual disease of the cerebral cortex," including "senile plaque" usually seen in much older people. © 2022 npr

Keyword: Alzheimers
Link ID: 28534 - Posted: 11.02.2022

By Jack Tamisiea An elephant’s trunk has 40,000 muscles and weighs more than a Burmese python. The appendage is strong enough to uproot a tree, yet sensitive enough to suction up fragile tortilla chips. But how does an elephant’s brain help accomplish these feats of dexterity? That has been difficult to study, according to Michael Brecht, a neuroscientist at the Humboldt University of Berlin. Weighing in excess of 10 pounds, the elephant’s brain degrades quickly after death and is a hassle to store. “I tend to think that the big animals are a bit neglected because we don’t do enough work on big brains,” Dr. Brecht said. Dr. Brecht and his colleagues were fortunate enough to gain access to a trove of elephant brains from animals that had died of natural causes or were euthanized for health reasons and ended up either frozen or in a fixative substance at the Leibniz Institute for Zoo and Wildlife Research in Berlin. In a study published Wednesday in the journal Science Advances, Dr. Brecht and his colleagues reported that elephants had more facial neurons than any other land mammal, which might contribute to trunk dexterity and other anatomical abilities. The study also helped to pinpoint major differences between the neural wirings of African savanna elephants and Asian elephants. Using the brains of four Asian elephants and four African savanna elephants, the researchers homed in on the facial nucleus, a bundle of neurons concentrated in the brainstem and hooked up to facial nerves. In mammals, these neurons serve as the control center for facial muscles. They’re in command whenever you wrinkle your nose, purse your lips or raise your eyebrows. They also help elephants employ their trunks. The researchers divided the facial nucleus into regions of neurons that controlled the elephant’s ears, lips and trunk. African elephants sported 63,000 facial neurons, while their Asian cousins had 54,000. The only mammals with more are dolphins, which pack nearly 90,000 facial neurons into their sensitive snouts. While his team expected both African savanna and Asian elephants to possess massive stores of facial neurons, Dr. Brecht said the discrepancy between the two species was noteworthy. © 2022 The New York Times Company

Keyword: Evolution; Pain & Touch
Link ID: 28533 - Posted: 10.28.2022

By Jackie Rocheleau For people haunted by recurring nightmares, untroubled sleep would be a dream come true. Now in a small experiment, neuroscientists have demonstrated a technique that, for some, may chase the bad dreams away. Enhancing the standard treatment for nightmare disorder with a memory-boosting technique cut down average weekly nightmares among a few dozen people from three to near zero, researchers report online October 27 in Current Biology. “The fact that they could actually make a big difference in the frequency of those nightmares is huge,” says Gina Poe, a neuroscientist at UCLA who wasn’t involved in the study. People with nightmare disorder fear the night not for the monsters under the bed, but the monsters in their dreams. Frequent, terrifying dreams disturb sleep and even affect well-being in waking life. The go-to nightmare disorder treatment is imagery rehearsal therapy, or IRT. In this treatment, patients reimagine nightmares with a positive spin, mentally rehearsing the new story line while awake. It reduces nightmares for most but fails for nearly a third of people. To boost IRT’s power, neuroscientist Sophie Schwartz of the University of Geneva and her colleagues leveraged a learning technique called targeted memory reactivation, or TMR. In this technique, a person focuses on learning something while a sound plays, and that same cue plays again during sleep. Experiencing the cue during sleep, which is important for memory storage, may reactivate and strengthen the associated memory (SN: 10/3/19). In the new study, the researchers gave 36 people with nightmare disorder training in IRT, randomly assigning half of them to rehearse their revised nightmares in silence. The other half rehearsed while a short piano chord, the TMR cue, played every 10 seconds for five minutes. © Society for Science & the Public 2000–2022.

Keyword: Sleep
Link ID: 28532 - Posted: 10.28.2022

By Nicola Jones What color is a tree, or the sky, or a sunset? At first glance, the answers seem obvious. But it turns out there is plenty of variation in how people see the world — both between individuals and between different cultural groups. A lot of factors feed into how people perceive and talk about color, from the biology of our eyes to how our brains process that information, to the words our languages use to talk about color categories. There’s plenty of room for differences, all along the way. For example, most people have three types of cones — light receptors in the eye that are optimized to detect different wavelengths or colors of light. But sometimes, a genetic variation can cause one type of cone to be different, or absent altogether, leading to altered color vision. Some people are color-blind. Others may have color superpowers. Our sex can also play a role in how we perceive color, as well as our age and even the color of our irises. Our perception can change depending on where we live, when we were born and what season it is. To learn more about individual differences in color vision, Knowable Magazine spoke with visual neuroscientist Jenny Bosten of the University of Sussex in England, who wrote about the topic in the 2022 Annual Review of Vision Science. This conversation has been edited for length and clarity. How many colors are there in the rainbow? Physically, the rainbow is a continuous spectrum. The wavelengths of light vary smoothly between two ends within the visible range. There are no lines, no sharp discontinuities. The human eye can discriminate far more than seven colors within that range. But in our culture, we would say that we see seven color categories in the rainbow: red, orange, yellow, green, blue, indigo and violet. That’s historical and cultural. © 2022 Annual Reviews

Keyword: Vision
Link ID: 28531 - Posted: 10.28.2022

Elizabeth Pennisi Think of the chattiest creatures in the animal kingdom and songbirds, dolphins, and—yes—humans probably come to mind. Turtles probably don’t register. But these charismatic reptiles also communicate using a large repertoire of clicks, snorts, and chortles. Now, by recording the “voices” of turtles and other supposedly quiet animals, scientists have concluded that all land vertebrate vocalizations—from the canary’s song to the lion’s roar—have a common root that dates back more than 400 million years. The findings imply animals began to vocalize very early in their evolutionary history—even before they possessed well-developed ears, says W. Tecumseh Fitch, a bioacoustician at the University of Vienna who was not involved with the work. “It suggests our ears evolved to hear these vocalizations.” Several years ago, University of Arizona evolutionary ecologist John Wiens and his graduate student Zhuo Chen started looking into the evolutionary roots of acoustic communication—basically defined as the sounds animals make with their mouths using their lungs. Combing the scientific literature, the duo compiled a family tree of all the acoustic animals known at the time, eventually concluding such soundmaking abilities arose multiple times in vertebrates between 100 million and 200 million years ago. But Gabriel Jorgewich-Cohen, an evolutionary biologist at the University of Zürich, noticed an oversight: turtles. Though Wiens and Chen had found that only two of 14 families of turtles made sounds, he was finding a lot more. He spent 2 years recording 50 turtle species in the act of “speaking.”

Keyword: Hearing; Evolution
Link ID: 28530 - Posted: 10.28.2022

By Erika Check Hayden Weeks after Valeria Schenkel took an experimental drug named after her, the daily seizures that had afflicted her from birth became less frequent. But the drug caused fluid to build up in her brain, and a year later, she died at age 3. The drug was given to only one other child, and she experienced the same side effect and nearly died last year. The drug contained snippets of genetic material tailor-made to turn off the mutated gene causing the extremely rare form of epilepsy that these children were born with. A handful of researchers and nonprofit organizations have raised millions of dollars to make these treatments, known as antisense drugs, for at least 19 children and adults with severe diseases that are too rare to garner interest from pharmaceutical companies. The treatments have helped some of these patients, raising hopes that the personalized approach might one day save thousands of lives. But the brain side effect, known as hydrocephalus, reported on Sunday at the American Neurological Association meeting in Chicago, is a blow for the niche medical field that has made rapid progress over the past five years. Hydrocephalus happens when too much fluid fills cavities in the brain, increasing pressure on brain tissue and risking lethal damage if untreated. “I think it’s worth saying: No question that encountering hydrocephalus has been a setback, sobering and important,” said Dr. Timothy Yu, the neurologist and genetics researcher at Boston Children’s Hospital who developed the drug, known as valeriasen. But traditional drug companies, he added, are not helping patients with thousands of rare, untreatable and rapidly progressing diseases that cause death and severe disabilities. Personalized genetic treatments may be their only hope. “We have to learn as much as we can from each and every one, because they’re just so incredibly valuable in every sense,” Dr. Yu said. Scientists first imagined creating “antisense oligonucleotide” drugs — pieces of custom-made DNA or RNA designed to correct for genetic errors in cells — in the 1960s. But it took decades to make stable and effective versions of such drugs. © 2022 The New York Times Company

Keyword: Epilepsy; Development of the Brain
Link ID: 28529 - Posted: 10.28.2022

By Hannah Thomasy Ned and Sunny stretch out together on the warm sand. He rests his head on her back, and every so often he might give her an affectionate nudge with his nose. The pair is quiet and, like many long-term couples, they seem perfectly content just to be in each other’s presence. The couple are monogamous, which is quite rare in the animal kingdom. But Sunny and Ned are a bit scalier that your typical lifelong mates — they are shingleback lizards that live at Melbourne Museum in Australia. In the wild, shinglebacks regularly form long-term bonds, returning to the same partner during mating season year after year. One lizard couple in a long-term study had been pairing up for 27 years and were still going strong when the study ended. In this way, the reptiles are more like some of the animal kingdom’s most famous long-term couplers, such as albatrosses, prairie voles and owl monkeys, and they confound expectations many people have about the personalities of lizards. “There’s more socially going on with reptiles than we give them credit for,” said Sean Doody, a conservation biologist at the University of South Florida. Social behavior in reptiles has been largely overlooked for decades, but a handful of dedicated scientists have begun unraveling reptiles’ cryptic social structures. With the help of camera traps and genetic testing, scientists have discovered reptiles living in family groups, caring for their young and communicating with each other in covert ways. And they aren’t only doing this because they love lizards. Currently, one in five reptile species are threatened with extinction; researchers say learning more about reptile sociality could be crucial for conservation. Humans have a long history of animosity toward reptiles, and influential twentieth century scientists added to the idea of reptiles as cold, unintelligent beasts. In the mid-1900s, Paul MacLean, a neuroscientist at Yale and then the National Institute of Mental Health, began developing the triune brain hypothesis. He theorized that the human brain contained three parts: the reptilian R-complex, which governed survival and basic instinctual behaviors; the paleomammalian complex, which controlled emotional behavior; and the neomammalian cortex, which was responsible for higher functions like problem-solving and language. © 2022 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 28528 - Posted: 10.26.2022

By Jan Claassen, Brian L. Edlow A medical team surrounded Maria Mazurkevich’s hospital bed, all eyes on her as she did … nothing. Mazurkevich was 30 years old and had been admitted to New York–Presbyterian Hospital at Columbia University on a blisteringly hot July day in New York City. A few days earlier, at home, she had suddenly fallen unconscious. She had suffered a ruptured blood vessel in her brain, and the bleeding area was putting tremendous pressure on critical brain regions. The team of nurses and physicians at the hospital’s neurological intensive care unit was looking for any sign that Mazurkevich could hear them. She was on a mechanical ventilator to help her breathe, and her vital signs were stable. But she showed no signs of consciousness. Mazurkevich’s parents, also at her bed, asked, “Can we talk to our daughter? Does she hear us?” She didn’t appear to be aware of anything. One of us (Claassen) was on her medical team, and when he asked Mazurkevich to open her eyes, hold up two fingers or wiggle her toes, she remained motionless. Her eyes did not follow visual cues. Yet her loved ones still thought she was “in there.” She was. The medical team gave her an EEG—placing sensors on her head to monitor her brain’s electrical activity—while they asked her to “keep opening and closing your right hand.” Then they asked her to “stop opening and closing your right hand.” Even though her hands themselves didn’t move, her brain’s activity patterns differed between the two commands. These brain reactions clearly indicated that she was aware of the requests and that those requests were different. And after about a week, her body began to follow her brain. Slowly, with minuscule responses, Mazurkevich started to wake up. Within a year she recovered fully without major limitations to her physical or cognitive abilities. She is now working as a pharmacist. © 2022 Scientific American,

Keyword: Consciousness; Brain imaging
Link ID: 28527 - Posted: 10.26.2022

Nina Lakhani The mystery behind the astronomical rise in neurological disorders like Parkinson’s disease and Alzheimer’s could be caused by exposure to environmental toxins that are omnipresent yet poorly understood, leading doctors warn. At a conference on Sunday, the country’s leading neurologists and neuroscientists will highlight recent research efforts to fill the gaping scientific hole in understanding of the role environmental toxins – air pollution, pesticides, microplastics, forever chemicals and more – play in increasingly common diseases like dementias and childhood developmental disorders. Humans may encounter a staggering 80,000 or more toxic chemicals as they work, play, sleep and learn – so many that it is almost impossible to determine their individual effects on a person, let alone how they may interact or the cumulative impacts on the nervous system over a lifespan. Some contact with environmental toxins is inevitable given the proliferation of plastics and chemical pollutants, as well as America’s hands off regulatory approach, but exposure is unequal. In the US, communities of color, Indigenous people and low income families are far more likely to be exposed to a myriad of pollutants through unsafe housing and water, manufacturing and agricultural jobs, and proximity to roads and polluting industrial plants, among other hazards. It’s likely genetic makeup plays a role in how susceptible people are to the pathological effects of different chemicals, but research has shown higher rates of cancers and respiratory disease in environmentally burdened communities. © 2022 Guardian News & Media Limited

Keyword: Alzheimers; Parkinsons
Link ID: 28526 - Posted: 10.26.2022