By Rodrigo Pérez Ortega There’s clear evidence that racial discrimination negatively affects the health of people of color over the course of their lives. It’s associated with depression, anxiety, and psychological stress; it increases blood pressure; and it has been shown to weaken the immune system. However, few studies have linked single discriminatory events to immediate health effects. Now, data from a first-of-its-kind study suggest a racist attack could raise a person’s stress biomarkers almost immediately. “The big question mark, for me, has always been, how does this happen? What’s the black box that’s in the middle of discrimination, stress, and health disparities?” says Tiffany Yip, a developmental psychologist at Fordham University who was not involved with the study. “I think that this paper addresses that mechanistic question.” For the proof-of-concept study, Soohyun Nam at Yale University’s School of Nursing and her team collaborated with Black churches and their communities to recruit 12 Black people between the ages of 30 and 55 living in the northeastern United States. After accounting for the participants’ baseline stress levels, the research team adapted standardized survey questions about discrimination and microaggressions—such as whether they believed they had been mistaken for a service worker because of their race—and asked participants to share any occurrences of these experiences through a smartphone app. The method, known as ecological momentary assessment (EMA), has previously been used to study physical activity and behavior—such as alcohol intake reduction or smoking frequency. But this is one of the first studies correlating stress biomarkers and racist experiences using this precise monitoring technique. Researchers also asked the participants to describe their mood five times a day over the course of a week using the same phone app. To measure their biological response, participants spat into a tube four times a day over 4 days and froze the samples until research staff collected them. The researchers then had the samples analyzed in the lab to measure levels of cortisol, a hormone released during emotional distress, and alpha amylase, an enzyme that breaks down sugars and is secreted in stressful situations.

Keyword: Stress; Hormones & Behavior
Link ID: 28481 - Posted: 09.17.2022

By Jackie Rocheleau After experimenting on a hen, his dog, his goldfish, and himself, dentist William Morton was ready. On Oct. 16, 1846, he hurried to the Massachusetts General Hospital surgical theater for what would be the first successful public test of a general anesthetic. His concoction of sulfuric ether and oil from an orange (just for the fragrance) knocked a young man unconscious while a surgeon cut a tumor from his neck. To the onlooking students and clinicians, it was like a miracle. Some alchemical reaction between the ether and the man’s brain allowed him to slip into a state akin to light sleep, to undergo what should have been a painful surgery with little discomfort, and then to return to himself with only a hazy memory of the experience. General anesthesia redefined surgery and medicine, but over a century later it still carries significant risks. Too much sedation can lead to neurocognitive disorders and may even shorten lifespan; too little can lead to traumatic and painful wakefulness during surgery. So far, scientists have learned that, generally speaking, anesthetic drugs render people unconscious by altering how parts of the brain communicate. But they still don’t fully understand why. Although anesthesia works primarily on the brain, anesthesiologists do not regularly monitor the brain when they put patients under. And it is only in the past decade that neuroscientists interested in altered states of consciousness have begun taking advantage of anesthesia as a research tool. “It’s the central irony” of anesthesiology, says George Mashour, a University of Michigan neuroanesthesiologist, whose work entails keeping patients unconscious during neurosurgery and providing appropriate pain management. Mashour is one of a small set of clinicians and scientists trying to change that. They are increasingly bringing the tools of neuroscience into the operating room to track the brain activity of patients, and testing out anesthesia on healthy study participants. These pioneers aim to learn how to more safely anesthetize their patients, tailoring the dose to individual patients and adjusting during surgery. They also want to better understand what governs the transitions between states of consciousness and even hope to crack the code of coma. © 2022 NautilusThink Inc, All rights reserved.

Keyword: Sleep; Consciousness
Link ID: 28480 - Posted: 09.17.2022

By Mark Johnson A study using the electronic health records of more than 6 million Americans over age 65 found those who had covid-19 ran a greater risk of receiving a new diagnosis of Alzheimer’s disease within a year. The study, led by researchers at Case Western Reserve University School of Medicine and published in the Journal of Alzheimer’s Disease, does not show that covid-19 causes Alzheimer’s, but adds to a growing body of work suggesting links between the two. The results suggest researchers should be tracking older patients who recover from covid to see if they go on to show signs of memory loss, declining brain function or Alzheimer’s disease. The study found that for every 1,000 seniors with covid-19, seven will be diagnosed with Alzheimer’s within a year, slightly above the five-in-a-thousand diagnosis rate for seniors who did not have covid. “We know that covid can affect the brain, but I don’t think anyone had looked at new diagnoses of Alzheimer’s,” said Pamela Davis, one of the study’s co-authors and a research professor at Case Western Reserve University School of Medicine. Colleague Rong Xu said she had expected to see some increase among seniors sickened by covid, but was surprised “by the extent of the increase and how rapidly it occurred.” The study, though “important and useful” was “limited,” said Gabriel de Erausquin, director of the Laboratory of Brain Development, Modulation and Repair at University of Texas Health San Antonio, who was not involved in the research. He cautioned that a diagnosis of Alzheimer’s disease is not necessarily confirmation of the disease. Doctors sometimes diagnose Alzheimer’s based on changes in behavior, or responses to a memory test. These are considered less accurate than imaging or spinal fluid tests that measure two types of proteins, beta-amyloid and phosphorylated tau, which accumulate abnormally in the brains of people with Alzheimer’s. Brain scans that look for structural changes, such as the shrinking of certain regions, are another more accurate indicator. © 1996-2022 The Washington Post

Keyword: Alzheimers
Link ID: 28479 - Posted: 09.17.2022

by Nora Bradford A well-studied brain response to sound, called the M100, appears earlier in life in autistic children than in their non-autistic peers, according to a new longitudinal study. The finding suggests that the auditory cortex in children with autism matures unusually quickly, a growth pattern seen previously in other brain regions. “It’s a demonstration that when we look for autism markers in the brain, they can be very age-specific,” says lead investigator J. Christopher Edgar, associate professor of radiology at the Children’s Hospital of Philadelphia in Pennsylvania. For that reason, longitudinal studies such as this one — in which Edgar and his colleagues assessed children at up to three different ages — are essential, he adds. “If the two populations being studied have different rates of brain maturation, then the pattern of findings changes across time.” At the time of the first magnetoencephalography (MEG) scan, when the children were 6 to 9 years old, those with autism were more likely to have an M100 response to a barely audible tone in the right hemisphere than non-autistic children were. But this difference disappeared in the next two visits, presumably because the M100 response typically appears during early adolescence. By contrast, the M50 response, which occurs throughout life, beginning in utero, showed no significant difference between the two groups at any visit. The team also evaluated ‘phase locking,’ a measure of how similar a participant’s neural activity is from scan to scan within a certain frequency band. Autistic participants demonstrated more mature phase-locking patterns at the first visit, which then diminished at the later two visits. © 2022 Simons Foundation

Keyword: Autism; Hearing
Link ID: 28478 - Posted: 09.17.2022

Sara Reardon More than 500,000 years ago, the ancestors of Neanderthals and modern humans were migrating around the world when a pivotal genetic mutation caused some of their brains to improve suddenly. This mutation, researchers report in Science1, drastically increased the number of brain cells in the hominins that preceded modern humans, probably giving them a cognitive advantage over their Neanderthal cousins. “This is a surprisingly important gene,” says Arnold Kriegstein, a neurologist at the University of California, San Francisco. However, he expects that it will turn out to be one of many genetic tweaks that gave humans an evolutionary advantage over other hominins. “I think it sheds a whole new light on human evolution.” When researchers first reported the sequence of a complete Neanderthal genome in 20142, they identified 96 amino acids — the building blocks that make up proteins — that differ between Neanderthals and modern humans, as well as some other genetic tweaks. Scientists have been studying this list to learn which of these changes helped modern humans to outcompete Neanderthals and other hominins. Cognitive advantage To neuroscientists Anneline Pinson and Wieland Huttner at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, Germany, one gene stood out. TKTL1 encodes a protein that is made when a fetus’s brain is first developing. A mutation in the human version changed one amino acid, resulting in a protein that is different from those found in hominin ancestors, Neanderthals and non-human primates. The researchers suspected that this protein could increase the proliferation of neural progenitor cells, which become neurons, as the brain develops, specifically in an area called the neocortex — a region involved in cognitive function. This, they reasoned, could contribute to modern humans’ cognitive advantage. © 2022 Springer Nature Limited

Keyword: Evolution; Genes & Behavior
Link ID: 28477 - Posted: 09.14.2022

By Erin Garcia de Jesús Human trash can be a cockatoo’s treasure. In Sydney, the birds have learned how to open garbage bins and toss trash around in the streets as they hunt for food scraps. People are now fighting back. Bricks, pool noodles, spikes, shoes and sticks are just some of the tools Sydney residents use to keep sulphur-crested cockatoos (Cacatua galerita) from opening trash bins, researchers report September 12 in Current Biology. The goal is to stop the birds from lifting the lid while the container is upright but still allowing the lid to flop open when a trash bin is tilted to empty its contents. This interspecies battle could be a case of what’s called an innovation arms race, says Barbara Klump, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Radolfzell, Germany. When cockatoos learn how to flip trash can lids, people change their behavior, using things like bricks to weigh down lids, to protect their trash from being flung about (SN Explores: 10/26/21). “That’s usually a low-level protection and then the cockatoos figure out how to defeat that,” Klump says. That’s when people beef up their efforts, and the cycle continues. Researchers are closely watching this escalation to see what the birds — and humans — do next. With the right method, the cockatoos might fly by and keep hunting for a different target. Or they might learn how to get around it. In the study, Klump and colleagues inspected more than 3,000 bins across four Sydney suburbs where cockatoos invade trash to note whether and how people were protecting their garbage. Observations coupled with an online survey showed that people living on the same street are more likely to use similar deterrents, and those efforts escalate over time. © Society for Science & the Public 2000–2022.

Keyword: Learning & Memory; Evolution
Link ID: 28476 - Posted: 09.14.2022

James Brunton Badenoch Monkeypox’s effect on the skin – the disfiguring rashes – and the flu-like symptoms have been well described, but few have investigated the neurological and psychiatric problems the virus might cause. There are historic reports of neurological complications in people infected with the related smallpox virus and in people vaccinated against smallpox, which contains the related vaccinia virus. So my colleagues and I wanted to know whether monkeypox causes similar problems. We looked at all the evidence from before the current monkeypox pandemic of neurological or psychiatric problems in people with a monkeypox infection. The results are published in the journal eClinicalMedicine. A small but noticeable proportion of people (2% to 3%) with monkeypox became very unwell and developed serious neurological problems, including seizure and encephalitis (inflammation of the brain that can cause long-term disability). We also found that confusion occurred in a similar number of people. It’s important to note, though, that these figures are based on a few studies with few participants. Besides the severe and rare brain problems, we found evidence of a broader group of people with monkeypox who had more common neurological symptoms including headache, muscle ache and fatigue. From looking at the studies, it was unclear how severe these symptoms were and how long they lasted. It was also unclear how many people with monkeypox had psychiatric problems - such as anxiety and depression - as few studies looked into it. Of those that did, low mood was frequently reported.. © 2010–2022, The Conversation US, Inc.

Keyword: Epilepsy; Learning & Memory
Link ID: 28475 - Posted: 09.14.2022

Jon Hamilton In some families, Alzheimer's disease seems inevitable. "Your grandmother has it, your mom has it, your uncle has it, your aunts have it, your cousin has it. I always assumed that I would have it," says Karen Douthitt, 57. "It was always in our peripheral vision," says Karen's sister June Ward, 61. "Our own mother started having symptoms at age 62, so it has been a part of our life." Nearly a decade ago, Karen, June, and an older sister, Susie Gilliam, 64, set out to learn why Alzheimer's was affecting so many family members. Since then, each sister has found out whether she carries a rare gene mutation that makes Alzheimer's inescapable. And all three have found ways to help scientists trying to develop treatments for the disease. I met Karen and June in 2015, at the first-ever conference for families with a particular type of genetic mutation in which Alzheimer's often appears in middle age. The annual conference is sponsored by the Alzheimer's Association and the Dominantly Inherited Alzheimer's Network Trials Unit, a research program run by Washington University School of Medicine in St. Louis. Karen and June had come to Washington, D.C., for the family conference because of something they had just learned about a cousin on their mother's side. The cousin had developed Alzheimer's in her 50s. And genetic tests showed that she carried a rare, inherited gene mutation called presenilin 1. It's one of three mutations that typically cause Alzheimer's to appear in middle age. The three gene mutations responsible for early Alzheimer's are unlike a better known gene called APOE4, which merely increases the likelihood somewhat that a person will develop Alzheimer's – and usually at age 65 or older. In contrast, the early-onset mutations, including presenilin 1, make it almost certain an individual will develop the disease, and usually before age 60. Each child of a parent who has the presenilin 1 mutation has a 50% chance of inheriting it. © 2022 npr

Keyword: Alzheimers; Genes & Behavior
Link ID: 28474 - Posted: 09.14.2022

Emily Willingham In 2016, pharmacologist Susan Howlett wrote up a study on how hormone levels during pregnancy affect heart function and sent it off to a journal. When the reviewers’ comments came back, two of the three had asked an unexpected question: where were the tissues from male mice? Because they were studying high hormone levels related to pregnancy, Howlett, at Dalhousie University in Halifax, Canada, and her team had used only female animals. “I was really surprised that they wanted us to repeat everything in males,” she said. Nonetheless, they obliged, and their findings were published in 2017. As expected, they found no effect of the hormone progesterone on heart function in males; in females, it influenced the activity of cardiac cells1. Howlett had mixed feelings about the request to add males. “It was a big ask and it was a lot more research.” But in general, she adds, it’s really important to factor sex into studies. “I’m a big proponent of doing experiments in both males and females.” Many of science’s gatekeepers — granting agencies and academic journals — feel the same way. Over the past decade or so, a growing list of funders and publishers, including the US National Institutes of Health (NIH) and the European Union, have been asking researchers to include two sexes in their work with cells and animal models. Two major catalysts motivated these policies. One was a growing recognition that sex-based differences, often related to hormone profiles or genes on sex chromosomes, can influence responses to drugs and other treatments. The other was the realization that including two sexes can increase the rigour of scientific inquiry, enhance reproducibility and open up questions for scientific pursuit. © 2022 Springer Nature Limited

Keyword: Sexual Behavior
Link ID: 28473 - Posted: 09.14.2022

ByRodrigo Pérez Ortega We humans are proud of our big brains, which are responsible for our ability to plan ahead, communicate, and create. Inside our skulls, we pack, on average, 86 billion neurons—up to three times more than those of our primate cousins. For years, researchers have tried to figure out how we manage to develop so many brain cells. Now, they’ve come a step closer: A new study shows a single amino acid change in a metabolic gene helps our brains develop more neurons than other mammals—and more than our extinct cousins, the Neanderthals. The finding “is really a breakthrough,” says Brigitte Malgrange, a developmental neurobiologist at the University of Liège who was not involved in the study. “A single amino acid change is really, really important and gives rise to incredible consequences regarding the brain.” What makes our brain human has been the interest of neurobiologist Wieland Huttner at the Max Planck Institute of Molecular Cell Biology and Genetics for years. In 2016, his team found that a mutation in the ARHGAP11B gene, found in humans, Neanderthals, and Denisovans but not other primates, caused more production of cells that develop into neurons. Although our brains are roughly the same size as those of Neanderthals, our brain shapes differ and we created complex technologies they never developed. So, Huttner and his team set out to find genetic differences between Neanderthals and modern humans, especially in cells that give rise to neurons of the neocortex. This region behind the forehead is the largest and most recently evolved part of our brain, where major cognitive processes happen. The team focused on TKTL1, a gene that in modern humans has a single amino acid change—from lysine to arginine—from the version in Neanderthals and other mammals. By analyzing previously published data, researchers found that TKTL1 was mainly expressed in progenitor cells called basal radial glia, which give rise to most of the cortical neurons during development. © 2022 American Association for the Advancement of Science.

Keyword: Development of the Brain; Evolution
Link ID: 28472 - Posted: 09.10.2022

Yasemin Saplakoglu You’re on the vacation of a lifetime in Kenya, traversing the savanna on safari, with the tour guide pointing out elephants to your right and lions to your left. Years later, you walk into a florist’s shop in your hometown and smell something like the flowers on the jackalberry trees that dotted the landscape. When you close your eyes, the store disappears and you’re back in the Land Rover. Inhaling deeply, you smile at the happy memory. Now let’s rewind. You’re on the vacation of a lifetime in Kenya, traversing the savanna on safari, with the tour guide pointing out elephants to your right and lions to your left. From the corner of your eye, you notice a rhino trailing the vehicle. Suddenly, it sprints toward you, and the tour guide is yelling to the driver to hit the gas. With your adrenaline spiking, you think, “This is how I am going to die.” Years later, when you walk into a florist’s shop, the sweet floral scent makes you shudder. “Your brain is essentially associating the smell with positive or negative” feelings, said Hao Li, a postdoctoral researcher at the Salk Institute for Biological Studies in California. Those feelings aren’t just linked to the memory; they are part of it: The brain assigns an emotional “valence” to information as it encodes it, locking in experiences as good or bad memories. And now we know how the brain does it. As Li and his team reported recently in Nature, the difference between memories that conjure up a smile and those that elicit a shudder is established by a small peptide molecule known as neurotensin. They found that as the brain judges new experiences in the moment, neurons adjust their release of neurotensin, and that shift sends the incoming information down different neural pathways to be encoded as either positive or negative memories. To be able to question whether to approach or to avoid a stimulus or an object, you have to know whether the thing is good or bad. All Rights Reserved © 2022

Keyword: Learning & Memory; Emotions
Link ID: 28471 - Posted: 09.10.2022

By Jonathan Moens An artificial intelligence can decode words and sentences from brain activity with surprising — but still limited — accuracy. Using only a few seconds of brain activity data, the AI guesses what a person has heard. It lists the correct answer in its top 10 possibilities up to 73 percent of the time, researchers found in a preliminary study. The AI’s “performance was above what many people thought was possible at this stage,” says Giovanni Di Liberto, a computer scientist at Trinity College Dublin who was not involved in the research. Developed at the parent company of Facebook, Meta, the AI could eventually be used to help thousands of people around the world unable to communicate through speech, typing or gestures, researchers report August 25 at arXiv.org. That includes many patients in minimally conscious, locked-in or “vegetative states” — what’s now generally known as unresponsive wakefulness syndrome (SN: 2/8/19). Most existing technologies to help such patients communicate require risky brain surgeries to implant electrodes. This new approach “could provide a viable path to help patients with communication deficits … without the use of invasive methods,” says neuroscientist Jean-Rémi King, a Meta AI researcher currently at the École Normale Supérieure in Paris. King and his colleagues trained a computational tool to detect words and sentences on 56,000 hours of speech recordings from 53 languages. The tool, also known as a language model, learned how to recognize specific features of language both at a fine-grained level — think letters or syllables — and at a broader level, such as a word or sentence. © Society for Science & the Public 2000–2022.

Keyword: Language; Robotics
Link ID: 28470 - Posted: 09.10.2022

By Alice Callahan Katherine Flegal wanted to be an archaeologist. But it was the 1960s, and Flegal, an anthropology major at the University of California, Berkeley, couldn’t see a clear path to this profession at a time when nearly all the summer archaeology field schools admitted only men. “The accepted wisdom among female archaeology students was that there was just one sure way for a woman to become an archaeologist: marry one,” Flegal wrote in a career retrospective published in the 2022 Annual Review of Nutrition. And so Flegal set her archaeology aspirations aside and paved her own path, ultimately serving nearly 30 years as an epidemiologist at the National Center for Health Statistics (NCHS), part of the US Centers for Disease Control and Prevention. There, she spent decades crunching numbers to describe the health of the nation’s people, especially as it related to body size, until she retired from the agency in 2016. At the time of her retirement, her work had been cited in 143,000 books and articles. In the 1990s, Flegal and her CDC colleagues published some of the first reports of a national increase in the proportion of people categorized as overweight based on body mass index (BMI), a ratio of weight and height. The upward trend in BMI alarmed public health officials and eventually came to be called the “obesity epidemic.” But when Flegal, along with other senior government scientists, published estimates on how BMI related to mortality — reporting that being overweight was associated with a lower death rate than having a “normal” BMI — she became the subject of intense criticism and attacks. Flegal and her coauthors were not the first to publish this seemingly counterintuitive observation, but they were among the most prominent. Some researchers in the field, particularly from the Harvard School of Public Health, argued that the findings would detract from the public health message that excess body fat was hazardous, and they took issue with some of the study’s methods. Flegal’s group responded with several subsequent publications reporting that the suggested methodological adjustments didn’t change their findings. © 2022 Annual Reviews

Keyword: Obesity
Link ID: 28469 - Posted: 09.10.2022

Short ribs glazed in a sweet sticky sauce and slow-cooked to perfection, potato chips hand-fried and tossed with a generous coating of sour cream, chicken wings battered and double-fried so that they stay crispy for hours. What is it about these, and other, mouth-watering — but incredibly fatty — foods that makes us reach out, and keep coming back for more? How they taste on the tongue is one part of the story, but to really understand what drives “our insatiable appetite for fat,” we have to examine what happens after fat is consumed, says Columbia University’s Charles Zuker, a neuroscientist and molecular geneticist who has been a Howard Hughes Medical Institute (HHMI) Investigator since 1989. Two years ago, Zuker and his team reported how sugar, upon reaching the gut, triggers signals that are sent to the brain, thus fueling cravings for sweet treats. Now, in an article published in Nature on September 7, 2022, they describe a similar gut-to-brain circuit that underlies a preference for fat. “The gut is the source of our great desire for fat and sugar,” says Zuker. The topic in question is an incredibly timely one, given the current global obesity epidemic. An estimated 13 percent of adults worldwide are obese — thrice that in 1975. In the US, that figure is even higher — at a staggering 42 percent. “It’s a very significant and important health problem,” says Zuker. Having a high body-mass index is a risk factor for stroke, diabetes, and several other diseases. “It’s clear that if we want to help make a difference here, we need to understand the biological basis for our strong appetite for fat and sugar,” he says. Doing so will help us design interventions in the future to “suppress this strong drive to consume” and combat obesity.

Keyword: Obesity; Hormones & Behavior
Link ID: 28468 - Posted: 09.10.2022

By Laurie McGinley Independent advisers to the Food and Drug Administration on Wednesday voted 7 to 2 to recommend approval of an experimental ALS drug with strong support from patients and advocates, making it likely the hotly debated treatment will be cleared by the agency within weeks. The vote was a stunning turnaround from late March when the panel voted 6 to 4 to recommend against FDA approval. At that meeting, the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee concluded the evidence from a single clinical trial — with just 137 patients and some follow-up data — was not sufficient to show the drug, called AMX0035, slowed a degenerative disease that usually kills people within three to five years. But on Wednesday, after hours of discussion, several advisers said that additional analyses submitted by the drug’s manufacturer, Cambridge-based Amylyx, bolstered the case for approval, even though uncertainties remain. Advisers were also affected by the disease’s severity and the lack of effective treatments. A vow by a top Amylyx official to pull the drug from the market if a larger study, with 600 patients, fails to show effectiveness was also a factor in the vote. The FDA, which usually follows the recommendation of its outside advisers but is not required to, is expected to decide whether to approve the drug by Sept. 29. The improved fortunes of the medicine came despite criticism from FDA staff as recently as last week about the treatment’s effectiveness, the conduct of its clinical trial and the researchers’ interpretation of the data. But the medicine is considered safe, and the agency has been under intense pressure from ALS patients and physicians who say the treatment holds promise for a fatal disease that typically causes rapid deterioration and death.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28467 - Posted: 09.10.2022

By Helen Santoro I barreled into the world — a precipitous birth, the doctors called it — at a New York City hospital in the dead of night. In my first few hours of life, after six bouts of halted breathing, the doctors rushed me to the neonatal intensive care unit. A medical intern stuck his pinky into my mouth to test the newborn reflex to suck. I didn’t suck hard enough. So they rolled my pink, 7-pound-11-ounce body into a brain scanner. Lo and behold, there was a huge hole on the left side, just above my ear. I was missing the left temporal lobe, a region of the brain involved in a wide variety of behaviors, from memory to the recognition of emotions, and considered especially crucial for language. My mother, exhausted from the labor, remembers waking up after sunrise to a neurologist, pediatrician and midwife standing at the foot of her bed. They explained that my brain had bled in her uterus, a condition called a perinatal stroke. They told her I would never speak and would need to be institutionalized. The neurologist brought her arms up to her chest and contorted her wrists to illustrate the physical disability I would be likely to develop. In those early days of my life, my parents wrung their hands wondering what my life, and theirs, would look like. Eager to find answers, they enrolled me in a research project at New York University tracking the developmental effects of perinatal strokes. But month after month, I surprised the experts, meeting all of the typical milestones of children my age. I enrolled in regular schools, excelled in sports and academics. The language skills the doctors were most worried about at my birth — speaking, reading and writing — turned out to be my professional passions. My case is highly unusual but not unique. Scientists estimate that thousands of people are, like me, living normal lives despite missing large chunks of our brains. Our myriad networks of neurons have managed to rewire themselves over time. But how? © 2022 The New York Times Company

Keyword: Development of the Brain; Language
Link ID: 28466 - Posted: 09.07.2022

Michael Heithaus Could you explain how fish sleep? Do they drift away on currents, or do they anchor themselves to a particular location when they sleep? – Laure and Neeraj, New York From the goldfish in your aquarium to a bass in a lake to the sharks in the sea – 35,000 species of fish are alive today, more than 3 trillion of them. All over the world, they swim in hot springs, rivers, ponds and puddles. They glide through freshwater and saltwater. They survive in the shallows and in the darkest depths of the ocean, more than five miles down. If those trillions of fish, three major types exist: bony fish, like trout and sardines; jawless fish, like the slimy hagfish; and sharks and rays, which are boneless – instead, they have skeletons made of firm yet flexible tissue called cartilage. And all of them, every last one, needs to rest. Whether you’re a human or a haddock, sleep is essential. It gives a body time to repair itself, and a brain a chance to reset and declutter. As a marine biologist, I’ve always wondered how fish can rest. After all, in any body of water, predators are all over the place, lurking around, ready to eat them. But somehow they manage, like virtually all creatures on Earth. See the mysterious spot off the coast of Mexico where sharks take a nap. How they do it Scientists are still learning about how fish sleep. What we do know: Their sleep is not like ours. © 2010–2022, The Conversation US, Inc.

Keyword: Sleep; Evolution
Link ID: 28465 - Posted: 09.07.2022

By Christina Jewett Juul Labs, fighting for its survival in the United States, on Tuesday tentatively agreed to pay $438.5 million to settle an investigation by nearly three dozen states over marketing and sales practices that they contend set off the nation’s teenage vaping crisis. The company said that it did not acknowledge any wrongdoing in the settlement, but that it was trying to “resolve issues from the past” while awaiting a decision by the Food and Drug Administration over whether it would be permitted to continue to sell its products. Juul has been trying to reposition itself as a seller of vaping products that could help adults quit smoking traditional cigarettes, in an effort to rehabilitate its tarnished reputation and improve its diminished market value. The tentative settlement prohibits the company from marketing to youth, funding education in schools and misrepresenting the level of nicotine in its products. But Juul had already discontinued several marketing practices and withdrawn many of its flavored pods that appealed to teenagers, under public pressure from lawmakers, parents and health experts a few years ago when the vaping crisis was at a peak. “We think that this will go a long way in stemming the flow of youth vaping,” William Tong, Connecticut’s attorney general, said at a news conference on Tuesday. “We are under no illusions and cannot claim that it will stop youth vaping. It continues to be an epidemic. It continues to be a huge problem. But we have essentially taken a big chunk out of what was once a market leader.” The multistate investigation found that the company appealed to young people by hiring young models, using social media to court teenagers and giving out free samples, he said. And, he added, the inquiry revealed that the company had a “porous” age verification system for its products and that 45 percent of its Twitter followers were ages 13 to 17. Jason Miyares, the attorney general for Virginia, pointed out in a statement that the company’s former strategy of selling flavors like mango and crème brûlée appealed to youth as did the sleek design of its device that was easy to conceal. One term of the settlement banned the company from depicting anyone under 35 in its marketing images, Mr. Miyares’ statement said. © 2022 The New York Times Company

Keyword: Drug Abuse
Link ID: 28464 - Posted: 09.07.2022

Perspective by Steven Petrow A few weeks ago, I mentioned to a friend that I was interested in learning more about psychedelics, especially how they might help me with depression and anxiety. That’s a broad category of plant medicines including psilocybin (“magic”) mushrooms, MDMA (ecstasy), DMT (Dimitri or the Businessman’s Trip), ketamine (“special K”) and some others. I’d been hesitant to be open about my search, because I’m old enough to remember the warnings about “bad trips” that scramble your brain. Imagine my surprise when my friend told me he’d recently taken his first “trip,” which he described as life-changing. I asked him — a real estate developer living in Northern California, married with kids — why he decided to try a psychedelic substance. “My work felt increasingly stale and meaningless,” he explained to me over a beer. “Despite a massive amount of reflection and coaching around how to break the rut, I felt as though I was still off track.” He and the others who have used these medicines spoke on the condition of anonymity because most of these psychedelics are Schedule I substances, meaning they are illegal to manufacture, buy, possess or distribute. When I confided my interest in psychedelics to a few other friends, several said they had tried the drugs and experienced several benefits: from easing anxiety to finding spiritual insights to combating depression and, among some with cancer, helping to reduce the fear of dying. They are hardly outliers. According to a new YouGovAmerica study, “one in four Americans say they’ve tried at least one psychedelic drug,” amounting to some 72 million U.S. adults. (The study included the medicines mentioned earlier, plus LSD, mescaline and salvia.) Was I missing a beat by not getting onboard?

Keyword: Depression; Drug Abuse
Link ID: 28463 - Posted: 09.07.2022

Nicola Davis Regular doses of a hormone may help to boost cognitive skills in people with Down’s syndrome, a pilot study has suggested. Researchers fitted seven men who have Down’s syndrome with a pump that provided a dose of GnRH, a gonadotropin-releasing hormone, every two hours for six months. Six out of the seven men showed moderate cognitive improvements after the treatment, including in attention and being able to understand instructions, compared with a control group who were not given the hormone. However, experts raised concerns about the methods used in the study, urging caution over the findings. The team behind the work said brain scans of the participants, who were aged between 20 and 37, given the hormone suggest they underwent changes in neural connectivity in areas involved in cognition. “[People] with Down’s syndrome have cognitive decline which starts in the 30s,” said Prof Nelly Pitteloud, co-author of the study from the University of Lausanne. “I think if we can delay that, this would be great, if the therapy is well tolerated [and] without side effects.” Writing in the journal Science, Pitteloud and colleagues said they previously found mice with an extra copy of chromosome 16 experienced an age-related decline in cognition and sense of smell, similar to that seen in people with Down’s syndrome – who have an extra copy of chromosome 21. In a series of experiments, the team found regular doses of gonadotropin-releasing hormone boosted both the sense of smell and cognitive performance of these mice. Pitteloud said no side effects were seen in the participants and that the hormone is already used to induce puberty in patients with certain disorders. “I think these data are of course very exciting, but we have to remain cautious,” said Pitteloud. She said larger, randomised control studies are now needed to confirm that the improvements were not driven by patients becoming less stressed during assessments and thus performing better. Prof Michael Thomas of Birkbeck, University of London, who studies cognitive development across the lifespan in Down’s syndrome, said the results were exciting. “For parents, this is good news: interventions can still yield benefits across the lifespan,” he said, although he noted it is not clear how applicable the hormone therapy would be for children. © 2022 Guardian News & Media Limited

Keyword: Hormones & Behavior; Development of the Brain
Link ID: 28462 - Posted: 09.03.2022