Scientists at the National Institutes of Health have identified new genetic risk factors for two types of non-Alzheimer’s dementia. These findings were published in Cell Genomics and detail how researchers identified large-scale DNA changes, known as structural variants, by analyzing thousands of DNA samples. The team discovered several structural variants that could be risk factors Lewy body dementia (LBD) and frontotemporal dementia (FTD). The project was a collaborative effort between scientists at the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA) at NIH. Structural variants have been implicated in a variety of neurological disorders. Unlike more commonly studied mutations, which often affect one or a few DNA building blocks called nucleotides, structural variants represent at least 50 but often hundreds, or even thousands, of nucleotides at once, making them more challenging to study. “If you imagine that our entire genetic code is a book, a structural variant would be a paragraph, page, or even an entire chapter that has been removed, duplicated, or inserted in the wrong place,” said Sonja W. Scholz, M.D., Ph.D., investigator in the neurogenetics branch of NINDS and senior author of this study. By combining cutting-edge computer algorithms capable of mapping structural variations across the whole genome with machine learning, the research team analyzed whole-genome data from thousands of patient samples and several thousand unaffected controls. A previously unknown variant in the gene TCPN1 was found in samples from patients with LBD, a disease, that like Parkinson’s disease, is associated with abnormal deposits of the protein alpha-synuclein in the brain. This variant, in which more than 300 nucleotides are deleted from the gene, is associated with a higher risk for developing LBD. While this finding is new for LBD, TCPN1 is a known risk factor for Alzheimer’s disease, which could mean that this structural variant plays a role in the broader dementia population.

Keyword: Alzheimers; Genes & Behavior
Link ID: 28775 - Posted: 05.10.2023

By Freda Kreier Pregnancy can do weird things to the body. For some bats, it can hamper their ability to “see” the world around them. Kuhl’s pipistrelle bats (Pipistrellus kuhlii) echolocate less frequently while pregnant, researchers report March 28 in BMC Biology. The change may make it harder for the tiny bats to detect prey and potential obstacles in the environment. The study is among the first to show that pregnancy can shape how nonhuman mammals sense their surroundings, says Yossi Yovel, a neuroecologist at Tel Aviv University in Israel. Nocturnal bats like Kuhl’s pipistrelles famously use sound to navigate and hunt prey in the dark (SN: 9/20/17). Their calls bounce off whatever is nearby and bats use the echoes to reconstruct what’s around them, a process aptly named echolocation. The faster a bat makes calls, the better it can make out its surroundings. But rapid-fire calling requires breathing deeply, which is something that pregnancy can get in the way of. “Although I’ve never been pregnant, I know that when I eat a lot, it’s more difficult to breathe,” Yovel says. So pregnancy — which can add a full gram to a 7-gram Kuhl’s pipistrelle and may push up on the lungs — might hamper echolocation. Yovel and colleagues tested their hypothesis by capturing 10 Kuhl’s pipistrelles, five of whom were pregnant, and training the bats to find and land on a platform. Recordings of the animals’ calls revealed that bats that weren’t pregnant made around 130 calls on average while searching for the platform. But bats that were pregnant made only around 110 calls, or 15 percent fewer. © Society for Science & the Public 2000–2023.

Keyword: Hearing; Hormones & Behavior
Link ID: 28774 - Posted: 05.10.2023

Sara Reardon For the second time, an experimental drug has been shown to reduce the cognitive decline associated with Alzheimer’s disease. On 3 May, pharmaceutical company Eli Lilly announced in a press release that its monoclonal antibody donanemab slowed mental decline by 35% for some participants in a 1,736-person trial — a rate comparable to that for competitor drug lecanemab. But researchers warn that until the full results are published, questions remain as to the drug’s clinical usefulness, as well as whether the modest benefit outweighs the risk of harmful side effects. Like lecanemab, donanemab targets amyloid protein, which is thought to cause dementia by accumulating in the brain and damaging neurons. The trial results provide strong evidence that amyloid is a key driver of Alzheimer’s, says Jeffrey Cummings, a neuroscientist at the University of Nevada, Las Vegas. “These are transformative in an enormously important way from a scientific point of view,” he adds. “They’re terrific.” But Marsel Mesulam, a neurologist at Northwestern University in Chicago, is more cautious. “The results that are described are extremely significant and impressive, but clinically their significance is doubtful,” he says, adding that the modest effect suggests that factors other than amyloid contribute to Alzheimer’s disease progression. “We’re heading to a new era — there’s room to cheer, but it’s an era that should make us all very sober, realizing that there will be no single magic bullet.” In the press release, Eli Lilly said that people with mild Alzheimer’s who received donanemab showed 35% less clinical decline over 18 months than did those who received a placebo, and 40% less decline in their ability to perform daily tasks. The company, based in Indianapolis, Indiana, says that it will present the full results at a conference in July and publish them in a peer-reviewed journal. It plans to apply for approval by the US Food and Drug Administration (FDA) in the next two months. Promising treatments © 2023 Springer Nature Limited

Keyword: Alzheimers
Link ID: 28773 - Posted: 05.06.2023

Tess McClure Every few months, Cohen “Coey” Irwin lies on his back and lets the walls close in. Lights move overhead, scanning over the tattoos covering his cheeks. He lies suspended, his head encased by a padded helmet, ears blocked, as his body is shunted into a tunnel. The noise begins: a rhythmic crashing, loud as a jackhammer. For the next hour, an enormous magnet will produce finely detailed images of Irwin’s brain. Irwin has spent much of his adult life addicted to smoking methamphetamine – or P, as the drug is known in New Zealand. He knows its effects intimately: the euphoria, the paranoia, the explosive violence, the energy, the tics that run through his neck and lips. Stepping outside the MRI machine, however, he can get a fresh view for the first time – looking in from the outside at what the drug has done to his internal organs. New Zealanders are some of the world’s biggest meth takers: wastewater testing has placed it in the top four consumers worldwide. The country’s physical isolation – 4,000km from the nearest major ports – makes importing hard drugs challenging and costly, but meth can be manufactured relatively cheaply and easily, and is derived from available pharmaceuticals. Almost a third of middle-aged New Zealanders have tried the drug, a University of Otago study found in 2020. In the backroom of Mātai research centre, Irwin thinks back to when it all started. He was a teenager when he tried P for the first time – trying to impress a girl on New Year’s Eve, in his home town of Porirua, Wellington. The girlfriend didn’t last, but the drug was love at first puff, he says, and would become one of the defining relationships of his life. “I remember it was the next day, the sun had risen, I was still awake with the people at the table I’d been smoking with. And I was instantly trying to find ways: how can we make money to get more?” Within a few years, he would be smoking every day. © 2023 Guardian News & Media Limited

Keyword: Drug Abuse; Brain imaging
Link ID: 28772 - Posted: 05.06.2023

Twelve people with persistent neurological symptoms after SARS-CoV-2 infection were intensely studied at the National Institutes of Health (NIH) and were found to have differences in their immune cell profiles and autonomic dysfunction. These data inform future studies to help explain persistent neurological symptoms in Long COVID. The findings, published in Neurology: Neuroimmunology & Neuroinflammation(link is external), may lead to better diagnoses and new treatments. People with post-acute sequelae of COVID-19 (PASC), which includes Long COVID, have a wide range of symptoms, including fatigue, shortness of breath, fever, headaches, sleep disturbances, and “brain fog,” or cognitive impairment. Such symptoms can last for months or longer after an initial SARS-CoV-2 infection. Fatigue and “brain fog” are among the most common and debilitating symptoms, and likely stem from nervous system dysfunction. Researchers used an approach called deep phenotyping to closely examine the clinical and biological features of Long COVID in 12 people who had long-lasting, disabling neurological symptoms after COVID-19. Most participants had mild symptoms during their acute infection. At the NIH Clinical Center, participants underwent comprehensive testing, which included a clinical exam, questionnaires, advanced brain imaging, blood and cerebrospinal fluid tests, and autonomic function tests. The results showed that people with Long COVID had lower levels of CD4+ and CD8+ T cells—immune cells involved in coordinating the immune system’s response to viruses—compared to healthy controls. Researchers also found increases in the numbers of B cells and other types of immune cells, suggesting that immune dysregulation may play a role in mediating Long COVID.

Keyword: Neuroimmunology
Link ID: 28771 - Posted: 05.06.2023

By Neelam Bohra Ayla Wing’s middle school students don’t always know what to make of their 26-year-old teacher’s hearing aids. The most common response she hears: “Oh, my grandma has them, too.” But grandma’s hearing aids were never like this: Bluetooth-enabled and connected to her phone, they allow Ms. Wing to toggle with one touch between custom settings. She can shut out the world during a screeching subway ride, hear her friends in noisy bars during a night out and even understand her students better by switching to “mumbly kids.” A raft of new hearing aids have hit the market in recent years, offering greater appeal to a generation of young adults that some experts say is both developing hearing problems earlier in life and — perhaps paradoxically — becoming more comfortable with an expensive piece of technology pumping sound into their ears. Some of the new models, including Ms. Wing’s, are made by traditional prescription brands, which usually require a visit to a specialist. But the Food and Drug Administration opened up the market last year when it allowed the sale of hearing aids over the counter. In response, brand names like Sony and Jabra began releasing their own products, adding to the new wave of designs and features that appeal to young consumers. “These new hearing aids are sexy,” said Pete Bilzerian, a 25-year-old in Richmond, Va., who has worn the devices since he was 7. He describes his early models as distinctly unsexy: “big, funky, tan-colored hearing aids with the molding that goes all around the ear.” But increasingly, those have given way to sleeker, smaller models with more technological capabilities. Nowadays, he said, no one seems to notice the electronics in his ear. “If it ever does come up as a topic, I just brush it off and say, ‘Hey, I got these very expensive AirPods.’” More people in Mr. Bilzerian’s age group might need the equivalent of expensive AirPods, experts say. By the time they turn 30, about a fifth of Americans today have had their hearing damaged by noise, the Centers for Disease Control and Prevention recently estimated. This number adds to the already substantial population of young people with hearing loss tied to genetics or medical conditions. © 2023 The New York Times Company

Keyword: Hearing
Link ID: 28770 - Posted: 05.06.2023

By Laura Sanders Like Dumbledore’s wand, a scan can pull long strings of stories straight out of a person’s brain — but only if that person cooperates. This “mind-reading” feat, described May 1 in Nature Neuroscience, has a long way to go before it can be used outside of sophisticated laboratories. But the result could ultimately lead to seamless devices that help people who can’t talk or otherwise communicate easily. The research also raises privacy concerns about unwelcome neural eavesdropping (SN: 2/11/21). “I thought it was fascinating,” says Gopala Anumanchipalli, a neural engineer at the University of California, Berkeley who wasn’t involved in the study. “It’s like, ‘Wow, now we are here already,’” he says. “I was delighted to see this.” As opposed to implanted devices that have shown recent promise, the new system requires no surgery (SN: 11/15/22). And unlike other external approaches, it produces continuous streams of words instead of having a more constrained vocabulary. For the new study, three people lay inside a bulky MRI machine for at least 16 hours each. They listened to stories, mostly from The Moth podcast, while functional MRI scans detected changes in blood flow in the brain. These changes are proxies for brain activity, albeit slow and imperfect measures. With this neural data in hand, computational neuroscientists Alexander Huth and Jerry Tang of the University of Texas at Austin and colleagues were able to match patterns of brain activity to certain words and ideas. The approach relied on a language model that was built with GPT, one of the forerunners that enabled today’s AI chatbots (SN: 4/12/23). © Society for Science & the Public 2000–2023.

Keyword: Brain imaging; Consciousness
Link ID: 28769 - Posted: 05.03.2023

By Oliver Whang Think of the words whirling around in your head: that tasteless joke you wisely kept to yourself at dinner; your unvoiced impression of your best friend’s new partner. Now imagine that someone could listen in. On Monday, scientists from the University of Texas, Austin, made another step in that direction. In a study published in the journal Nature Neuroscience, the researchers described an A.I. that could translate the private thoughts of human subjects by analyzing fMRI scans, which measure the flow of blood to different regions in the brain. Already, researchers have developed language-decoding methods to pick up the attempted speech of people who have lost the ability to speak, and to allow paralyzed people to write while just thinking of writing. But the new language decoder is one of the first to not rely on implants. In the study, it was able to turn a person’s imagined speech into actual speech and, when subjects were shown silent films, it could generate relatively accurate descriptions of what was happening onscreen. “This isn’t just a language stimulus,” said Alexander Huth, a neuroscientist at the university who helped lead the research. “We’re getting at meaning, something about the idea of what’s happening. And the fact that that’s possible is very exciting.” The study centered on three participants, who came to Dr. Huth’s lab for 16 hours over several days to listen to “The Moth” and other narrative podcasts. As they listened, an fMRI scanner recorded the blood oxygenation levels in parts of their brains. The researchers then used a large language model to match patterns in the brain activity to the words and phrases that the participants had heard. © 2023 The New York Times Company

Keyword: Brain imaging; Consciousness
Link ID: 28768 - Posted: 05.03.2023

Sara Reardon The little voice inside your head can now be decoded by a brain scanner — at least some of the time. Researchers have developed the first non-invasive method of determining the gist of imagined speech, presenting a possible communication outlet for people who cannot talk. But how close is the technology — which is currently only moderately accurate — to achieving true mind-reading? And how can policymakers ensure that such developments are not misused? Most existing thought-to-speech technologies use brain implants that monitor activity in a person’s motor cortex and predict the words that the lips are trying to form. To understand the actual meaning behind the thought, computer scientists Alexander Huth and Jerry Tang at the University of Texas at Austin and their colleagues combined functional magnetic resonance imaging (fMRI), a non-invasive means of measuring brain activity, with artificial intelligence (AI) algorithms called large language models (LLMs), which underlie tools such as ChatGPT and are trained to predict the next word in a piece of text. In a study published in Nature Neuroscience on 1 May, the researchers had 3 volunteers lie in an fMRI scanner and recorded the individuals’ brain activity while they listened to 16 hours of podcasts each1. By measuring the blood flow through the volunteers’ brains and integrating this information with details of the stories they were listening to and the LLM’s ability to understand how words relate to one another, the researchers developed an encoded map of how each individual’s brain responds to different words and phrases. Next, the researchers recorded the participants’ fMRI activity while they listened to a story, imagined telling a story or watched a film that contained no dialogue. Using a combination of the patterns they had previously encoded for each individual and algorithms that determine how a sentence is likely to be constructed based on other words in it, the researchers attempted to decode this new brain activity. The video below shows the sentences produced from brain recordings taken while a study participant watched a clip from the animated film Sintel about a girl caring for a baby dragon. © 2023 Springer Nature Limited

Keyword: Brain imaging; Consciousness
Link ID: 28767 - Posted: 05.03.2023

By Wynne Parry For the first time, researchers have determined how a human olfactory receptor captures an airborne scent molecule, the pivotal chemical event that triggers our sense of smell. Whether it evokes roses or vanilla, cigarettes or gasoline, every scent starts with free-floating odor molecules that latch onto receptors in the nose. Multitudes of such unions produce the perception of the smells we love, loathe or tolerate. Researchers therefore want to know in granular detail how smell sensors detect and respond to odor molecules. Yet human smell receptors have resisted attempts to visualize how they work in detail — until now. In a recent paper published in Nature, a team of researchers delineated the elusive three-dimensional structure of one of these receptors in the act of holding its quarry, a compound that contributes to the aroma of Swiss cheese and body odor. “People have been puzzled about the actual structure of olfactory receptors for decades,” said Michael Schmuker, who uses chemical informatics to study olfaction at the University of Hertfordshire in England. Schmuker was not involved in the study, which he describes as “a real breakthrough.” He and others who study our sense of smell say that the reported structure represents a step toward better understanding how the nose and brain jointly wring from airborne chemicals the sensations that warn of rotten food, evoke childhood memories, help us find mates and serve other crucial functions. The complexity of the chemistry that the nose detects has made olfaction particularly difficult to explain. Researchers think that human noses possess about 400 types of olfactory receptors, which are tasked with detecting a vastly larger number of odoriferous “volatiles,” molecules that vaporize readily, from the three-atom, rotten-egg-smelling hydrogen sulfide to the much larger, musky-scented muscone. (One recent estimate put the number of possible odor-bearing compounds at 40 billion or more.) == All Rights Reserved © 2023

Keyword: Chemical Senses (Smell & Taste)
Link ID: 28766 - Posted: 05.03.2023

By Sara Reardon Many people who have come close to death or have been resuscitated report a similar experience: Their lives flash before their eyes, memorable moments replay, and they may undergo an out-of-body experience, sensing they’re looking at themselves from elsewhere in the room. Now, a small study mapping the brain activity of four people while they were dying shows a burst of activity in their brains after their hearts stop. The authors say the finding, published today in the Proceedings of the National Academy of Sciences, may explain how a person’s brain could replay conscious memories even after the heart has stopped. It “suggests we are identifying a marker of lucid consciousness,” says Sam Parnia, a pulmonologist at New York University Langone Medical Center who was not involved in the study. Although death has historically been medically defined as the moment when the heart irreversibly stops beating, recent studies have suggested brain activity in many animals and humans can continue for seconds to hours. In 2013, for instance, University of Michigan neurologist Jimo Borjigin and team found that rats’ brains showed signs of consciousness up to 30 seconds after their hearts had stopped beating. “We have this binary concept of life and death that is ancient and outdated,” Parnia says. Still, despite the numerous reports over hundreds of years from people who have been resuscitated following clinical death or nearly died, “I was shocked to realize we know almost nothing” about brain activity during the dying process, Borjigin says. For the current study, she and her team looked at the medical records of four people who were in comas and on life support on whom physicians had placed electroencephalography caps. None of the patients had any chance of survival.

Keyword: Attention; Consciousness
Link ID: 28765 - Posted: 05.03.2023

By Tim Vernimmen This story starts in an unusual place for an article about human nutrition: a cramped, humid and hot room somewhere in the Zoology building of the University of Oxford in England, filled with a couple hundred migratory locusts, each in its own plastic box. It was there, in the late 1980s, that entomologists Stephen Simpson and David Raubenheimer began working together on a curious job: rearing these notoriously voracious insects, to try and find out whether they were picky eaters. Every day, Simpson and Raubenheimer would weigh each locust and feed it precise amounts of powdered foods containing varying proportions of proteins and carbohydrates. To their surprise, the young scientists found that whatever food the insects were fed, they ended up eating almost exactly the same amount of protein. In fact, locusts feeding on food that was low in protein ate so much extra in order to reach their protein target that they ended up overweight — not chubby on the outside, since their exoskeleton doesn’t allow for bulges, but chock-full of fat on the inside. Inevitably, this made Simpson and Raubenheimer wonder whether something similar might be causing the documented rise in obesity among humans. Many studies had reported that even as our consumption of fats and carbohydrates increased, our consumption of protein did not. Might it be that, like locusts, we are tricked into overeating, in our case by the irresistible, low-protein, ultraprocessed foods on the shelves of the stores where we do most of our foraging? That’s what Raubenheimer and Simpson, both now at the University of Sydney, argue in their recent book “Eat Like the Animals” and in an overview in the Annual Review of Nutrition. © 2023 Annual Reviews

Keyword: Obesity; Attention
Link ID: 28764 - Posted: 05.03.2023

By McKenzie Prillaman Cracking the code to brain cancer treatment might start with cracking the brain’s protective shield. Nearly impenetrable walls of jam-packed cells line most of the brain’s blood vessels. Although this blood-brain barrier protects the organ from harmful invaders, it also prevents many medications from reaching the brain. Now, scientists can get a powerful chemotherapy drug into the human brain by temporarily opening its protective shield with ultrasound and tiny bubbles. The early-stage clinical trial, described May 2 in the Lancet Oncology, could lead to new treatments for those with brain cancer. Better treatments are especially needed for glioblastoma, a common and aggressive type of brain tumor. Even after surgical removal, another mass tends to grow in its place. “There’s really no established treatment for when the tumors come back,” says neurosurgeon Adam Sonabend of the Northwestern University Feinberg School of Medicine in Chicago. Patients with recurrent glioblastomas “don’t have any meaningful therapeutic options, so we were exploring new ways of treating them.” After the initial tumor has been removed, patients typically receive a relatively weak chemotherapy drug that can bypass the brain’s barricade. More potent drugs could help destroy any lingering disease — if the medicines could break through the barrier. © Society for Science & the Public 2000–2023.

Keyword: Brain imaging
Link ID: 28763 - Posted: 05.03.2023

By Sofia Quaglia With a large blade resembling a bread knife—but without the jagged edges—Stephanie Forkel slices through the human brain lying in front of her on the dissection table. A first-year university student, Forkel is clad in an apron and protective gear. It’s her first day working in the morgue at a university hospital in Munich, Germany, where the brains of people who’ve donated their bodies to science are examined for research. Her contact lenses feel dry because of the dense formaldehyde hanging in the air. But that’s not the only reason she squints a little harder. When she looks down at the annotated brain diagram in the textbook she’s supposed to use for reference, the real human brain in front of her looks nothing like the illustrated one. That was Forkel’s first eureka moment: The standard reference shape of the brain and real brains were actually vastly divergent. As she continued her studies, she confirmed that, indeed, “every individual brain looked very different,” she recounts decades later. A growing body of research now confirms there are plenty of physical dissimilarities between individual brains, particularly when it comes to white matter—the material nestled beneath the much-prized gray matter. And it’s not just anatomical. White matter hosts connections between the brain’s sections, like a city’s streets and avenues. So behavioral patterns can arise from even small physical differences in white matter, according to a late 2022 Science paper penned by Forkel and a colleague.1 Forkel is now one of a host of researchers probing subtle differences in white matter to better understand the extent of its role in making us who we are—including how much white matter dictates variations between people’s everyday behavior, and whether it’s implicated in how some patients recover better than others from life-threatening brain injuries. © 2023 NautilusNext Inc.,

Keyword: Development of the Brain
Link ID: 28762 - Posted: 05.03.2023

By Jaya Padmanabhan Speaking two languages provides the enviable ability to make friends in unusual places. A new study suggests that bilingualism may also come with another benefit: improved memory in later life. Studying hundreds of older patients, researchers in Germany found that those who reported using two languages daily from a young age scored higher on tests of learning, memory, language and self-control than patients who spoke only one language. The findings, published in the April issue of the journal Neurobiology of Aging, add to two decades of work suggesting that bilingualism protects against dementia and cognitive decline in older people. “It’s promising that they report that early and middle-life bilingualism has a beneficial effect on cognitive health in later life,” said Miguel Arce Rentería, a neuropsychologist at Columbia University who was not involved in the study. “This would line up with the existing literature.” In recent years, scientists have gained a greater understanding of bilingualism and the aging brain, though not all their findings have aligned. Some have found that if people who have fluency in two languages develop dementia, they’ll develop it at a later age than people who speak one language. But other research has shown no clear benefit from bilingualism. Neuroscientists hypothesize that because bilingual people switch fluidly between two languages, they may be able to deploy similar strategies in other skills — such as multitasking, managing emotions and self-control — that help delay dementia later on. The new study tested 746 people age 59 to 76. Roughly 40 percent of the volunteers had no memory problems, while the others were patients at memory clinics and had experienced confusion or memory loss. © 2023 The New York Times Company

Keyword: Alzheimers; Language
Link ID: 28761 - Posted: 04.29.2023

Nicola Davis Science correspondent From loud snores to twitching paws, dogs often appear to have a penchant for a good snooze. But researchers have said elderly canines with dementia appear to spend less time slumbering than those with healthy brains – mirroring patterns seen in humans. It has long been known that people with dementia can experience sleep problems, including finding it harder to get to sleep. Researchers have also found changes in the brainwaves of people with dementia during sleep – including decreased slow brain waves that occur during non-rapid eye movement deep sleep. These are important in memory consolidation and appear to be linked to the activity of the brain’s system for clearing away waste. Now it seems sleep impairment may occur in dogs experiencing a condition similar to dementia in humans. “Changes in sleep habits should be expected in older dogs, and could be a harbinger of decline in cognition,” said Prof Natasha Olby, senior author of a study at North Carolina State University. Writing in the journal Frontiers in Veterinary Science, Olby and colleagues reported on their study of 28 dogs aged between 10 and 16 years old. The canines’ brainwaves were recorded by electroencephalogram (EEG) while the dogs took a two-hour afternoon nap. The researchers also assessed owners’ answers to a questionnaire and each dog’s performance on a range of problem-solving, memory and attention tasks, to provide a score indicating whether the dog had, or was at risk of, canine dementia. Twenty of the dogs were deemed to have cognitive impairment, with this judged to be severe in eight of them. Combining their data, the team found dogs with higher dementia scores took longer to fall asleep and spent less time sleeping. © 2023 Guardian News & Media Limited

Keyword: Alzheimers; Sleep
Link ID: 28760 - Posted: 04.29.2023

by Kyle H. Kallman In 2010, when I was 18, a sleep study confirmed what kids at sleepovers and camp, and my freshman-year dorm mate who slept with headphones blaring heavy metal, already knew: I snored, and very loudly. The breathing passages in my nose, throat and mouth weren’t staying open, forcing my brain to wake up from deep sleep and open my airways. Over 30 times an hour. I awoke each morning exhausted. At the time, I thought it was normal to feel terrible every morning. “He’s a typical teenager,” said my mom when I slept in until the evening on weekends. My dad’s solution was pouring water on me so I could “seize the day!” I was a regular night owl who hated mornings. I never felt fully awake until the afternoon. Kyle H. Kallman wears a mask for his CPAP machine. (Kyle H. Kallman) But my physician suggested I get tested for sleep apnea since my levels of sleepiness were off the charts, even for a teen. And he warned me that the health effects of sleep apnea over time could be bad: stroke, heart problems, diabetes, and in some cases, even a shortened life span. A specialist looked at my test and said I needed a continuous positive airway pressure machine, a clunky contraption that sits beside your bed and straps on your face at night, providing a little constant air pressure that basically keeps your airways open as you sleep. No way was I going to do that. Sleep apnea seemed like a problem for old people — most CPAP users start at age 55 — and I was living in a college dorm and dating. If I ever brought somebody back to my college dorm room, they’d see the dorky machine on my nightstand and any possibility of romance would end. Besides, I didn’t think snoring was a big deal — I didn’t hear it.

Keyword: Sleep
Link ID: 28759 - Posted: 04.29.2023

By Aimee Cunningham Fentanyl, a deadly synthetic opioid, is killing a growing number of children and teens in the United States. More than 1,500 kids under the age of 20 died from fentanyl in 2021, four times as many as in 2018, says epidemiologist Julie Gaither of the Yale School of Medicine, who will present the data May 1 at the Pediatric Academic Societies meeting in Washington, D.C. The fentanyl deaths account for nearly all of the opioid-related deaths in this age group in 2021. Fentanyl is a lab-made opioid used for pain treatment that is 30 to 50 times more potent than heroin, making it lethal at a much smaller dose. The drug is also manufactured and sold illegally and is increasingly found contaminating counterfeit prescription drugs, or entirely replacing the drug a buyer expects to get (SN: 5/1/18). “That’s primarily the story of what’s happening among teenagers,” says pediatrician and addiction provider Sarah Bagley of the Boston University Chobanian & Avedisian School of Medicine. They intend to purchase and use one kind of drug or substance but unknowingly ingest fentanyl. “People are not anticipating that they are going to be exposed to fentanyl, and then they are, and that results in an overdose.” Some of the signs that a person is experiencing an overdose include falling asleep, losing consciousness, gurgling or choking sounds and weak or no breathing. “This change in the drug supply, where you just have a much more potent opioid, is really driving it all,” says Bagley, who was not involved in the work. © Society for Science & the Public 2000–2023.

Keyword: Drug Abuse
Link ID: 28758 - Posted: 04.29.2023

By Geoffrey Giller From the brightly colored poison frogs of South America to the prehistoric-looking newts of the Western US, the world is filled with beautiful, deadly amphibians. Just a few milligrams of the newt’s tetrodotoxin can be fatal, and some of those frogs make the most potent poisons found in nature. In recent years, scientists have become increasingly interested in studying poisonous amphibians and are starting to unravel the mysteries they hold. How is it, for example, that the animals don’t poison themselves along with their would-be predators? And how exactly do the ones that ingest toxins in order to make themselves poisonous move those toxins from their stomachs to their skin? Even the source of the poison is sometimes unclear. While some amphibians get their toxins from their diet, and many poisonous organisms get theirs from symbiotic bacteria living on their skin, still others may or may not make the toxins themselves — which has led scientists to rethink some classic hypotheses. Over the long arc of evolution, animals have often turned to poisons as a means of defense. Unlike venoms — which are injected via fang, stinger, barb, or some other specialized structure for offensive or defensive purposes — poisons are generally defensive toxins a creature makes that must be ingested or absorbed before they take effect. Amphibians tend to store their poisons in or on their skin, presumably to increase the likelihood that a potential predator is deterred or incapacitated before it can eat or grievously wound them. Many of their most powerful toxins — like tetrodotoxin, epibatidine and the bufotoxins originally found in toads — are poisons that interfere with proteins in cells, or mimic key signaling molecules, thus disrupting normal function. © 2023 Annual Reviews

Keyword: Neurotoxins
Link ID: 28757 - Posted: 04.29.2023

By Kate Golembiewski On the one hand, this headgear looks like something a cyberfish would wear. On the other, it’s not far from a fashion statement someone at the Kentucky Derby might make. But scientists didn’t just affix this device for laughs: They are curious about the underlying brain mechanisms that allow fish to navigate their world, and how such mechanisms relate to the evolutionary roots of navigation for all creatures with brain circuitry. “Navigation is an extremely important aspect of behavior because we navigate to find food, to find shelter, to escape predators,” said Ronen Segev, a neuroscientist at Ben-Gurion University of the Negev in Israel who was part of a team that fitted 15 fish with cybernetic headgear for a study published on Tuesday in the journal PLOS Biology. Putting a computer on a goldfish to study how the neurons fire in its brain while navigating wasn’t easy. It takes a careful hand because a goldfish’s brain, which looks a bit like a small cluster of lentils, is only half an inch long. “Under a microscope, we exposed the brain and put the electrodes inside,” said Lear Cohen, a neuroscientist and doctoral candidate at Ben-Gurion who performed the surgeries to attach the devices. Each of those electrodes was the diameter of a strand of human hair. It was also tricky to find a way to perform the procedure on dry land without harming the test subject. “The fish needs water and you need him not to move,” he said. He and his colleagues solved both problems by pumping water and anesthetics into the fish’s mouth. Once the electrodes were in the brain, they were connected to a small recording device, which could monitor neuronal activity and which was sealed in a waterproof case, mounted on the fish’s forehead. To keep the computer from weighing the fish down and impeding its ability to swim, the researchers attached buoyant plastic foam to the device. © 2023 The New York Times Company

Keyword: Learning & Memory
Link ID: 28756 - Posted: 04.26.2023