By Veronique Greenwood This morning, when the sun came up, billions of humans opened their eyes and admitted into their bodies a shaft of light from space. When the stream of photons struck the retina, neurons fired. And in every organ, in nearly every cell, elaborate machinery stirred. Each cell’s circadian clock, a complex of proteins whose levels rise and fall with the sun, clicked into gear. That clock synchronizes our bodies to the light-dark cycle of the planet by controlling the expression of more than 40% of our genome. Genes for immune signals, brain messengers and liver enzymes, to name just a few, are all transcribed to make proteins when the clock says it’s time. That means you are not, biochemically, the same person at 10 p.m. that you are at 10 a.m. It means that evenings are a more dangerous time to take large doses of the painkiller acetaminophen: Liver enzymes that protect against overdose become scarce then. It means that vaccines given in the morning and evening work differently, and that night-shift workers, who chronically disobey their clocks, have higher rates of heart disease and diabetes. People whose clocks run fast or slow are trapped in a hideous state of perpetual jet lag. “We are linked to this day in ways that I think people just push off,” the biochemist Carrie Partch tells me. If we understand the clock better, she has argued, we might be able to reset it. With that information, we might shape the treatment of diseases, from diabetes to cancer. For more than a quarter century, Partch has lived among the orchestrators of the circadian clock, the proteins whose rise and fall control its workings. As a postdoc, she produced the first visualization of the bound pair of proteins at its heart, CLOCK and BMAL1. Since then, she has continued to make visible the whorls and twists of those and other clock proteins while charting how changes to their structure add or subtract time from the day. Her achievements in pursuit of that knowledge have brought her some of the highest honors in this field of science: the Margaret Oakley Dayhoff Award from the Biophysical Society in 2018, and the National Academy of Sciences Award in Molecular Biology in 2022. Simons Foundation All Rights Reserved © 2023

Keyword: Biological Rhythms
Link ID: 28957 - Posted: 10.12.2023

Nicola Davis Science correspondent When it comes to avoiding unwanted male attention, researchers have found some frogs take drastic action: they appear to feign death. Researchers say the findings shed new light on the European common frog, suggesting females do not simply put up with the male scramble for mates – a situation in which several males can end up clinging to a female, sometimes fatally. “It was previously thought that females were unable to choose or defend themselves against this male coercion,” said Dr Carolin Dittrich, the first author of the study from the Natural History Museum of Berlin. But the research suggests this may not be the case. “Females in these dense breeding aggregations are not passive as previously thought,” Dittrich said. Writing in the journal Royal Society Open Science, Dittrich and her co-author, Dr Mark-Oliver Rödel, report how they placed each male frog in a box with two females: one large and one small. The mating behaviour was then recorded on video. The results, obtained from 54 females who experienced the clutches of a male, revealed that 83% of females gripped by a male tried rotating their body. Release calls such as grunts and squeaks were emitted by 48% of clasped females – all of whom also rotated their body. Tonic immobility – stiffening with arms and legs outstretched in a pose reminiscent of playing dead – occurred in 33% of all females clasped by a male, with the team adding it tended to occur alongside rotating and calling. Smaller females, they note, more frequently employed all three tactics together than larger ones. While unusual, tonic immobility – it turned out – had been seen before. “I found a book written in 1758 by Rösel von Rosenhoff describing this behaviour, which was never mentioned again,” Dittrich said. © 2023 Guardian News & Media Limited

Keyword: Sexual Behavior
Link ID: 28956 - Posted: 10.12.2023

McKenzie Prillaman Players in an ‘overweight football league’ warm up before a match in Germany. To join, members must have a BMI of at least 31. Credit: Ina Fassbender/AFP via Getty As an obesity physician, Fatima Cody Stanford has treated many people whose weight was causing them health problems. She has plenty of success stories: one woman, for instance, returned “stunning” cholesterol, blood-pressure and blood-sugar readings after working with Stanford for about ten years. But the woman still wanted more treatment. She was fixated on her body mass index, or BMI, which classified her as having obesity. “She wants to lose more weight”, says Stanford, who is at Massachusetts General Hospital and Harvard Medical School in Boston. BMI, which is calculated by dividing weight by height squared, has been used for several decades as an international standard to determine healthy weights. It serves as a proxy for body fat, and higher numbers can indicate increased risk for metabolic disease and death. But BMI does not measure body fat, and it also ignores factors that affect how healthy someone is at a given weight, including age, sex and race. Not everyone with a high BMI has poor health or a raised risk of death1–3. That’s why there is a small but growing movement to go beyond BMI when diagnosing and treating obesity, which the World Health Organization (WHO) recognizes as a chronic disease. In June, the American Medical Association (AMA) called for more weight-related metrics to be used in conjunction with BMI owing to its imperfections and questionable history. But, with global rates of obesity having tripled over the past 50 years, and a wave of cutting-edge weight-loss drugs now hitting the market, a high BMI still reigns as the main criterion for obesity treatment. Specialists worry that the surging demand for the drugs will exacerbate reliance on BMI as a solo diagnostic tool.

Keyword: Obesity
Link ID: 28955 - Posted: 10.12.2023

Linda Geddes Science correspondent The former Premier League goalkeeper Brad Friedel once said that to be able to work well in the box, you have to be able to think outside the box. Now scientific data supports the idea that goalies’ brains really do perceive the world differently – their brains appear able to merge signals from the different senses more quickly, possibly underpinning their unique abilities on the football pitch. Goalkeeping is the most specialised position in football, with the primary objective of stopping the opposition from scoring. But while previous studies have highlighted differences in physiological and performance profiles between goalkeepers and other players, far less was known about whether they have different perceptual or cognitive abilities. “Unlike other football players, goalkeepers are required to make thousands of very fast decisions based on limited or incomplete sensory information,” said Michael Quinn, a former goalkeeper in the Irish Premiership, who is now studying for a master’s degree in behavioural neuroscience at University College Dublin. Suspecting that this ability might hinge on an enhanced capacity to combine information from different senses, Quinn and researchers at Dublin City University and University College Dublin recruited 60 professional goalkeepers, outfield players and age-matched non-players to do a series of tests, looking for differences in their ability to distinguish sounds and flashes as separate from one another. Doing so enabled them to estimate volunteers’ temporal binding windows – the timeframe in which different sensory signals are fused together in the brain. The study, published in Current Biology, found that goalkeepers had a narrower temporal binding window relative to outfielders and non-soccer players. © 2023 Guardian News & Media Limited

Keyword: Attention; Vision
Link ID: 28954 - Posted: 10.10.2023

Mariana Lenharo For more than a century, researchers have known that people are generally very good at eyeballing quantities of four or fewer items. But performance at sizing up numbers drops markedly — becoming slower and more prone to error — in the face of larger numbers. Now scientists have discovered why: the human brain uses one mechanism to assess four or fewer items and a different one for when there are five or more. The findings, obtained by recording the neuron activity of 17 human participants, settle a long-standing debate on how the brain estimates how many objects a person sees. The results were published in Nature Human Behaviour1 on 2 October. The finding is relevant to the understanding of the nature of thinking, says psychologist Lisa Feigenson, the co-director of the Johns Hopkins University Laboratory for Child Development in Baltimore, Maryland. “Fundamentally, the question is one of mental architecture: what are the building blocks that give rise to human thought?” The limits of the human ability to estimate large quantities have puzzled many generations of scientists. In an 1871 Nature article2, economist and logician William Stanley Jevons described his investigations into his own counting skills and concluded “that the number five is beyond the limit of perfect discrimination, by some persons at least”. Some researchers have argued that the brain uses a single estimation system, one that is simply less precise for higher numbers. Others hypothesize that the performance discrepancy arises from there being two separate neuronal systems to quantify objects. But experiments have failed to determine which model is correct. Then, a team of researchers had a rare opportunity to record the activity of individual neurons inside the brains of people who were awake. All were being treated for seizures at the University Hospital Bonn in Germany, and had microelectrodes inserted in their brains in preparation for surgery. © 2023 Springer Nature Limited

Keyword: Attention
Link ID: 28953 - Posted: 10.10.2023

By Matt Richtel Approximately 20 percent of adolescents had symptoms of major depressive disorder in 2021 — the first full calendar year of the pandemic — but less than half who needed treatment received it, according to a new study. The research, published in JAMA Pediatrics, found that treatment was most lacking for minority adolescents, particularly those who are Latino and mixed-race. Major depressive disorder is a chronic condition that surfaces in episodes of depressed mood and loss of joy, with symptoms lasting at least two weeks. It is distinct from persistent depressive disorder, in which symptoms last two years or more. Previous research showed that the prevalence of major depressive disorder among adolescents nearly doubled recently, rising to 15.8 percent in 2019 from 8.1 percent in 2009. The Covid-19 pandemic amplified this trend as it caused isolation, uncertainty, loneliness and fear of illness among family members. The new study on the prevalence of major depressive disorder in 2021 drew from a nationally representative sample of 10,700 adolescents, ages 12 to 17, whose experiences were recorded by the National Survey on Drug Use and Health. The study found some sharp differences in the prevalence of the condition across racial and ethnic groups. About 14.5 percent of Black adolescents, 14.6 percent of Asian adolescents and 20 percent of white adolescents reported symptoms of major depressive disorder. Latino adolescents experienced major depressive disorder at a slightly higher rate, around 23 percent. Though mixed-race and Latino adolescents had the highest rates of major depressive disorder, they had the lowest rates of treatment, the study found. Twenty-one percent of mixed-race adolescents and 29 percent of Latino adolescents with the condition received treatment for it, compared with nearly half of white adolescents. Treatment rates for Asian and Black adolescents fell in between. © 2023 The New York Times Company

Keyword: Depression
Link ID: 28952 - Posted: 10.10.2023

By Sandra G. Boodman Bridget Houser felt despairing. In the months before her 2018 wedding, Houser, who had never struggled with her weight, noticed that it inexplicably began to creep up. In response she doubled the length of her runs to eight miles, took back-to-back high intensity workout classes and often consumed only water, coffee and fruit during the day before a spartan, mostly vegetable, dinner. Yet no matter what Houser did, her weight stubbornly increased and her oval face grew round, a transformation that was glaringly obvious in comparison with her identical twin sister. Houser wondered whether the five pounds she gained despite her herculean effort was a corollary of other problems. For the previous two years she had battled a string of maladies: first daily headaches, then crippling anxiety, followed by insomnia, hair loss and acne, something she’d never endured as a teenager. “Stress was the universal explanation,” recalled Houser, a controller for a small business in Chicago. When doctors suggested that her upcoming marriage might be a cause of her problems, Houser considered, then rejected, the theory. It just didn’t jibe with her feelings. In early 2019, about six months after her wedding, Houser insisted that her doctors perform several tests. They ultimately revealed that her symptoms weren’t the result of stress or marital misgivings but of a serious illness that had been smoldering for years. After successful treatment followed by a long recovery Houser, now 34, feels far better than she did during those miserable years in her late 20s. “I wish I’d been nicer to myself and not blamed myself for what was going on,” she said.

Keyword: Hormones & Behavior
Link ID: 28951 - Posted: 10.10.2023

Hannah Devlin Science correspondent Pregnancy leads to a permanent rewiring of neurons, according to research that gives new insights into the influence of hormones on behaviour. The research, in mice, revealed that their parenting instincts were triggered by changes in the brain that occur in response to oestrogen and progesterone late in pregnancy. Similar changes are likely to occur in the human brain, according to scientists, who said the work could pave the way for fresh understanding into parenting behaviour and postpartum mental health. Dr Jonny Kohl, who led the research at London’s Francis Crick Institute, said: “We know that the female body changes during pregnancy to prepare for bringing up young. One example is the production of milk, which starts long before giving birth. Our research shows that such preparations are taking place in the brain, too.” The findings are consistent with brain imaging research in women showing changes to brain volume and brain activity that endure long after pregnancy. Although Kohl pointed out that “parenting is obviously a lot more complex in humans”. “We have NCT classes, observational learning, all these environmental influences,” he added. “We don’t have to rely on those hormonal changes to such a degree.” a newborn baby boy is checked by nurses in a hospital maternity theatre Smoking in pregnancy increases risk of premature birth threefold, study finds Read more The studies were carried out in mice, which undergo a dramatic shift in behaviour, with virgin females showing no interest in pups, and mouse mothers spending most of their time looking after young. Previously it had been widely assumed that the onset of this behaviour occurred during or just after birth, possibly triggered by hormones such as oxytocin. However, the latest research puts the change at an earlier stage and also suggests that the changes may be permanent. © 2023 Guardian News & Media Limited

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 28949 - Posted: 10.07.2023

by Angie Voyles Askham About once a month throughout 2012, researchers from four labs at the University of California, San Francisco filed into a conference room in the early morning to hear the latest news on their ambitious project. The heads of the labs — Arturo Alvarez-Buylla, Scott Baraban, Arnold Kriegstein and John Rubenstein — had formed the company Neurona Therapeutics in 2008 to develop a new approach to treating neurological conditions, using cell therapy. Their goal was to transplant inhibitory interneurons into people’s nervous systems to treat the overexcited circuits that can give rise to conditions such as epilepsy, Alzheimer’s disease and neuropathic pain. These meetings had grown tense as researchers within the four groups struggled to see eye to eye on data interpretation, particularly when Cory Nicholas, then a postdoctoral researcher in Kriegstein’s lab, presented his protocol for producing the inhibitory interneurons. On those days, Nicholas would open his slide deck to reveal images of fluorescent cells on a large screen behind him — red and white branching blobs against a black background. Then the questions would come from Baraban’s group. Why do some of the cells seem to be the wrong kind? Are they forming tumors? Can we see the neighboring images? There were some in the audience who thought they were being shown only the best images, says Joy Sebe, a postdoc in Baraban’s lab at the time. Nicholas, for his part, says he welcomed the questioning — in science, he says, “your job is to challenge” — and Daniel Vogt, who was a postdoc Rubenstein’s lab at the time, says the back and forth was simply part of the scientific process. © 2023 Simons Foundation

Keyword: Epilepsy
Link ID: 28948 - Posted: 10.07.2023

By Mark Johnson Using a host of high-tech tools to simulate brain development in a lab dish, Stanford University researchers have discovered several dozen genes that interfere with crucial steps in the process and may lead to autism, a spectrum of disorders that affects about one in every 36 Americans, impairing their ability to communicate and interact with others. The results of a decade of work, the findings published in the journal Nature may one day pave the way for scientists to design treatments that allow these phases of brain development to proceed unimpaired. The study delves into a 20-year-old theory that suggests one cause of autism may be a disruption of the delicate balance between two types of nerve cells found in the brain’s cerebral cortex, the area responsible for higher-level processes such as thought, emotion, decision-making and language. Some nerve cells in this region of the brain excite other nerve cells, encouraging them to fire; other cells, called interneurons, do the opposite. Too much excitation can impair focus in the brain and cause epilepsy, a seizure disorder that is more common in people with autism than in the general population. Scientists therefore believe a proper balance requires more of the inhibiting interneurons. In the developing fetus, these nerve cells start out deep in the brain in a region called the subpallium, then migrate slowly to the cerebral cortex. The process begins mid-gestation and ends in the infant’s second year of life, said Sergiu Pasca, a Stanford University professor of psychiatry and behavioral sciences who led the study. Pasca’s team, which included researchers from the University of California at San Francisco and the Icahn School of Medicine at Mount Sinai, tested 425 genes that have been linked to neurodevelopmental disorders to determine which ones interfere with the generation and migration of interneurons. Genes linked to autism were among those identified in the study. “What’s really cool about this paper is that autism is a collection of different behaviors, but we don’t have [an] understanding of how those behaviors are connected to differences in the brain,” said James McPartland, a professor of child psychiatry and psychology at the Yale School of Medicine, who was not involved in the study. The new work advances research into autism by “beginning to create a fundamental understanding of the building blocks of brain development,” he said.

Keyword: Autism; Genes & Behavior
Link ID: 28947 - Posted: 10.07.2023

By Stephanie Pappas Your bedmate is whimpering in their sleep and perhaps thrashing about. It looks like a nightmare. Should you wake them? Nope, experts say. As terrible as whatever visions that are running through their head might be, waking someone from a nightmare is more likely to ensure that they’ll remember the bad dream. And if someone appears physically distressed in their sleep like this, it’s more likely that they’re having a night terror than a nightmare; night terrors are different neurological experiences. Nightmares are a normal part of dreaming, says Deirdre Barrett, a dream researcher at Harvard Medical School and author of The Committee of Sleep (Oneiroi Press, 2001). They almost always happen in rapid eye movement (REM) sleep, the stage of sleep marked by brain activity that looks very similar to that of an awake brain. “Except for being scary, they look like every other dream,” Barrett says. During REM sleep, the brain areas responsible for long-term memory storage show altered activation, so people don’t tend to remember their nightmares unless those sleep tales are scary enough to wake them up. Once a dreamer awakens, their long-term memory regions come back on line. Most of the time, someone having a nightmare will be indistinguishable from a peaceful dreamer. During a nightmare, heart rate increases by seven beats per minute on average, says Michael Schredl, a dream and sleep researcher at the Central Institute of Mental Health in Germany. Otherwise the sleeper typically lies still in bed: during REM sleep, muscles are paralyzed, which keeps people from acting out their dreams. If someone is moving around, talking in their sleep or sleepwalking while appearing distressed, it’s more likely a night terror, which occurs during non-REM sleep, Schredl says.

Keyword: Sleep
Link ID: 28946 - Posted: 10.07.2023

By Marco Giancotti I’m lying down in a white cylinder barely wider than my body, surrounded on all sides by a mass of sophisticated machinery the size of a small camper van. It’s an fMRI machine, one of the technological marvels of modern neuroscience. Two small inflatable cushions squeeze my temples, keeping my head still. “We are ready to begin the next batch of exercises,” I hear Dr. Horikawa’s gentle voice saying. We’re underground, in one of the laboratories of Tokyo University’s Faculty of Medicine, Hongo Campus. “Do you feel like proceeding?” “Yes, let’s go,” I answer. The machine sets in motion again. A powerful current grows inside the cryogenically cooled wires that coil around me, showering my head with radio waves, knocking the hydrogen atoms inside my head off their original spin axis, and measuring the rate at which the axis recovers afterward. To the sensors around me, I’m now as transparent as a glass of water. Every tiny change of blood flow anywhere inside my brain is being watched and recorded in 3-D. A few seconds pass, then a synthetic female voice speaks into my ears over the electronic clamor: “top hat.” I close my eyes and I imagine a top hat. A few seconds later a beep tells me I should rate the quality of my mental picture, which I do with a controller in my hand. The voice speaks again: “fire extinguisher,” and I repeat the routine. Next is “butterfly,” then “camel,” then “snowmobile,” and so on, for about 10 minutes, while the system monitors the activation of my brain synapses. For most people, this should be a rather simple exercise, perhaps even satisfying. For me, it’s a considerable strain, because I don’t “see” any of those things. For each and every one of the prompts, I rate my mental image “0” on a 0 to 5 scale, because as soon as I close my eyes, what I see are not everyday objects, animals, and vehicles, but the dark underside of my eyelids. I can’t willingly form the faintest of images in my mind. And, although it isn’t the subject of the current experiment, I also can’t conjure sounds, smells, or any other kind of sensory stimulation inside my head. I have what is called “aphantasia,” the absence of voluntary imagination of the senses. I know what a top hat is. I can describe its main characteristics. I can even draw an above-average impression of one on a piece of paper for you. But I can’t visualize it mentally. What’s wrong with me? © 2023 NautilusNext Inc.,

Keyword: Consciousness; Attention
Link ID: 28945 - Posted: 10.05.2023

By Tim Vernimmen For humans, division of labor has become a necessity: No person in the world has all the knowledge and skills to perform all the tasks that are required to keep our highly technological societies afloat. This has made us entirely dependent on each other, leaving us individually vulnerable. We really can’t make it on our own. From archaeological findings, we can reconstruct more or less how this situation evolved. Initially, everyone was doing more or less the same thing. But because food was shared among people living in hunter-gatherer groups, some were able to specialize in tasks other than finding food, such as fashioning tools, treating illnesses or cultivating plants. These skills enriched the group but made the specialists even more dependent on others. This further reinforced cooperation among group members and pushed our species to even higher levels of specialization — and prosperity. “Societies that have highly developed task-sharing and division of labor between group members are conspicuous because of their exceptional ecological success,” says Michael Taborsky, a behavioral biologist at the University of Bern in Switzerland. And he doesn’t just mean us: Extensive division of labor also can be seen among many social insects — ants, wasps, bees and termites — in which individuals in large colonies often specialize in particular tasks, making them impressively effective. “It is no exaggeration,” Taborsky says, “to say that societies” — of both humans and social insects — “predominate life on Earth.” But how did this division of labor evolve? Why does it seem to be rare outside of our species and the social insects? Is it, in fact, as rare as it seems? Taborsky, who has studied cooperation in animals for decades, has become increasingly interested in these questions. In March 2023, he and Barbara Taborsky, his wife and colleague, organized a scientific workshop on the topic in Berlin to which they invited a number of other experts. Over the course of two days, the group discussed how division of labor may have evolved over time, and what mechanisms allow it to develop, over and over again, in every colony of certain species. One of the invited scientists was Jennifer Fewell, a social insect biologist at Arizona State University who coauthored an influential overview of division of labor in the Annual Review of Entomology in 2001 and has studied the subject for decades. In social insect colonies, she says, “there is no central controller telling everybody what to do, but instead, the division of labor emerges from the interaction between individuals.” © 2023 Annual Reviews

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 28944 - Posted: 10.05.2023

By Carl Zimmer In more than 1,500 animal species, from crickets and sea urchins to bottlenose dolphins and bonobos, scientists have observed sexual encounters between members of the same sex. Some researchers have proposed that this behavior has existed since the dawn of the animal kingdom. But the authors of a new study of thousands of mammalian species paint a different picture, arguing that same-sex sexual behavior evolved when mammals started living in social groups. Although the behavior does not produce offspring to carry on the animals’ genes, it could offer other evolutionary advantages, such as smoothing over conflicts, the researchers proposed. “It may contribute to establishing and maintaining positive social relationships,” said José Gómez, an evolutionary biologist at the Experimental Station of Arid Zones in Almería, Spain, and an author of the new study. But Dr. Gómez cautioned that the study, published on Tuesday in the journal Nature Communications, could not shed much light on sexual orientation in humans. “The type of same-sex sexual behavior we have used in our analysis is so different from that observed in humans that our study is unable to provide an explanation for its expression today,” he said. Previous studies of same-sex sexual behavior have typically involved careful observations of a single species, or a small group of them. Dr. Gómez and his colleagues instead looked for the big evolutionary patterns that gave rise to the behavior in some species but not others. The researchers surveyed the 6,649 species of living mammals that arose from reptilelike ancestors starting roughly 250 million years ago. Looking over the scientific literature, they noted which of them had been seen carrying out same-sex sexual behaviors — defined as anything from courtships and mating to forming long-term bonds. The researchers ended up with a list of 261 species, or about 4 percent of all mammalian species, that exhibited these same-sex behaviors. Males and females were about equally likely to be observed carrying out same-sex sexual behavior, the analysis showed. In some species, only one sex did. But in still others — including cheetahs and white-tailed deer — both males and females engaged in same-sex sexual behavior. © 2023 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 28943 - Posted: 10.05.2023

Mara Gordon Right around the time Ozempic came out, I started to change the way I practice medicine. As the new class of weight-loss drug ushered in a highly medicalized era of Americans' obsession with being thin, I decided I was done with trying to get my patients to lose weight. Sometimes I call myself a "body-positive doctor," but that isn't it, exactly, because I don't expect all of my patients to love their bodies at all times. With my students, I call it practicing "weight-neutral medicine." I've found a great community of like-minded health care providers with the Health at Every Size movement, which promotes the idea that people can be healthy without focusing on weight loss. This change started for me, as many of my major realizations do, from reading. I read memoirs by fat authors like Roxane Gay, Lindy West, and Kiese Laymon, who wrote about the many ways they were made to feel terrible about their bodies, often at the doctor's office. It was unsettling to recognize myself in some of the encounters they described. I had told my own patients, dozens of times: "Your knee pain might get better if you just lost a few pounds." As if my patients hadn't thought of that already. As if they hadn't already tried. Reading these books also forced me to reckon with my own relationship to my weight and my experiences in health care. As a chubby teen, I remember a visceral unease before each appointment at the pediatrician's office, the fear I felt stepping on the scale. I remember the doctor who chided my mom for buying 2% milk, not skim. Then, when I lost weight in my 20s, appointments with the doctor were transformed. I could focus on the issues I wanted to discuss, rather than visits being dominated by talk of cutting calories. © 2023 npr

Keyword: Obesity
Link ID: 28942 - Posted: 10.05.2023

By Katherine Harmon Courage On the surface, sleep seems obvious, essential. It comes in long, languid, predictable waves, washing over humans and elephants, birds and fish and beetles. It comes bearing restoration, repair, learning. It follows an ancestral rhythm played deep within our cells, cued by the movement of our planet around our star. Perhaps we could believe this nice, simple fantasy, were it not for an irksome little eyeless fish. More than a decade ago, this fish—the Mexican tetra (Astyanax mexicanus)—caught the eye of a graduate student at New York University. It was not new to science—it had been the subject of fascination for aquarists and researchers for decades, who marveled at its ghostly appearance and the splash of skin where its eyes should have been. But other quirks of the fish turned out to be even more mysterious. In Manhattan, the fish were far from their place of origin: a collection of unassuming caves strung through northeastern Mexico. Inside these caves, it is pitch dark, always cool, quiet, and rather boring. A seemingly perfect place to sleep. So Erik Duboué, the curious graduate student, decided to test if these fish showed any unusual sleep habits. One night in 2009, he made a 2 a.m. visit to the lab and noticed something strange about these sightless fish: They seemed wide awake. On further investigation, he found that despite their soporific native environs, they actually hardly sleep at all. In fact, he discovered, they doze just about three and a half hours out of each 24-hour period. And their bouts of sleep seem to come on entirely randomly and only in brief spurts. Curiously, these eyeless cavefish seem to have been flourishing on this quiescence interruptus for hundreds of thousands of years. “What you have is a fish that is completely healthy—it just doesn’t need to sleep,” says Duboué, who is now a molecular geneticist at Florida Atlantic University. Since then, Duboué and others have been studying the strange sleep of these wakeful creatures—prodding them in the lab to rouse them from their occasional slumber and plumbing their DNA. Combined with investigations into other animals, as well as some peculiar experiments that have sent humans to sleep in caves, scientists are uncovering new, closely guarded truths about sleep that have eluded us in our bright, rhythmic world. © 2023 NautilusNext Inc.

Keyword: Sleep; Evolution
Link ID: 28941 - Posted: 10.03.2023

Jon Hamilton A team of researchers has developed a new way to study how genes may cause autism and other neurodevelopmental disorders: by growing tiny brain-like structures in the lab and tweaking their DNA. These "assembloids," described in the journal Nature, could one day help researchers develop targeted treatments for autism spectrum disorder, intellectual disability, schizophrenia, and epilepsy. "This really accelerates our effort to try to understand the biology of psychiatric disorders," says Dr. Sergiu Pașca, a professor of psychiatry and behavioral sciences at Stanford University and an author of the study. The research suggests that someday "we'll be able to predict which pathways we can target to intervene" and prevent these disorders, adds Kristen Brennand, a professor of psychiatry at Yale who was not involved in the work. The study comes after decades of work identifying hundreds of genes that are associated with autism and other neurodevelopmental disorders. But scientists still don't know how problems with these genes alter the brain. "The challenge now is to figure out what they're actually doing, how disruptions in these genes are actually causing disease," Pașca says. "And that has been really difficult." For ethical reasons, scientists can't just edit a person's genes to see what happens. They can experiment on animal brains, but lab animals like rodents don't really develop anything that looks like autism or schizophrenia. So Pașca and a team of scientists tried a different approach, which they detailed in their new paper. The team did a series of experiments using tiny clumps of human brain cells called brain organoids. These clumps will grow for a year or more in the lab, gradually organizing their cells much the way a developing brain would. And by exposing an organoid to certain growth factors, scientists can coax it into resembling tissue found in brain areas including the cortex and hippocampus. © 2023 npr

Keyword: Epilepsy; Autism
Link ID: 28940 - Posted: 10.03.2023

By Stephanie Pappas If you’ve ever awoken from a vivid dream only to find that you can’t remember the details by the end of breakfast, you’re not alone. People forget most of the dreams they have—though it is possible to train yourself to remember more of them. Dreaming happens mostly (though not always exclusively) during rapid eye movement (REM) sleep. During this sleep stage, brain activity looks similar to that in a waking brain, with some very important differences. Key among them: during REM sleep, the areas of the brain that transfer memories into long-term storage—as well as the long-term storage areas themselves—are relatively deactivated, says Deirdre Barrett, a dream researcher at Harvard Medical School and author of the book The Committee of Sleep (Oneiroi Press, 2001). This may be a side effect of REM’s role in memory consolidation, according to a 2019 study on mice in the journal Science. Short-term memory areas are active during REM sleep, but those only hang on to memories for about 30 seconds. “You have to wake up from REM sleep, generally, to recall a dream,” Barrett says. If, instead, you pass into the next stage of sleep without rousing, that dream will never enter long-term memory. REM sleep occurs about every 90 minutes, and it lengthens as the night drags on. The first REM cycle of the night is typically just a few minutes long, but by the end of an eight-hour night of sleep, a person has typically been in the REM stage for a good 20 minutes, Barrett says. That’s why the strongest correlation between any life circumstance and your memory of dreams is the number of hours you’ve slept. If you sleep only six hours, you’re getting less than half of the dream time of an eight-hour night, she says. Those final hours of sleep are the most important for dreaming. And people tend to remember the last dream of the night—the one just before waking. © 2023 Scientific American

Keyword: Sleep; Learning & Memory
Link ID: 28939 - Posted: 10.03.2023

Sara Reardon Scientists have identified two types of brain cell linked to a reduced risk of dementia in older people — even those who have brain abnormalities that are hallmarks of Alzheimer’s disease1. The finding could eventually lead to new ways to protect these cells before they die. The results were published in Cell on 28 September. The most widely held theory about Alzheimer’s attributes the disease to a build-up of sticky amyloid proteins in the brain. This leads to clump-like ‘plaques’ of amyloid that slowly kill neurons and eventually destroy memory and cognitive ability. But not everyone who develops cognitive impairment late in life has amyloid clumps in their brain, and not everyone with amyloid accumulation develops Alzheimer’s. Neurobiologist Hansruedi Mathys at the University of Pittsburgh School of Medicine in Pennsylvania and neuroscientist Li-Huei Tsai and computer scientist Manolis Kellis at the Massachusetts Institute of Technology in Cambridge and their colleagues decided to investigate this disconnect. To do so, they used data from a massive study that tracks cognitive and motor skills in thousands of people throughout old age. The researchers examined tissue samples from 427 brains from participants who had died. Some of those participants had dementia typical of advanced Alzheimer’s disease, some had mild cognitive impairment and the remainder had no sign of impairment. The researchers isolated cells from each participant’s prefrontal cortex, the region involved in higher brain function. To classify the cells, they sequenced all the active genes in each one. This allowed them to create an atlas of the brain showing where the different cell types occur. The scientists identified two key cell types that had a specific genetic marker. One had active genes coding for reelin, a protein associated with brain disorders such as schizophrenia, and the other had active genes that code for somatostatin, a hormone that regulates processes throughout the body. © 2023 Springer Nature Limited

Keyword: Alzheimers; Genes & Behavior
Link ID: 28938 - Posted: 09.29.2023

By Alice Callahan Q: I routinely drink three or four cups of coffee per day, but often wonder if this is too much. Should I consider cutting back? Coffee can be many things: a morning ritual, a cultural tradition, a productivity hack and even a health drink. Studies suggest, for instance, that coffee drinkers live longer and have lower risks of Type 2 diabetes, Parkinson’s disease, cardiovascular conditions and some cancers. “Overall, coffee does more good than bad,” said Rob van Dam, a professor of exercise and nutrition sciences at the Milken Institute School of Public Health at George Washington University. But between your breakfast brew, lunchtime latte and afternoon espresso, is it possible to have too much? And if so, how can you tell? Coffee contains thousands of chemical compounds, many of which may influence health, said Marilyn Cornelis, an associate professor of preventive medicine at Northwestern University Feinberg School of Medicine. But coffee is also the largest source of caffeine for people in the United States, and that’s where most of the risks associated with coffee consumption come from, she said. Having too much caffeine can cause a racing heart, jitteriness, anxiousness, nausea or trouble sleeping, said Jennifer Temple, a professor of exercise and nutrition sciences at the University at Buffalo. But “most people are kind of well tuned with their response to caffeine,” Dr. Cornelis said, and when they begin to experience even mild symptoms of having too much, they cut back. © 2023 The New York Times Company

Keyword: Drug Abuse
Link ID: 28937 - Posted: 09.29.2023