Functional neurologic disorder (FND) refers to a group of motor, sensory, or cognitive symptoms caused by an abnormality in how the brain functions. FND is distinct from other neurologic conditions such as epilepsy, stroke, and multiple sclerosis in that there is no overt structural damage in the brain. It's a dysfunction of the connections within the brain (the “software”) rather than the structure of the brain itself (the “hardware”). People with FND can experience involuntary movements, nonepileptic seizures, dizziness, blindness, numbness, fatigue, and pain. Memory and concentration also may be affected. An estimated four to 12 people per 100,000 will develop FND, according to the National Institutes of Health. Risk factors include adverse life experiences, having fibromyalgia or other disorders with no identifiable causes, and physical injury. Some people with FND have experienced abuse or neglect in their lives. FND is more common in women and occurs most frequently in people between the ages of 20 and 50, although adolescents and older people also can develop it. Symptoms can include leg and arm weakness or paralysis; nonepileptic convulsions; tremor; sudden, brief involuntary twitching or jerking of a muscle or group of muscles; tics; involuntary muscle contractions that cause slow, repetitive movements or abnormal postures; problems with walking, posture, or balance; speech or voice difficulties; persistent dizziness; and clouded thinking. To diagnose FND and distinguish it from other neurologic conditions, doctors (generally neurologists or neuropsychiatrists) conduct physical and neurologic examinations and ask questions about the person's health and medical and family histories. To evaluate for potential co-occurring conditions and to assist in developing a treatment plan, doctors also may order imaging scans and perform focused mental health and social history screenings. Other tests, which screen for other neurologic disorders, could include electromyography (to record electrical activity in muscles) and electroencephalography (to monitor the brain's electrical activity).

Keyword: Epilepsy; Muscles
Link ID: 28734 - Posted: 04.12.2023

By Bruce Bower Human hair recovered in a Mediterranean island cave has yielded Europe’s oldest direct evidence of people taking hallucinogenic drugs, researchers say. By around 3,000 years ago, visitors at Es Càrritx cave on Menorca — perhaps shamans who performed spiritual and healing rituals — consumed plants containing mind-altering and vision-inducing substances, say archaeologist Elisa Guerra-Doce of the University of Valladolid in Spain and colleagues. Signs of human activity at the cave, including more than 200 human graves arrayed in a chamber at the entrance, were previously dated to between around 3,600 and 2,800 years ago. Researchers had also found a hoard of objects in a small pit within an inner cave chamber, including six wooden containers, each containing locks of human hair. Chemical analyses of one container’s locks, possibly from more than one person, detected three psychoactive plant substances that had been ingested and absorbed into the hair over nearly a year, the scientists report April 6 in Scientific Reports. Two substances, atropine and scopolamine from nightshade plants, induce disorientation, hallucinations and altered physical sensations. Another, ephedrine, boosts energy and alertness. Shamans would have known how to handle and consume these potentially toxic plants safely, the investigators say. Individuals intent on preserving ancient traditions hid hair and other ritually significant objects at Es Càrritx as Menorca’s growing population spurred social changes between 3,000 and 2,800 years ago, the researchers speculate. Burial rituals had included dyeing strands of hair on corpses a reddish color and later cutting off some locks to be put in containers left near graves. © Society for Science & the Public 2000–2023.

Keyword: Drug Abuse
Link ID: 28733 - Posted: 04.09.2023

Miryam Naddaf Virtual models representing the brains of people with epilepsy could help to enable more-effective treatments of the disease by showing neurosurgeons precisely which zones are responsible for seizures. The models, created using a computational system known as the Virtual Epileptic Patient (VEP), have been developed as part of the Human Brain Project (HBP), a ten-year European initiative focused on digital brain research. The approach is being tested in a clinical trial called EPINOV, to evaluate whether it improves the success rate of epilepsy surgery. “It’s an example of personalized medicine,” says Aswin Chari, a neurosurgeon at University College London. VEP uses “the patient’s own brain scans [and] the patient’s own brainwave-recording data to build a model and improve our understanding of where their seizures are coming from”. Life-changing surgery Epileptic seizures are brought on by abnormal brain activity, and around one-third of the 50 million people living with epilepsy worldwide do not respond to anti-seizure drugs. “For those people, surgery is a huge game changer,” says Chari. It aims to free patients from seizures by removing parts of the epileptogenic zone — the brain region that is thought to initiate seizures. To identify the epileptogenic zone, clinicians currently use scanning techniques such as magnetic resonance imaging (MRI) and electroencephalogram (EEG) to investigate brain activity. They also perform stereoelectroencephalography (SEEG), which involves placing up to 16 electrodes, each 7 centimetres long, through the skull to monitor the activity of specific areas for 1–2 weeks. © 2023 Springer Nature Limited

Keyword: Epilepsy; Brain imaging
Link ID: 28732 - Posted: 04.09.2023

By Amber Dance Isabelle Lousada was in her early 30s when she collapsed at her Philadelphia wedding in 1995. A London architect, she had suffered a decade of mysterious symptoms: tingling fingers, swollen ankles, a belly distended by her enlarged liver. The doctors she first consulted suggested she had chronic fatigue syndrome or that she’d been partying and drinking too hard. But her new brother-in-law, a cardiologist, felt that something else must be going on. A fresh series of doctor’s visits led, finally, to the proper diagnosis: Malformed proteins had glommed together inside Lousada’s bloodstream and organs. Those giant protein globs are called amyloid, and the diagnosis was amyloidosis. Amyloid diseases that affect the brain, such as Alzheimer’s and Parkinson’s diseases, receive the lion’s share of attention from medical professionals and the press. In contrast, amyloid diseases that affect other body parts are less familiar and rarely diagnosed conditions, says Gareth Morgan, a biochemist at Boston University Chobanian & Avedisian School of Medicine. Physicians may struggle to recognize and distinguish them, especially in early stages. Treatment options have also been limited — Lousada, now CEO of the nonprofit Amyloidosis Research Consortium in Newton, Massachusetts, was fortunate to survive thanks to a stem cell transplant that is too grueling or unsuitable for many with amyloidosis. Several new medications have come out in the last five years — and these, Lousada says, “have been real game-changers.” But although these therapies can block the formation of new, damaging amyloid, they can’t dissolve the amyloid that’s already built up. The body has natural processes to do so, but these are often too slow to clear years’ worth of built-up amyloid, especially in older individuals. And so patients still deal with amyloid clogging their organs, and people still die of amyloidosis, even if they survive longer than they once did. © 2023 Annual Reviews

Keyword: Alzheimers; Parkinsons
Link ID: 28731 - Posted: 04.09.2023

Nicola Davis Science correspondent From squabbling over who booked a disaster holiday to differing recollections of a glorious wedding, events from deep in the past can end up being misremembered. But now researchers say even recent memories may contain errors. Scientists exploring our ability to recall shapes say people can make mistakes after just a few seconds – a phenomenon the team have called short-term memory illusions. “Even at the shortest term, our memory might not be fully reliable,” said Dr Marte Otten, the first author of the research from the University of Amsterdam. “Particularly when we have strong expectations about how the world should be, when our memory starts fading a little bit – even after one and a half seconds, two seconds, three seconds – then we start filling in based on our expectations.” Writing in the journal Plos One, Otten and colleagues note previous research has shown that when people are presented with a rotated or mirror-image letter, they often report seeing the letter in its correct orientation. While this had previously been put down to participants mis-seeing the shape, Otten and colleagues had doubts. “We thought that they are more likely to be a memory effect. So you saw it correctly, but as soon as you commit it to memory stuff starts going wrong,” said Otten. To investigate further, the researchers carried out four experiments. In the first, participants were screened to ensure they were able to complete basic visual memory tasks before being presented with a circle of six or eight letters, one or two of which were mirror-image forms. After a matter of seconds, participants were shown a second circle of letters which they were instructed to ignore – this acted as a distraction. They were then asked to select, from a series of options, a target shape that had been at particular location in the first circle, and rate their confidence in this choice. © 2023 Guardian News & Media Limited

Keyword: Learning & Memory
Link ID: 28730 - Posted: 04.09.2023

By David Marchese As the founding director of the Johns Hopkins Center for Psychedelic and Consciousness Research, Dr. Roland Griffiths has been a pioneer in investigating the ways in which psychedelics can help treat depression, addiction and, in patients with a life-threatening cancer diagnosis, psychological distress. He has also looked at how the use of psychedelics can produce transformative and long-lasting feelings of human interconnectedness and unity. One could surely classify his achievements using various medical and scientific terms, but I’ll just put it like this: Griffiths has expanded the knowledge of how we might better learn to live. Now he is learning to die. Griffiths, who is 76, has been diagnosed with Stage 4 metastatic colon cancer. It’s a diagnosis, in all likelihood terminal, that for him has brought forth transcendently positive feelings about existence and what he calls the great mystery of consciousness. “We all know that we’re terminal,” says Griffiths, who since being diagnosed has established an endowment at Johns Hopkins to study psychedelics and their potential for increasing human flourishing. “So I believe that in principle we shouldn’t need this Stage 4 cancer diagnosis to awaken. I’m excited to communicate, to shake the bars and tell people, ‘Come on, let’s wake up!’ ” Can we start with your current prognosis? [Laughs.] Prognosis is a 50 percent chance that I’ll make it to Halloween.1 1 Soon after we spoke, Griffiths was removed from the drug trial he was participating in because of a lack of positive results. That likely means his survival timeline is now shorter than it was at the time of our interview. And how are you feeling about that? In spite of that, life has been more beautiful, more wonderful than ever. When I first got that diagnosis, because I work out regularly, I watch my diet, I sleep well, this came out of left field. There was this period in which it felt like I was going to wake up and say, “Boy, that was” — to put it in psychedelic language — “a bummer, a bad dream.” But soon after that I started to contemplate the different psychological states that would be naturally forthcoming with a diagnosis like mine: depression, anxiety, denial, anger, or adopting some belief system of religious outcomes, which as a scientist I was not cut out to do. I went through those, exploring what life would be like if I inhabited those reactions, and I quickly concluded that that was not a wise way to live. I have a long-term meditation practice. © 2023 The New York Times Company

Keyword: Drug Abuse
Link ID: 28729 - Posted: 04.09.2023

Visual: Andrew Bret Wallis/The Image Bank via Getty Images By Lina Tran At 25, Dasha Kiper moved in with a 98-year-old man. She’d just left a graduate program in clinical psychology; Mr. Kessler was a Holocaust survivor in the early stages of Alzheimer’s disease, whose son had hired Kiper as a live-in caregiver. One day, Mr. Kessler clambers onto a chair to replace the battery in a smoke detector. When he ignores her instructions to come down, Kiper loses her cool. She shouts that he’s incapable of changing the battery and doing much of anything for himself. Later, Kiper is filled with remorse. She should have known better than to yell at a nonagenarian with dementia. This is the focus of Kiper’s “Travelers to Unimaginable Lands: Stories of Dementia, the Caregiver, and the Human Brain” — not the mind of the patient, but the caregiver. Often, the spouses, children, and loved ones of people living with dementia succumb to arguing or pleading with their patients, despite reason. “We want to reestablish a shared reality,” Kiper writes. “It’s not cruelty but desperation that drives us to confront them with the truth.” Caregivers aren’t mere observers to cognitive decline but the “invisible victims” of dementia disorders, Kiper writes. They traverse warped realities that operate under different rules of time and memory. One caregiver says, referring to a famous case study by neurologist and author Oliver Sacks, it’s “like being an anthropologist on Mars.” But a caregiver’s slip-up isn’t necessarily the result of character flaws or a lapse in compassion. Rather, Kiper shows the healthy brain is riddled with cognitive biases that impede the work of caring for a person with an impaired mind. This takes a heavy toll. “People always ask about the patient,” one exasperated woman tells Kiper, after recounting how her husband, who doesn’t recognize her, takes to locking her out of their apartment each night. She starts carrying a spare key to let herself in after he falls asleep. “Let me tell you something, the patient is fine; it’s the caregiver who’s going crazy.”

Keyword: Alzheimers; Stress
Link ID: 28728 - Posted: 04.09.2023

By Simon Makin Waves of cerebrospinal fluid which normally wash over brains during sleep can be made to pulse in the brains of people who are wide awake, a new study finds. The clear fluid may flush out harmful waste, such as the sticky proteins that accumulate in Alzheimer’s disease (SN: 7/15/18). So being able to control the fluid’s flow in the brain could possibly one day have implications for treating certain brain disorders. “I think this [finding] will help with many neurological disorders,” says Jonathan Kipnis, a neuroscientist at Washington University in St. Louis who was not involved in the study. “Think of Formula One. You can have the best car and driver, but without a great maintenance crew, that driver will not win the race.” Spinal fluid flow in the brain is a major part of that maintenance crew, he says. But he and other researchers, including the study’s authors, caution that any potential therapeutic applications are still far off. In 2019, neuroscientist Laura Lewis of Boston University and colleagues reported that strong waves of cerebrospinal fluid wash through our brains while we slumber, suggesting that one unappreciated role of sleep may be to give the brain a deep clean (SN: 10/31/19). And the team showed that the slow neural oscillations that characterize deep, non-REM sleep occur in lockstep with the waves of spinal fluid through the brain. “If you drop your clothes in a bath of water, eventually dirt will come out. But if you swish them back and forth, things are moving much more effectively,” Lewis says. “That’s the analogy I think of.” These flows were far larger than the small, rhythmic influences that one’s breathing and heartbeat have on spinal fluid. © Society for Science & the Public 2000–2023.

Keyword: Sleep
Link ID: 28727 - Posted: 04.01.2023

Suzana Herculano-Houzel Neuroscientists have long assumed that neurons are greedy, hungry units that demand more energy when they become more active, and the circulatory system complies by providing as much blood as they require to fuel their activity. Indeed, as neuronal activity increases in response to a task, blood flow to that part of the brain increases even more than its rate of energy use, leading to a surplus. This increase is the basis of common functional imaging technology that generates colored maps of brain activity. Scientists used to interpret this apparent mismatch in blood flow and energy demand as evidence that there is no shortage of blood supply to the brain. The idea of a nonlimited supply was based on the observation that only about 40% of the oxygen delivered to each part of the brain is used – and this percentage actually drops as parts of the brain become more active. It seemed to make evolutionary sense: The brain would have evolved this faster-than-needed increase in blood flow as a safety feature that guarantees sufficient oxygen delivery at all times. Functional magnetic resonance imaging is one of several ways to measure the brain. But does blood distribution in the brain actually support a demand-based system? As a neuroscientist myself, I had previously examined a number of other assumptions about the most basic facts about brains and found that they didn’t pan out. To name a few: Human brains don’t have 100 billion neurons, though they do have the most cortical neurons of any species; the degree of folding of the cerebral cortex does not indicate how many neurons are present; and it’s not larger animals that live longer, but those with more neurons in their cortex. I believe that figuring out what determines blood supply to the brain is essential to understanding how brains work in health and disease. It’s like how cities need to figure out whether the current electrical grid will be enough to support a future population increase. Brains, like cities, only work if they have enough energy supplied. © 2010–2023, The Conversation US, Inc.

Keyword: Stroke; Brain imaging
Link ID: 28726 - Posted: 04.01.2023

By Z Paige L’Erario New Research Points to Causes for Brain Disorders with No Obvious Injury A picture of a human brain taken by a positron emission tomography scanner, also called PET scan, is seen on a screen on January 9, 2019, at the Regional and University Hospital Center of Brest in France. Credit: Fred Tanneau/Getty Images “Stop faking!” Imagine hearing those words moments after your doctor diagnosed you with, say, a stroke or a brain tumor. That sounds absurd but for many people diagnosed with a condition called functional neurological disorder (FND), this is exactly what happens. Although the disorder is not well known to many people, FND is actually one of the most common conditions that neurologists like myself encounter. In it, abnormal brain functioning causes symptoms to appear. FND comes in many forms, with symptoms that can include seizures, feelings of weakness and movement disorders. People may lose consciousness or their ability to move or walk. Or they may experience abnormal tremors or tics. It can be highly disabling and just as costly as structural neurological conditions such as amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, multiple sclerosis and Parkinson’s disease. Although men can develop FND, young to middle-aged women receive this diagnosis most frequently. And during the first two years of the COVID pandemic, FND briefly made international headlines when functional tic-like behaviors spread with social media usage, particularly among adolescent girls.

Keyword: Brain imaging; Stress
Link ID: 28725 - Posted: 04.01.2023

By Elizabeth Preston Several years ago, Christian Rutz started to wonder whether he was giving his crows enough credit. Rutz, a biologist at the University of St. Andrews in Scotland, and his team were capturing wild New Caledonian crows and challenging them with puzzles made from natural materials before releasing them again. In one test, birds faced a log drilled with holes that contained hidden food, and could get the food out by bending a plant stem into a hook. If a bird didn’t try within 90 minutes, the researchers removed it from the dataset. But, Rutz says, he soon began to realize he was not, in fact, studying the skills of New Caledonian crows. He was studying the skills of only a subset of New Caledonian crows that quickly approached a weird log they’d never seen before—maybe because they were especially brave, or reckless. The team changed their protocol. They began giving the more hesitant birds an extra day or two to get used to their surroundings, then trying the puzzle again. “It turns out that many of these retested birds suddenly start engaging,” Rutz says. “They just needed a little bit of extra time.” Scientists are increasingly realizing that animals, like people, are individuals. They have distinct tendencies, habits, and life experiences that may affect how they perform in an experiment. That means, some researchers argue, that much published research on animal behavior may be biased. Studies claiming to show something about a species as a whole—that green sea turtles migrate a certain distance, say, or how chaffinches respond to the song of a rival—may say more about individual animals that were captured or housed in a certain way, or that share certain genetic features. That’s a problem for researchers who seek to understand how animals sense their environments, gain new knowledge, and live their lives. © 2023 NautilusNext Inc.,

Keyword: Evolution; Intelligence
Link ID: 28724 - Posted: 04.01.2023

By Lucy Odling-Smee Philip Kass spends 90% of his day lying on a twin bed in a sparsely decorated room that used to belong to his niece. He takes most meals with a plate balanced on his chest, and he usually watches television because reading is too stressful. “I’m barely living,” he told me on a warm night in June last year. Ever since a back injury 23 years ago, pain has been eating away at Kass’s life. It has cost him his career, his relationships, his mobility and his independence. Now 55, Kass lives with his sister and her family in San Francisco, California. He occasionally joins them for dinner, which means he’ll eat while standing. And once a day he tries to walk four or five blocks around the neighbourhood. But he worries that any activity, walking too briskly or sitting upright for more than a few minutes, will trigger a fresh round of torment that can take days or weeks to subside. Philip Kass has dealt with pain for more than two decades. Some of what Kass describes is familiar. I have been pinned to the floor by spinal pain several times in my life. In my twenties, I was immobilized for three months. In my thirties and forties, each episode of severe pain lasted more than a year. I spent at least another half decade standing or pacing through meetings, meals and movies — for fear that even a few minutes spent sitting would result in weeks of disabling pain. For years, I read anything I could find to better understand why my pain persisted.

Keyword: Pain & Touch
Link ID: 28723 - Posted: 03.29.2023

By Bethany Brookshire Cockroaches are changing up their sex lives, and it’s all our fault. Faced with sweet poisoned bait, roaches first ended up with a mutation that made them hate sweets, hindering their mating strategies. Now, more roach mutations are emerging, showing you can’t keep a good pest down. Like many animals, cockroaches have a sweet tooth, and that preference for sugar plays a central role in their reproductive activities. When a male roach targets a female roach, he will back up to her, secreting a solution called a nuptial gift from the tergal gland under his wings. The solution is full of proteins, fats and sugars, what some researchers call the chocolate of roach food. The female cockroach will crawl up on his back to take a sample, and while she is occupied, the male will whip out a hooked penis to latch onto her reproductive tract. They will then turn back to back and do the deed for about 90 minutes. Humans have aimed to exploit this love of sweet stuff to push cockroaches — particularly the German cockroaches that turn up in American homes — out of our spaces. For decades, people used poisoned roach baits baited with solutions containing glucose. Cockroaches took the bait. But some time in the late 20th century, a new mutation arose — glucose aversion. No one knows how many roaches now hate the sweet stuff, but Coby Schal, an evolutionary biologist at North Carolina State University, suspects the mutation is very common. “There are more and more papers being published on the fact that a whole suite of baits don’t work so well,” he said. This lack of a sweet tooth saved cockroaches from death, but it hurt their sex lives. The gift that normal males secrete contains maltose, a sugar that cockroach saliva transforms into glucose. But if females had the glucose averse mutation, they did not find the male secretions sexy and turned away before the male could hook on. © 2023 The New York Times Company

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 28722 - Posted: 03.29.2023

ByJennifer Couzin-Frankel A class of Alzheimer’s drugs that aims to slow cognitive decline, including the antibody lecanemab that was granted accelerated approval in the United States in January, can cause brain shrinkage, researchers report in a new analysis. Although scientists and drug developers have documented this loss of brain volume in clinical trial participants for years, the scientific review, published yesterday in Neurology, is the first to look at data across numerous studies. It also links the brain shrinkage to a better known side effect of the drugs, brain swelling, which often presents without symptoms. “We don’t fully know what these changes might imply,” says Jonathan Jackson, a cognitive neuroscientist at Massachusetts General Hospital. But, “These data are extremely concerning, and it’s likely these changes are detrimental.” The analysis, which found that trial participants taking these Alzheimer’s drugs often developed more brain shrinkage than when they were on a placebo, alarmed Scott Ayton, a neuroscientist at the Florey Institute of Neuroscience and Mental Health in Melbourne, Australia, who led the work. “We’re talking about the possibility of brain damage” from treatment, says Ayton, who was invited by Eisai to join an advisory board on lecanemab’s rollout in Australia if the drug is approved there. “I find it very peculiar that these data, which are very important, have been completely ignored by the field.” A spokesperson for Eisai suggested there are benign theories for the brain shrinkage, too. The company said that although participants in its pivotal trial did experience “greater cortical volume loss on lecanemab relative to placebo,” those reductions may be due to antibody clearing the protein beta amyloid from the brain, and reducing inflammation. © 2023 American Association for the Advancement of Science.

Keyword: Alzheimers; Brain imaging
Link ID: 28721 - Posted: 03.29.2023

A National Institutes of Health team has identified a compound already approved by the U.S. Food and Drug Administration that keeps light-sensitive photoreceptors alive in three models of Leber congenital amaurosis type 10 (LCA 10), an inherited retinal ciliopathy disease that often results in severe visual impairment or blindness in early childhood. LCA 10 is caused by mutations of the cilia-centrosomal gene (CEP290). Such mutations account for 20% to 25% of all LCA – more than any other gene. In addition to LCA, CEP290 mutations can cause multiple syndromic diseases involving a range of organ systems. Using a mouse model of LCA10 and two types of lab-created tissues from stem cells known as organoids, the team screened more than 6,000 FDA-approved compounds to identify ones that promoted survival of photoreceptors, the types of cells that die in LCA, leading to vision loss. The high-throughput screening identified five potential drug candidates, including Reserpine, an old medication previously used to treat high blood pressure. Observation of the LCA models treated with Reserpine shed light on the underlying biology of retinal ciliopathies, suggesting new targets for future exploration. Specifically, the models showed a dysregulation of autophagy, the process by which cells break down old or abnormal proteins, which in this case resulted in abnormal primary cilia, a microtubule organelle that protrudes from the surface of most cell types. In LCA10, CEP290 gene mutations cause dysfunction of the primary cilium in retinal cells. Reserpine appeared to partially restore autophagy, resulting in improved primary cilium assembly.

Keyword: Vision
Link ID: 28720 - Posted: 03.29.2023

By Jack Tamisiea Even a fisher’s yarn would sell a whale shark short. These fish—the biggest on the planet—stretch up to 18 meters long and weigh as much as two elephants. The superlatives don’t end there: Whale sharks also have one of the longest vertical ranges of any sea creature, filter feeding from the surface of the ocean to nearly 2000 meters down into the inky abyss. Swimming between bright surface waters and the pitch black deep sea should strain the shark’s eyes, making their lifestyle impossible. But researchers have now uncovered the genetic wiring that prevents this from happening. The study, published this week in the Proceedings of the National Academy of Sciences, pinpoints a genetic mutation that makes a visual pigment in the whale shark’s retina more sensitive to temperature changes. As a result, the pigments—which sense blue light in dark environments—are activated in the chilly deep sea and deactivated when the sharks return to the balmy surface to feed, allowing them to prioritize different parts of their vision at different depths. Ironically, the genetic alteration is surprisingly similar to one that degrades pigments in human retinas, causing night blindness. It remains unclear why whale sharks dive so deep. Because prey is scarce at these depths, the behavior may be linked to mating. But whatever they do, the sharks rely on a light-sensing pigment in their retinas called rhodopsin to navigate the dark waters. Although the pigments are less useful in sunny habitats, they help many vertebrates, including humans, detect light in dim environments. In the deep sea, the rhodopsin pigments in whale shark eyes are specifically calibrated to see blue light—the only color that reaches these depths. Previous research has revealed bottom-dwelling cloudy catsharks (Scyliorhinus torazame) have similarly calibrated pigments in their eyes to spot blue light. But these small sharks are content in the deep, making whale sharks the only known sharks to sport these pigments in the shallows. In lighter waters, these blue light–sensing pigments could act as a hindrance to seeing other kinds of light, but whale sharks are still able to maneuver with ease as they vacuum up seafood.

Keyword: Vision; Genes & Behavior
Link ID: 28719 - Posted: 03.25.2023

By Emily Underwood Many of our defining traits — including the languages we speak and how we connect with others — can be traced back at least in part to our earliest experiences. Although our brains remain malleable throughout our lives, most neuroscientists agree that the changes that occur in the womb and in the first few years of life are among the most consequential, with an outsize effect on our risk of developmental and psychiatric conditions. “Early on in life, the brain is still forming itself,” says Claudia Lugo-Candelas, a clinical psychologist at Columbia University and coauthor of an overview of the prenatal origins of psychiatric illness in the Annual Review of Clinical Psychology. Starting from a tiny cluster of stem cells, the brain develops into a complex organ of roughly 100 billion neurons and trillions of connections in just nine months. Compared to the more subtle brain changes that occur later in life, Lugo-Candelas says, what happens in utero and shortly after birth “is like building the house, versus finishing the deck.” But just how this process unfolds, and why it sometimes goes awry, has been a hard mystery to crack, largely because so many of the key events are difficult to observe. The first magnetic resonance imaging (MRI) scans of baby and fetal brains were taken back in the early 1980s, and doctors seized on the tool to diagnose major malformations in brain structure. But neuroimaging tools that can capture the baby brain’s inner workings in detail and spy on fetal brain activity in pregnant moms are much newer developments. Today, this research, coupled with long-term studies that follow thousands of individual children for years, is giving scientists new insights into how the brain develops. These advances have propelled researchers to a different stage than they were in even five years ago, says Damien Fair, a neuroscientist at the University of Minnesota who studies developmental conditions like autism and attention deficit hyperactivity disorder (ADHD). © 2023 Annual Reviews

Keyword: Development of the Brain; ADHD
Link ID: 28718 - Posted: 03.25.2023

By Emily Anthes The prevalence of autism spectrum disorder in American children rose between 2018 and 2020, continuing a long-running trend, according to a study released by the Centers for Disease Control and Prevention on Thursday. In 2020, an estimated one in 36 8-year-olds had autism, up from one in 44 in 2018. The prevalence was roughly 4 percent in boys and 1 percent in girls. The rise does not necessarily mean that autism has become more common among children, and it could stem from other factors, such as increased awareness and screening. “I have a feeling that this is just more discovery,” said Catherine Lord, a professor of psychiatry at the University of California, Los Angeles medical school, who was not involved in the research. “The question is what’s happening next to these kids, and are they getting services?” The rise was especially sharp among Black, Hispanic, and Asian or Pacific Islander children. For the first time, autism was significantly more prevalent among 8-year-olds in these groups than in white children, who have traditionally been more likely to receive autism diagnoses. “These patterns might reflect improved screening, awareness and access to services among historically underserved groups,” the researchers wrote. But why the prevalence in these children has surpassed that in white children is an open question that requires more investigation, Dr. Lord said. An accompanying study, also published on Thursday, suggests that the pandemic may have disrupted or delayed the detection of autism in younger children. © 2023 The New York Times Company

Keyword: Autism
Link ID: 28717 - Posted: 03.25.2023

By Nora Bradford For the first time, scientists have recorded brain waves from freely moving octopuses. The data reveal some unexpected patterns, though it’s too early to know how octopus brains control the animals’ behavior, researchers report February 23 in Current Biology. “Historically, it’s been so hard to do any recordings from octopuses, even if they’re sedated,” says neuroscientist Robyn Crook of San Francisco State University, who was not involved in the study. “Even when their arms are not moving, their whole body is very pliable,” making attaching recording equipment tricky. Octopuses also tend to be feisty and clever. That means they don’t usually put up with the uncomfortable equipment typically used to record brain waves in animals, says neuroethologist Tamar Gutnick of the University of Naples Federico II in Italy. To work around these obstacles, Gutnick and colleagues adapted portable data loggers typically used on birds, and surgically inserted the devices into three octopuses. The researchers also placed recording electrodes inside areas of the octopus brain that deal with learning and memory. The team then recorded the octopuses for 12 hours while the cephalopods went about their daily lives — sleeping, swimming and self-grooming — in tanks. Some brain wave patterns emerged across all three octopuses in the 12-hour period. For instance, some waves resembled activity in the human hippocampus, which plays a crucial role in memory consolidation. Other brain waves were similar to those controlling sleep-wake cycles in other animals. © Society for Science & the Public 2000–2023.

Keyword: Brain imaging
Link ID: 28716 - Posted: 03.25.2023

By Meghan Rosen The patient arrived at the hospital one hot night in Masi-Manimba, an agricultural town unfurled along the Democratic Republic of the Congo’s Lukula River. He couldn’t speak, he couldn’t walk, he was conscious but “barely could make … gestures,” says Béatrice Kasita, a nurse who was there when he came in. She remembers his deformed posture, how his body curved into a fetal position. He was also unusually drowsy — a telltale sign of his illness. The patient, a 27-year-old man, had been brought in by a medical team screening villagers for sleeping sickness, a deadly parasitic disease spread via the bite of a blood-feeding fly. Since the first case report in the late 14th century, the illness has ebbed and flowed in sub-Saharan Africa. Across the continent, the predominant form of sleeping sickness shows up in about two dozen countries, most cases now occurring in the DRC. The disease is a nightmarish scourge that can maim the brain and ultimately kill. But today, cases hover near an all-time low. In 2021, the World Health Organization reported just 747 cases of the predominant form, down from more than 37,000 in 1998. That precipitous plunge came out of decades of work, millions of screenings, spinal taps upon spinal taps, toxic treatments and the rapid rise of safer though often burdensome ones, countless IV infusions, long hospital days and nights, medicine lugged to remote villages, and communities on constant alert for sleeping sickness’s insidious symptoms. Now, a promising drug has fanned hope for halting transmission of the disease. Called acoziborole, the drug is taken by mouth in just a single dose. Kasita’s patient, who arrived at the hospital in June 2017, was among the first to try it. © Society for Science & the Public 2000–2023.

Keyword: Sleep
Link ID: 28715 - Posted: 03.23.2023