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Rachel Zamzow Andrew Whitehouse never expected his work as an autism researcher to put him in danger. But that’s exactly what happened soon after he and his colleagues reported in 2020 that few autism interventions used in the clinic are backed by solid evidence. Within weeks, a range of clinicians, therapy providers and professional organizations had threatened to sue Whitehouse or had issued complaints about him to his employer. Some harassed his family, too, putting their safety at risk, he says. For Whitehouse, professor of autism research at the Telethon Kids Institute and the University of Western Australia in Perth, the experience came as a shock. “It’s so absurd that just a true and faithful reading of science leads to this,” he says. “It’s an untold story.” In fact, Whitehouse’s findings were not outliers. Another 2020 study—the Autism Intervention Meta-Analysis, or Project AIM for short—plus a string of reviews over the past decade also highlight the lack of evidence for most forms of autism therapy. Yet clinical guidelines and funding organizations have continued to emphasize the efficacy of practices such as applied behavior analysis (ABA). And early intervention remains a near-universal recommendation for autistic children at diagnosis. The field urgently needs to reassess those claims and guidelines, says Kristen Bottema-Beutel, associate professor of special education at Boston College in Massachusetts, who worked on Project AIM. “We need to understand that our threshold of evidence for declaring something evidence-based is rock-bottom low,” she says. “It is very unlikely that those practices actually produce the changes that we’re telling people they do.” © 1986–2022 The Scientist.

Keyword: Autism
Link ID: 28291 - Posted: 04.20.2022

By Apoorva Mandavilli A small biotech company that trumpeted an exciting new treatment for Alzheimer’s disease is now under fire for irregularities in its research results, after several studies related to its work were retracted or questioned by scientific journals. The company, Cassava Sciences, based in Austin, Texas, announced last summer that its drug, simufilam, improved cognition in Alzheimer’s patients in a small clinical trial, describing it as the first such advance in treatment of the disease. Cassava later initiated a larger trial. The drug’s potential garnered enormous attention from investors. Alzheimer’s disease affects roughly six million Americans, a number that is expected to double by 2050, and an effective treatment would be lucrative. Cassava’s stock soared, by more than 1,500 percent at one point. The company was worth nearly $5 billion last summer. But many scientists have been deeply skeptical of the company’s claims, asserting that Cassava’s studies were flawed, its methods opaque and its results improbable. Families of some trial participants have said they see improvements. But critics noted that the trial reporting better cognition due to simufilam lacked a placebo group, and asserted that the Alzheimer’s patients were not followed long enough to confirm that any improvements in cognition were genuine. Some experts went further, accusing the company of manipulating its scientific results. In response to the allegations, in December The Journal of Neuroscience published “expressions of concern” regarding two brain studies authored by the company’s chief collaborator, Hoau-Yan Wang, a professor at the City University of New York. One was co-written by Lindsay H. Burns, chief scientist at Cassava. The journal editors also noted errors in the images accompanying the latter study. (An “expression of concern” indicates that the editors have reason to question the integrity and accuracy of a paper.) © 2022 The New York Times Company

Keyword: Alzheimers
Link ID: 28290 - Posted: 04.20.2022

Diana Kwon Susannah Cahalan was 24 years old when her world turned upside down. Cahalan was living a busy life as a news reporter at the New York Post when she suddenly began experiencing sensitivity to light, numbness in her limbs, and an unsettling feeling that something was not quite right in her body and her brain. One day at work, she found herself inexplicably going from crying hysterically to skipping giddily down a hall. After a seizure landed her in the hospital, her condition rapidly worsened. She started having delusions and hallucinations, believing that her father was a murderer, that she was being secretly recorded, and that she could age people using her mind. In a matter of weeks, walking, speaking, and swallowing became difficult. She eventually became immobile and unresponsive, lying in her hospital bed in a catatonic state. Despite her worsening condition, dozens of specialists from various fields—psychiatry, neurology, internal medicine—couldn’t figure out what was wrong. Numerous blood tests and brain scans failed to generate answers. To many who saw her, Cahalan’s condition looked indistinguishable from mental illnesses such as bipolar disorder or schizophrenia, in which people can experience delusions and hallucinations that make it difficult for them to distinguish what’s real and what’s not. It wasn’t until a neurologist asked Cahalan to draw a clock that the problem became clear. Cahalan had drawn all the numbers on just one side of the clock face, indicating that there was a problem in the functioning of one half of her brain. A brain biopsy confirmed what the doctor had suspected. Cahalan had anti-NMDAR encephalitis, a rare autoimmune disease in which the body produces antibodies that attack the NMDA receptor, a protein found throughout the brain. The condition had only been discovered in the early 2000s, just a few years prior to Cahalan’s diagnosis, by neurologist Josep Dalmau, then at the University of Pennsylvania. This diagnosis was much-needed good news for sufferers of the mysterious condition—their disease was treatable. After receiving immunotherapy, Cahalan was able to fully recover. © 1986–2022 The Scientist.

Keyword: Schizophrenia; Neuroimmunology
Link ID: 28289 - Posted: 04.20.2022

Joan L. Luby, M.D., John N. Constantino, M.D., Deanna M. Barch, Ph.D. Numerous studies of children in the US across decades have shown striking correlations between poverty and less-than-optimal physical and mental health and developmental outcomes. Trauma, poor health care, inadequate nutrition, and increased exposures to psychosocial stress and environmental toxins—all of which have significant negative developmental impact—are likely to be involved. The effects of elevated stress on child-caregiver relationships appear to be particularly detrimental, unsurprising in that nurturing and supportive caregiver relationships are foundational for healthy development in early childhood. For adults whose job options are unconducive to their role as parents (such as working multiple jobs or night shift hours), or for whom family support is unavailable, or for those do not have the material resources they need, the resulting stress may result in sleep disruption, depression, and anxiety—all of which translate to poor developmental trajectories for their children. Other health and developmental risks often associated with poverty include lead and other pollutants in air and water, poor nutrition (often related to living in “food desert” areas where healthy foods such as fresh fruits and vegetables are scarce), neighborhood violence, and trauma. “Toxic stress” that exceeds a child’s ability to adapt can occur when the burden of stressful life experience overwhelms the brain’s regulatory capacity, or when the compensatory abilities of brain and body are compromised. A lack of cognitive stimulation (due to such factors as the absence of books and educational materials in the home, poor immersion in language, and a lack of after school or other enrichment activities) or disruption of sleep and circadian rhythms (by neighborhood noise or parents’ irregular work schedules) is likely to impact brain development and emotional and behavioral regulation when these systems are rapidly developing. © 2022 The Dana Foundation.

Keyword: Development of the Brain; Brain imaging
Link ID: 28288 - Posted: 04.16.2022

By Sabrina Imbler Sign up for Science Times Get stories that capture the wonders of nature, the cosmos and the human body. Get it sent to your inbox. One morning in the Panamanian rainforest, a small fruit bat sized up his competition. The odds did not appear to be in his favor. The winged mammal, a Seba’s short-tailed bat, weighed about half an ounce. But his six opponents, fringe-lipped bats, were twice as heavy and occupying the shrouded corner where the small bat wanted to roost. Even worse, the larger bats are known to feast on small animals, such as frogs, katydids and smaller bats — including Seba’s short-tailed bats. None of this fazed the Seba’s short-tailed bat, which proceeded to scream, shake his wings and hurl his body at the posse of bigger bats, slapping one in the face more than 50 times. “I’ve never seen anything like it,” said Ahana Aurora Fernandez, a behavioral biologist at the Natural History Museum, Berlin, who viewed a recording of the bats but was not involved in the research that produced it. “It’s one bat against six,” Dr. Fernandez said. “He shows no fear at all.” The tiny bat’s belligerence paid off as the big bats fled. The corner clear, the Seba’s short-tailed bat moved in, joined a minute later by his female companion, who had nonchalantly watched the fight from nearby. This fun-size brawl and two similar bat bullying incidents in other roosts were observed by Mariana Muñoz-Romo, a biologist at the Smithsonian Tropical Research Institute, and her colleagues, who had been monitoring the sexual preferences of the larger fringe-lipped bats. In a paper published in March in the journal Behaviour, they asked how often tiny bats antagonize bigger ones. When it comes with a risk of being eaten, why pick a fight? The researchers originally set out to study fringe-lipped bats, who were recently discovered to smear a sticky, fragrant substance on their arms, potentially to attract mates. The animals also have impressive appetites, and have been observed eating sizable frogs. © 2022 The New York Times Company

Keyword: Aggression; Hearing
Link ID: 28287 - Posted: 04.16.2022

By Sharon Oosthoek Despite their excellent vision, one city-dwelling colony of fruit bats echolocates during broad daylight — completely contrary to what experts expected. A group of Egyptian fruit bats (Rousettus aegyptiacus) in downtown Tel Aviv uses sound to navigate in the middle of the day, researchers report in the April 11 Current Biology. The finding greatly extends the hours during which bats from this colony echolocate. A few years ago, some team members had noticed bats clicking while they flew under low-light conditions. The midday sound-off seems to help the bats forage and navigate, even though they can see just fine. Bats that are active during the day are unusual. Out of the more than 1,400 species, roughly 10 are diurnal. What’s more, most diurnal bats don’t use echolocation during the day, relying instead on their vision to forage and avoid obstacles. They save echolocation for dim light or dark conditions. So that’s why, two years ago, a group of Tel Aviv researchers were surprised when they noticed a bat smiling during the day. They were looking over photos from their latest study of Egyptian fruit bats when they noticed one with its mouth slightly parted and upturned. “When an Egyptian fruit bat is smiling, he’s echolocating — he’s producing clicks with his tongue and his mouth is open,” says Ofri Eitan, a bat researcher at Tel Aviv University. “But this was during the day, and these bats see really well.” When Eitan and his colleagues looked through other photos — thousands of them — many showed smiling bats in broad daylight. The team showed in 2015 that the diurnal Egyptian fruit bats do use echolocation outdoors under various low light conditions, at least occasionally. But the researchers hadn’t looked at whether the bats were echolocating during midday hours when light levels are highest. © Society for Science & the Public 2000–2022.

Keyword: Hearing; Evolution
Link ID: 28286 - Posted: 04.16.2022

Kayt Sukel Each night, as you transition into deep sleep from wakefulness, your body undergoes a remarkable transformation. Your muscles relax. Your breathing slows. Your temperature and blood pressure drop. Even your brain activity changes, decelerating into slow, coordinated waves. Despite these remarkable physiological changes, scientists are now learning that the brain is far from idle during sleep. Rather, it remains hard at work, facilitating memory and learning while uncoupled from the external world. “For a long time, we believed that being awake all day depleted you and that sleep was what was required to restore and reinvigorate the whole body, including the brain,” says Robert Stickgold, a pioneering sleep researcher at Harvard Medical School. “It turns out that rest has very little to do with the function of sleep—rather, our brain is sorting and consolidating the information we learned during the day so we can better access it when it’s needed.” Anyone who has ever pulled an all-nighter knows the effect that sleep deprivation can have on cognitive function, including one’s ability to learn and retain new information. Yet, over the last few decades, neuroscientists across the globe have learned that sleep plays an integral role in memory—and it is a role that is highly conserved across the animal kingdom. To better understand how sleep helps us remember, these researchers have been working to characterize not only the physiological changes observed during sleep, but also the neural mechanisms underlying them. Nearly every animal on earth, from fruit flies to non-human primates, experiences some form of sleep, a naturally recurring state of altered consciousness and inhibited sensory activity. And while the exact amount of time spent in slumber, and the patterns of neural activity, differ from animal to animal, humans are no different. We need sleep to thrive. © 2022 The Dana Foundation.

Keyword: Sleep; Learning & Memory
Link ID: 28285 - Posted: 04.16.2022

by Peter Hess Two separate sets of neurons govern the social difficulties and repetitive behaviors associated with mutations in TSHZ3, a top autism candidate gene, according to a new mouse study. The results could help advance a circuit-level understanding of autism, says co-lead investigator Laurent Fasano, senior researcher at the French National Center for Scientific Research and Aix-Marseille University in Marseille, France. “Although we know that the results obtained with animal models will not necessarily be transposable to humans, we hope that our results will stimulate additional studies that will benefit autistic people.” In the new work, Fasano and his colleagues homed in on cortical projection neurons, which connect the cerebral cortex to other brain regions, and striatal cholinergic interneurons, which produce the chemical messenger acetylcholine in the striatum. Together, these cell types form part of the corticostriatal circuit, the dysfunction of which has been implicated in autism. “Whereas many studies have linked defective development and function of the corticostriatal pathway to autism, there is little evidence for an implication of striatal cholinergic interneurons,” says co-lead investigator Lydia Kerkerian-Le Goff, senior researcher at the French National Center for Scientific Research and Aix-Marseille University. Picking out specific cell types in the corticostriatal circuit and linking them to distinct autism-related behaviors is important, says Michael Ragozzino, professor of behavioral neuroscience at the University of Illinois Chicago, who was not involved in the study. The study’s results suggest that repetitive behaviors and social deficits, autism’s core traits, have different neurobiological roots, he says. “This may also suggest that different therapeutics may need to be developed to effectively treat both symptom domains.” © 2022 Simons Foundation

Keyword: Autism
Link ID: 28284 - Posted: 04.16.2022

By Andrew Jacobs Psychedelic compounds like LSD, Ecstasy and psilocybin mushrooms have shown significant promise in treating a range of mental health disorders, with participants in clinical studies often describing tremendous progress taming the demons of post-traumatic stress disorder, or finding unexpected calm and clarity as they face a terminal illness. But exactly how psychedelics might therapeutically rewire the mind remains an enigma. A group of neuroscientists in London thought advanced neuroimaging technology that peered deep into the brain might provide some answers. They included 43 people with severe depression in a study sponsored by Imperial College London, and gave them either psilocybin, the active ingredient in magic mushrooms, or a conventional antidepressant; the participants were not told which one they would receive. Functional magnetic resonance imaging, which captures metabolic function, took two snapshots of their brain activity — the day before receiving the first dose and then roughly three weeks after the final one. What they found, according to a study published Monday in the journal Nature Medicine, was illuminating, both figuratively and literally. Over the course of three weeks, participants who had been given the antidepressant escitalopram reported mild improvement in their symptoms, and the scans continued to suggest the stubborn, telltale signs of a mind hobbled by major depressive disorder. Neural activity was constrained within certain regions of the brain, a reflection of the rigid thought patterns that can trap those with depression in a negative feedback loop of pessimism and despair. By contrast, the participants given psilocybin therapy reported a rapid and sustained improvement in their depression, and the scans showed flourishes of neural activity across large swaths of the brain that persisted for the three weeks. That heightened connectivity, they said, resembled the cognitive agility of a healthy brain that, for example, can toggle between a morning bout of melancholia, a stressful day at work and an evening of unencumbered revelry with friends. © 2022 The New York Times Company

Keyword: Depression; Drug Abuse
Link ID: 28283 - Posted: 04.13.2022

by Niko McCarty A new miniature, head-mounted microscope can simultaneously record the activity of thousands of neurons at different depths within the brains of freely moving mice. The smallest functional two-photon microscope to date, it can image neurons almost anywhere in the brain, with subcellular resolution. The device, called MINI2P (miniature two-photon microscope), can also collect data from the same cluster of neurons over several weeks, making it useful for long-term behavioral studies. “If you really want to understand what is behind cognition or failures in cognition, like in autism, you need to look at the interaction between neurons,” says lead investigator Edvard Moser, professor of neuroscience at the Kavli Institute for Systems Neuroscience in Trondheim, Norway. Other devices that measure neuronal activity, such as Neuropixels 2.0, record signals from more than 10,000 sites in the brain at once. But they have a low spatial resolution and cannot always determine which specific neuron is firing at any given time. Other miniature microscopes have also, traditionally, relied on visible light, which illuminates the surface of tissue, but are limited to imaging about 2,000 neurons. The new device can monitor a brain area measuring 500 by 500 micrometers and can capture data on more than 10,000 neurons at once. A typical mouse brain is roughly the size of a pea and contains about 85 million neurons. The MINI2P uses infrared light to capture the activity of neurons engineered to express GCaMP, a protein that binds to calcium ions during an action potential and emits a fluorescent signal in reply. The microscope measures that fluorescence using an infrared laser beam. © 2022 Simons Foundation

Keyword: Brain imaging
Link ID: 28282 - Posted: 04.13.2022

Rhitu Chatterjee For the first time in a decade, overdose deaths among teens in the United States rose dramatically in 2020 and kept rising through 2021 as well. That's according to the results of a new study published Tuesday in JAMA. "This is very alarming because what we've seen in other parts of the population is that when overdose death rates start to rise, they tend to continue to do so for quite some time," says Joe Friedman, a public health researcher at the University of California, Los Angeles, and the lead author of the new study. "We're still really in the early days in terms of teen overdose. And that makes this an especially important time to intervene," he adds. Friedman and his colleagues found that fatal overdoses among adolescents nearly doubled from 492 in 2019 to 954 in 2020, an increase of 94%. There was an additional 20% rise in 2021 compared to the previous year. The highest rates were among Native American and Alaskan Native teens, followed by Latino teens. "For decades, we've seen overdose rates rising among adults, and teens have been insulated from that," says Friedman. "And now, for the first time, the overdose crisis is reaching teens as well." It appears that the rise in deaths was fueled not by greater numbers of teens using drugs – substance use in this age group actually went down during the pandemic – but by use of dangerous and highly potent forms of fentanyl. The study found that fentanyl-related deaths increased from 253 in 2019 to 680 the following year. And in 2021, 77% of all teen overdose deaths involved fentanyl. © 2022 npr

Keyword: Drug Abuse
Link ID: 28281 - Posted: 04.13.2022

By Jake Buehler Earthen piles built by a chicken-like bird in Australia aren’t just egg incubators — they may also be crucial for the distribution of key nutrients throughout the ecosystem. In the dry woodlands of South Australia, sandy mounds rise between patches of many-stemmed “mallee” eucalyptus trees. These monuments — big enough to smother a parking space — are nests, painstakingly constructed by the malleefowl bird. By inadvertently engineering a patchwork of nutrients and churned soil, the industrious malleefowl may be molding surrounding plant and soil communities and even blunting the spread of fire, researchers report March 27 in the Journal of Ecology. Such ecosystem impacts suggest malleefowl conservation could benefit many species, says Heather Neilly, an ecologist at the Australian Landscape Trust in Calperum Station. The species is currently listed as “vulnerable” and declining by the International Union for Conservation of Nature. Some animals — termed “ecosystem engineers” — produce habitats for other species by shaping the environment around them. Beavers build dams that create homes for pond-dwelling lifeforms. In deserts, owls and giant lizards support plant and animal life with their burrows (SN: 10/8/19; SN: 1/19/21). “In Australia in particular, the focus has largely been on our array of digging mammals,” Neilly says. But malleefowl (Leipoa ocellata) — found throughout western and southern Australia — also perturb the soil. They and their close relatives are “megapodes,” a group of fowl native to Australasia and the South Pacific that have the unusual habit of incubating their eggs much like alligators do: in a massive pile of rotting compost. Heat from the decaying vegetation — locked in with an insulating sand layer on top — regulates the eggs’ temperature, and the young scratch their way to the surface upon hatching. © Society for Science & the Public 2000–2022.

Keyword: Sexual Behavior; Evolution
Link ID: 28280 - Posted: 04.13.2022

By Annie Roth and Hisako Ueno The reign of Japan’s monkey queen has just begun. Last year, Yakei, a 9-year-old female Japanese macaque, fought several other macaques, including her own mother, to become the alpha of her troop. That made Yakei the first known female troop leader in the history of Takasakiyama Natural Zoological Garden in Southern Japan, which was established in 1952 and is home to over 1,000 macaques. But during her first breeding season as queen, which began in November 2021 and concluded in March 2022, a messy love triangle threatened to weaken her grip on power. According to officials at the park, the macaque that Yakei showed interest in mating with, a 15-year-old male named Goro, rejected her advances despite their coupling during a previous breeding season. Meanwhile, an 18-year-old macaque named Luffy did his best to woo Yakei, much to her displeasure. Japanese macaques are polyamorous and scientists were worried that Yakei would not be able to maintain her status while pursuing and rejecting potential mates. Tensions run high during breeding season, and a challenge from a spurned male could easily rob Yakei, an average-sized female, of her rank. Yakei rose to power by defeating her troop’s alpha male, but he was elderly and less formidable than the average young male. Fortunately for Yakei, no other macaques attempted to usurp her throne this season and the queen remained the troop’s alpha at the end of March, according to reserve officials. Her continued rule has surprised scientists and given them an opportunity to observe how macaque society functions under a matriarchy. Despite having to maintain her supremacy, Yakei managed to have a successful breeding season. After Goro gave her the cold shoulder, she spent many weeks playing the field, expressing interest in no fewer than five males. Among these males was Chris, a male ranked 10th in the troop, and Shikao, who holds the rank just below Chris. But the only male the reserve is sure she mated with was Maruo. Maruo, Yakei’s mate. © 2022 The New York Times Company

Keyword: Aggression; Sexual Behavior
Link ID: 28279 - Posted: 04.13.2022

By Benjamin Ehrlich Hour after hour, year after year, Santiago Ramón y Cajal sat alone in his home laboratory, head bowed and back hunched, his black eyes staring down the barrel of a microscope, the sole object tethering him to the outside world. His wide forehead and aquiline nose gave him the look of a distinguished, almost regal, gentleman, although the crown of his head was as bald as a monk’s. He had only a crowd of glass bottles for an audience, some short and stout, some tall and thin, stopped with cork and filled with white powders and colored liquids; the other chairs, piled high with journals and textbooks, left no room for anyone else to sit. Stained with dye, ink and blood, the tablecloth was strewn with drawings of forms at once otherworldly and natural. Colorful transparent slides, mounted with slivers of nervous tissue from sacrificed animals still gummy to the touch from chemical treatments, lay scattered on the worktable. With his left thumb and forefinger, Cajal adjusted the corners of the slide as if it were a miniature picture frame under the lens of his microscope. With his right hand, he turned the brass knob on the side of the instrument, muttering to himself as he drew the image into focus: brownish-black bodies resembling inkblots and radiating threadlike appendages set against a transparent yellow background. The wondrous landscape of the brain was finally revealed to him, more real than he could have ever imagined. In the late 19th century most scientists believed the brain was composed of a continuous tangle of fibers as serpentine as a labyrinth. Cajal produced the first clear evidence that the brain is composed of individual cells, later termed neurons, that are fundamentally the same as those that make up the rest of the living world. He believed that neurons served as storage units for mental impressions such as thoughts and sensations, which combined to form our experience of being alive: “To know the brain is equivalent to ascertaining the material course of thought and will,” he wrote. The highest ideal for a biologist, he declared, is to clarify the enigma of the self. In the structure of neurons, Cajal thought he had found the home of consciousness itself. © 2022 Scientific American

Keyword: Brain imaging
Link ID: 28278 - Posted: 04.13.2022

Max Kozlov When neuroscientist Jakob Seidlitz took his 15-month-old son to the paediatrician for a check-up last week, he left feeling unsatisfied. There wasn’t anything wrong with his son — the youngster seemed to be developing at a typical pace, according to the height and weight charts the physician used. What Seidlitz felt was missing was an equivalent metric to gauge how his son’s brain was growing. “It is shocking how little biological information doctors have about this critical organ,” says Seidlitz, who is based at the University of Pennsylvania in Philadelphia. Soon, he might be able to change that. Working with colleagues, Seidlitz has amassed more than 120,000 brain scans — the largest collection of its kind — to create the first comprehensive growth charts for brain development. The charts show visually how human brains expand quickly early in life and then shrink slowly with age. The sheer magnitude of the study, published in Nature on 6 April1, has stunned neuroscientists, who have long had to contend with reproducibility issues in their research, in part because of small sample sizes. Magnetic resonance imaging (MRI) is expensive, meaning that scientists are often limited in the number of participants they can enrol in experiments. “The massive data set they assembled is extremely impressive and really sets a new standard for the field,” says Angela Laird, a cognitive neuroscientist at Florida International University in Miami. Even so, the authors caution that their database isn’t completely inclusive — they struggled to gather brain scans from all regions of the globe. The resulting charts, they say, are therefore just a first draft, and further tweaks would be needed to deploy them in clinical settings. If the charts are eventually rolled out to paediatricians, great care will be needed to ensure that they are not misinterpreted, says Hannah Tully, a paediatric neurologist at the University of Washington in Seattle. “A big brain is not necessarily a well-functioning brain,” she says. © 2022 Springer Nature Limited

Keyword: Development of the Brain; Brain imaging
Link ID: 28277 - Posted: 04.09.2022

By Alla Katsnelson A dog gives a protective bark, sensing a nearby stranger. A cat slinks by disdainfully, ignoring anyone and everyone. A cow moos in contentment, chewing its cud. At least, that’s what we may think animals feel when they act the way they do. We take our own lived experiences and fill in gaps with our imaginations to better understand and relate to the animals we encounter. Often, our assumptions are wrong. Take horse play, for example. Many people assume that these muscular, majestic animals are roughhousing just for the fun of it. But in the wild, adult horses rarely play. When we see them play in captivity, it isn’t necessarily a good sign, says Martine Hausberger, an animal scientist at CNRS at the University of Rennes in France. Hausberger, who raises horses on her farm in Brittany, began studying horse welfare about three decades ago, after observing that people who keep horses often misjudge cues about the animals’ behavior. Adult horses that play are often ones that have been restrained, Hausberger says. Play seems to discharge the stress from that restriction. “When they have the opportunity, they may exhibit play, and at that precise moment they may be happier,” she says. But “animals that are feeling well all the time don’t need this to get rid of the stress.” Scientists studying animal behavior and animal welfare are making important strides in understanding how the creatures we share our planet with experience the world. “In the last decade or two, people have gotten bolder and more creative in terms of asking what animals’ emotional states are,” explains Georgia Mason, a behavioral biologist and animal welfare scientist at the University of Guelph in Canada. They’re finding thought-provoking answers amid a wide array of animals. © Society for Science & the Public 2000–2022.

Keyword: Emotions; Evolution
Link ID: 28276 - Posted: 04.09.2022

By Paula Span On a recent afternoon in Bastrop, Texas, Janet Splawn was walking her dog, Petunia, a Pomeranian-Chihuahua mix. She said something to her grandson, who lives with her and had accompanied her on the stroll. But he couldn’t follow; her speech had suddenly become incoherent. “It was garbled, like mush,” Ms. Splawn recalled a few days later from a hospital in Austin. “But I got mad at him for not understanding. It was kind of an eerie feeling.” People don’t take chances when 87-year-olds develop alarming symptoms. Her grandson drove her to the nearest hospital emergency room, which then transferred her to a larger hospital for a neurology consultation. The diagnosis: a transient ischemic attack, or T.I.A. For decades, patients have been relieved to hear that phrase. The sudden onset of symptoms like weakness or numbness (often on one side), loss of vision (often in one eye) and trouble with language (speaking, understanding or both) — if resolved in a few minutes — is considered “transient.” Whew. But in a recent editorial in JAMA, two neurologists called for doctors and patients to abandon the term transient ischemic attack. It’s too reassuring, they argued, and too likely to lead someone with passing symptoms to wait until the next morning to call a doctor or let a week go by before arranging an appointment. That’s dangerous. Better, they said, to call a T.I.A. what it is: a stroke. More specifically, a minor ischemic stroke. (Almost 90 percent of strokes, which afflict 795,000 Americans a year, are ischemic, meaning they result from a clot that reduces blood flow to the brain.) Until recently, T.I.A.s “were played down,” said Dr. J. Donald Easton, a neurologist recently retired from the University of California, San Francisco, and an author of the editorial. “The person thinks, ‘Oh, it’s over. It goes away, so all is well.’ But all is not well. There’s trouble to come, and it’s coming soon.” The advent of brain imaging — first CT scans in the late 1970s, then the more precise M.R.I.s in the 1990s — has shown that many T.I.A.s, sometimes called ministrokes, cause visible and permanent brain damage. © 2022 The New York Times Company

Keyword: Stroke
Link ID: 28275 - Posted: 04.09.2022

By Lenny Bernstein Researchers have found variations in a small number of genes that appear to dramatically increase the likelihood of developing schizophrenia in some people. The interplay of a wide array of other genes is implicated for most people with schizophrenia, a severe brain disorder characterized by hallucinations, delusions and inability to function. But for some who possess mutations in the 10 genes identified in the new study, published Wednesday in the journal Nature, the likelihood of developing the disease can be 10, 20 and even 50 times greater. The discovery could one day lead to advances in diagnosis of, and therapy for, the disease, according to the lead author of the study, Tarjinder Singh, of the Broad Institute at MIT and Harvard, which led an effort that involved years of work by dozens of research institutions worldwide. “This is the biological clue that leads to better therapies,” Singh said in an interview. “But the key thing is, we haven’t had any meaningful clues for the longest time.” Ken Duckworth, chief medical officer for the National Alliance on Mental Illness, a nationwide advocacy group, said the study is an important development in the neuroscience that underlies schizophrenia. But he said it is difficult to predict how soon such basic research would pay off for people living with the disease. “This is a big step forward for science that may pay a long-term return for people with schizophrenia and the people who live with them,” Duckworth said. But, he said, “if this is a 17-inning game and they’ve gotten us from the first to the second inning, how does this help someone today?” Less than 1 percent of the U.S. population is believed to have schizophrenia, which is generally treated with an array of powerful antipsychotic medications. The disease reduces life expectancy by about 15 years, according to the new research. Scientists have long recognized a hereditary component to the disease, along with other factors such as environment. The work of isolating these genes could not have been accomplished even 10 or 15 years ago, Singh said, before the sequencing of the human genome and the spread of technology that allows such genetic detective work to be conducted in laboratories around the world. © 1996-2022 The Washington Post

Keyword: Schizophrenia; Genes & Behavior
Link ID: 28274 - Posted: 04.09.2022

By Richard Sandomir Terry Wallis, who spontaneously regained his ability to speak after a traumatic brain injury left him virtually unresponsive for 19 years, and who then became a subject of a major study that showed how a damaged brain could heal itself, died on March 29 in a rehabilitation facility in Searcy, Ark. He was 57. He had pneumonia and heart problems, said his brother George Wallis, who confirmed the death. Terry Wallis was 19 when the pickup truck he was in with two friends skidded off a small bridge in the Ozark Mountains of northern Arkansas and landed upside down in a dry riverbed. The accident left him in a coma for a brief time, then in a persistent vegetative state for several months. One friend died; the other recovered. Until 2003, Mr. Wallis lay in a nursing home in a minimally conscious state, able to track objects with his eyes or blink on command. But on June 11, 2003, he effectively returned to the world when, upon seeing his mother, Angilee, he suddenly said, “Mom.” At the sight of the woman he was told was his adult daughter, Amber, who was six weeks old at the time of the accident, he said, “You’re beautiful,” and told her that he loved her. “Within a three-day period, from saying ‘Mom’ and ‘Pepsi,’ he had regained verbal fluency,” said Dr. Nicholas Schiff, a professor of neurology and neuroscience at Weill Cornell Medicine in Manhattan who led imaging studies of Mr. Wallis’s brain. The findings were presented in 2006 in The Journal of Clinical Investigation. “He was disoriented,” Dr. Schiff, in a phone interview, said of Mr. Wallis’s emergence. “He thought it was still 1984, but otherwise he knew all the people in his family and had that fluency.” Mr. Wallis’s brain scans — the first ever of a late-recovering patient — revealed changes in the strength of apparent connections within the back of the brain, which is believed to have helped his conscious awareness, and in the midline cerebellum, an area involved in motor control, which may have accounted for the very limited movement in his arms and legs while he was minimally conscious. © 2022 The New York Times Company

Keyword: Consciousness
Link ID: 28273 - Posted: 04.09.2022

Yasemin Saplakoglu A mosquito watches you through a lattice of microscopic lenses. You stare back, fly swatter in hand, closely tracking the bloodsucker with your humble single-lens eyes. But it turns out that the way you see each other — and the world — may have more in common than you might think. A study published last month in Science Advances found that inside mammalian eyes, mitochondria, the organelles that power cells, may serve a second role as microscopic lenses, helping to focus light on the photoreceptor pigments that convert the light into neural signals for the brain to interpret. The findings, which draw a striking parallel between mammalian eyes and the compound eyes of insects and other arthropods, suggest that our own eyes have hidden levels of optical complexity, and that evolution has found new uses for very old parts of our cellular anatomy. Abstractions navigates promising ideas in science and mathematics. Journey with us and join the conversation. The lens at the very front of the eye focuses light from the environment onto a thin layer of tissue called the retina in the back. There, photoreceptor cells — cones that paint our world in color and rods that help us navigate in low light — absorb the light and translate it into nerve signals that propagate into the brain. But light-sensitive pigments sit at the very ends of photoreceptors, right behind a thick bundle of mitochondria. The odd placement of this bundle turns the mitochondria into seemingly unnecessary, light-scattering obstacles. The mitochondria are the “final hurdle” for the light particles, said Wei Li, a senior investigator at the National Eye Institute and senior author on the paper. For years, vision scientists couldn’t make sense of this odd placement of these organelles — after all, most cells have their mitochondria hugging their center organelle, the nucleus. All Rights Reserved © 2022

Keyword: Vision
Link ID: 28272 - Posted: 04.06.2022