By Christina Jewett and Julie Creswell New York, California and several other states announced a $462 million settlement with Juul Labs on Wednesday, resolving lawsuits claiming that the company aggressively marketed its e-cigarettes to young people and fueled a vaping crisis. The agreement brings many of the company’s legal woes to a conclusion, with settlements reached with 47 states and territories, and 5,000 individuals and local governments. Juul is in the middle of a trial in Minnesota, an unusual case in which a settlement has not been reached. But the company’s efforts to broker deals over the lawsuits have cost it nearly $3 billion so far, an enormous sum for a company still seeking official regulatory approval to keep selling its products. The latest settlement resolved the claims of New York, California, Colorado, the District of Columbia, Illinois, Massachusetts and New Mexico. It follows other lawsuit settlements that took Juul to task for failing to warn young users that the high levels of nicotine in their e-cigarettes would prove addictive. California contended in its lawsuit that for months, Juul did not disclose in its advertising that its devices contained nicotine. It detailed the company’s early marketing efforts, which included handing out free samples of the e-cigarettes in 2015 at trendy events, including a “Nocturnal Wonderland” in San Bernardino and a “Movies All Night Slumber Party” in Los Angeles. The New York lawsuit noted that the company embraced the use of social media hashtags like #LightsCameraVapor. Attorneys general in those states conducted investigations that they said had found that Juul executives were aware that their initial marketing lured teenage users into buying its sleek vaping pens, but did little to address the problem as the adolescent vaping rate exploded. In New York City and the Hamptons, the company held glamorous parties and “falsely led consumers to believe that its vapes were safer than cigarettes and contained less nicotine,” Letitia James, New York’s attorney general, said in a press event Wednesday. © 2023 The New York Times Company

Keyword: Drug Abuse
Link ID: 28740 - Posted: 04.15.2023

by Sarah DeWeerdt Many papers about autism-linked genes note that the genes are expressed throughout both the central and the peripheral nervous systems. The proportion of such prolific genes may be as high as two-thirds, according to one 2020 analysis. Yet few studies delve into what those genes are actually doing outside the brain. That’s starting to change. Although autism is typically thought of as a brain condition, a critical mass of researchers has started to investigate how the condition alters neurons elsewhere in the body. Their work — part of a broader trend in neuroscience to look beyond the brain — hints that the role of the peripheral nervous system in autism is, well, anything but peripheral: Neuronal alterations outside the brain may help to explain a host of the condition’s characteristic traits. Much of the research so far focuses on touch and the workings of the gut, but there is increasing interest in other sensory and motor neurons, as well as the autonomic nervous system, which orchestrates basic body functions such as heartbeat, blood pressure, breathing and digestion. It’s difficult to pinpoint whether some autism traits arise in the peripheral nervous system or the central nervous system; in many cases, complex feedback loops link the two. “Your nervous system doesn’t know that we’ve divided it that way,” says Carissa Cascio, associate professor of psychiatry and behavioral sciences at Vanderbilt University in Nashville, Tennessee. But at least some peripheral changes may offer novel treatment targets. And drugs that act in the peripheral nervous system could also prove more effective and have fewer side effects than brain-based therapies, says Julia Dallman, associate professor of biology at the University of Miami in Coral Gables, Florida. © 2023 Simons Foundation

Keyword: Autism
Link ID: 28739 - Posted: 04.15.2023

By Azeen Ghorayshi Morénike Giwa Onaiwu was shocked when day care providers flagged some concerning behaviors in her daughter, Legacy. The toddler was not responding to her name. She avoided eye contact, didn’t talk much and liked playing on her own. But none of this seemed unusual to Dr. Onaiwu, a consultant and writer in Houston. “I didn’t recognize anything was amiss,” she said. “My daughter was just like me.” Legacy was diagnosed with autism in 2011, just before she turned 3. Months later, at the age of 31, Dr. Onaiwu was diagnosed as well. Autism, a neurodevelopmental disorder characterized by social and communication difficulties as well as repetitive behaviors, has long been associated with boys. But over the past decade, as more doctors, teachers and parents have been on the lookout for early signs of the condition, the proportion of girls diagnosed with it has grown. In 2012, the Centers for Disease Control and Prevention estimated that boys were 4.7 times as likely as girls to receive an autism diagnosis. By 2018, the ratio had dipped to 4.2 to 1. And in data released by the agency last month, the figure was 3.8 to 1. In that new analysis, based on the health and education records of more than 226,000 8-year-olds across the country, the autism rate in girls surpassed 1 percent, the highest ever recorded. More adult women like Dr. Onaiwu are being diagnosed as well, raising questions about how many young girls continue to be missed or misdiagnosed. “I think we just are getting more aware that autism can occur in girls and more aware of the differences,” said Catherine Lord, a psychologist and autism researcher at the University of California, Los Angeles. © 2023 The New York Times Company

Keyword: Autism; Sexual Behavior
Link ID: 28737 - Posted: 04.12.2023

Alison Abbott When neurologist Reisa Sperling stepped up to receive her lifetime achievement award at an international Alzheimer’s conference last December, she was more excited about the future than about celebrating the past. What thrilled Sperling, who won the award for her work on clinical trials of Alzheimer’s treatments, was a sense of hope, which has been conspicuously missing from research into the disease for many years. Most other attendees felt the same. Just a few months before the meeting, researchers had announced that an antibody drug called lecanemab clearly lowered the amount of amyloid protein plaques — a tell-tale sign of the disease — in the brains of participants in a clinical trial, and slowed their cognitive decline. Sperling, who runs a laboratory at Harvard Medical School in Boston, Massachusetts, was buoyant as she gripped the microphone tightly. After spending more than 30 frustrating years in Alzheimer’s research, she said, there was finally proof that she and her colleagues were on the right track. “But still, it isn’t enough,” she said. In the trial, treatment led to a 25% slowing of decline, enough to give participants a few extra months of independent living1. “But actually conquering a destructive disease that affects tens of millions of people worldwide is a different story,” she says. What’s more, lecanemab, marketed in the United States as Leqembi, makes for a tough treatment regime. It has to be infused through a vein by a nursing professional. And because the drug can cause potentially life-threatening brain swelling and bleeds, people taking it have to be monitored regularly.

Keyword: Alzheimers
Link ID: 28736 - Posted: 04.12.2023

By Oliver Whang What is the relationship between mind and body? Maybe the mind is like a video game controller, moving the body around the world, taking it on joy rides. Or maybe the body manipulates the mind with hunger, sleepiness and anxiety, something like a river steering a canoe. Is the mind like electromagnetic waves, flickering in and out of our light-bulb bodies? Or is the mind a car on the road? A ghost in the machine? Maybe no metaphor will ever quite fit because there is no distinction between mind and body: There is just experience, or some kind of physical process, a gestalt. These questions, agonized over by philosophers for centuries, are gaining new urgency as sophisticated machines with artificial intelligence begin to infiltrate society. Chatbots like OpenAI’s GPT-4 and Google’s Bard have minds, in some sense: Trained on vast troves of human language, they have learned how to generate novel combinations of text, images and even videos. When primed in the right way, they can express desires, beliefs, hopes, intentions, love. They can speak of introspection and doubt, self-confidence and regret. But some A.I. researchers say that the technology won’t reach true intelligence, or true understanding of the world, until it is paired with a body that can perceive, react to and feel around its environment. For them, talk of disembodied intelligent minds is misguided — even dangerous. A.I. that is unable to explore the world and learn its limits, in the ways that children figure out what they can and can’t do, could make life-threatening mistakes and pursue its goals at the risk of human welfare. “The body, in a very simple way, is the foundation for intelligent and cautious action,” said Joshua Bongard, a roboticist at the University of Vermont. “As far as I can see, this is the only path to safe A.I.” At a lab in Pasadena, Calif., a small team of engineers has spent the past few years developing one of the first pairings of a large language model with a body: a turquoise robot named Moxie. About the size of a toddler, Moxie has a teardrop-shaped head, soft hands and alacritous green eyes. Inside its hard plastic body is a computer processor that runs the same kind of software as ChatGPT and GPT-4. Moxie’s makers, part of a start-up called Embodied, describe the device as “the world’s first A.I. robot friend.” © 2023 The New York Times Company

Keyword: Intelligence; Robotics
Link ID: 28735 - Posted: 04.12.2023

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