By Julian Nowogrodzki Millions of adults around the world take potent drugs such as Wegovy to shed pounds. Should kids do the same? That question is growing more urgent in the face of mounting evidence that children and adolescents, as well as adults, slim down if they take the latest generation of obesity drugs. Clinical trials1,2 have shown that many adolescents with obesity lose substantial amounts of weight on these drugs, which work by mimicking a natural hormone called glucagon-like peptide 1 (GLP-1). The GLP-1 mimics semaglutide, commonly sold as Ozempic and Wegovy, and liraglutide, marketed as Saxenda and Victoza, are approved in the United States and Europe to treat obesity in children as young as 12. Now a trial has produced some of the first data on anti-obesity drugs in even younger children: those aged 6 to 11. The study3 reports that children who were treated with liraglutide showed a decrease in their body mass index (BMI), a measure of obesity. The results were published on 10 September in The New England Journal of Medicine. Nature asked specialists in obesity about the costs and benefits of giving the GLP-1 mimics to youngsters who are still growing and developing. Why test powerful weight-loss drugs on kids? Most kids with obesity become teens with obesity and then adults with obesity. Many young children with severe obesity have “already developed significant health issues”, says physician Sarah Ro, who directs the University of North Carolina Physicians Network Weight Management Program and has served as a consultant to Novo Nordisk, the manufacturer of semaglutide. Her clinic in Hillsborough treats children with severe obesity who have health issues such as high blood pressure, type 2 diabetes or an advanced form of liver disease linked to excess weight. © 2024 Springer Nature Limited

Keyword: Obesity; Development of the Brain
Link ID: 29482 - Posted: 09.18.2024

By Max Kozlov A low-cost diabetes drug slows ageing in male monkeys and is particularly effective at delaying the effects of ageing on the brain, finds a small study that tracked the animals for more than three years1. The results raise the possibility that the widely used medication, metformin, could one day be used to postpone ageing in humans. Monkeys that received metformin daily showed slower age-associated brain decline than did those not given the drug. Furthermore, their neuronal activity resembled that of monkeys about six years younger (equivalent to around 18 human years) and the animals had enhanced cognition and preserved liver function. This study, published in Cell on 12 September, helps to suggest that, although dying is inevitable, “ageing, the way we know it, is not”, says Nir Barzilai, a geroscientist at the Albert Einstein College of Medicine in New York City, who was not involved in the study. Metformin has been used for more than 60 years to lower blood-sugar levels in people with type 2 diabetes — and is the second most-prescribed medication in the United States. The drug has long been known to have effects beyond treating diabetes, leading researchers to study it against conditions such as cancer, cardiovascular disease and ageing. Data from worms, rodents, flies and people who have taken the drug for diabetes suggest the drug might have anti-ageing effects. But its effectiveness against ageing had not been tested directly in primates, and it is unclear whether its potential anti-ageing effects are achieved by lowering blood sugar or through a separate mechanism. This led Guanghui Liu, a biologist who studies ageing at the Chinese Academy of Sciences in Beijing, and his colleagues to test the drug on 12 elderly male cynomolgus macaques (Macaca fasciucularis); another 16 elderly monkeys and 18 young or middle-aged animals served as a control group. Every day, treated monkeys received the standard dose of metformin that is used to control diabetes in humans. The animals took the drug for 40 months, which is equivalent to about 13 years for humans. © 2024 Springer Nature Limited

Keyword: Development of the Brain; Obesity
Link ID: 29481 - Posted: 09.14.2024

By Emily Anthes The common marmoset is a certified chatterbox. The small, South American monkey uses an array of chirps, whistles and trills to defend its territory, flag the discovery of food, warn of impending danger and find family members hidden by dense forest foliage. Marmosets also use distinct calls to address different individuals, in much the same way that people use names, new research suggests. The findings make them the first nonhuman primates known to use name-like vocal labels for individuals. Until this year, only humans, dolphins and parrots were known to use names when communicating. In June, however, scientists reported that African elephants appeared to use names, too; researchers made the discovery by using artificial intelligence-powered software to detect subtle patterns in the elephants’ low-pitched rumbles. In the new study, which was published in Science last month, a different team of researchers also used A.I. to uncover name-like labels hiding in the calls of common marmosets. The discovery, which is part of a burgeoning scientific effort to use sophisticated computational tools to decode animal communication, could help shed light on the origins of language. And it raises the possibility that name-bestowing behavior may be more widespread in the animal kingdom than scientists once assumed. “I think what it’s telling us is that it’s likely that animals actually have names for each other a lot more than maybe we ever conceived,” said George Wittemyer, a conservation biologist at Colorado State University who led the recent elephant study but was not involved in the marmoset research. “We just never were really looking properly.” Marmosets are highly social, forming long-term bonds with their mates and raising their offspring cooperatively in small family groups. They produce high-pitched, whistle-like “phee calls” to communicate with other marmosets who might be hidden among the treetops. “They start to exchange phee calls when they lose eyesight of each other,” said David Omer, a neuroscientist at the Hebrew University of Jerusalem who led the new study. © 2024 The New York Times Company

Keyword: Animal Communication; Language
Link ID: 29480 - Posted: 09.14.2024

By Angie Voyles Askham Nathaniel Daw has never touched a mouse. As professor of computational and theoretical neuroscience at Princeton University, he mainly works with other people’s data to construct models of the brain’s decision-making process. So when a collaborator came to him a few years ago with confusing data from mice that had performed a complex decision-making task in the lab, Daw says his best advice was just to fit the findings to the tried-and-true model of reward prediction error (RPE). That model relies on the idea that dopaminergic activity in the midbrain reflects discrepancies between expected and received rewards. Daw’s collaborator, Ben Engelhard, had measured the activity of dopamine neurons in the ventral tegmental area (VTA) of mice as they were deciding how to navigate a virtual environment. And although the virtual environment was more complex than what a mouse usually experiences in the real world, an RPE-based model should have held, Daw assumed. “It was obvious to me that there was this very simple story that was going to explain his data,” Daw says. But it didn’t. The neurons exhibited a wide range of responses, with some activated by visual cues and others by movement or cognitive tasks. The classic RPE model, it turned out, could not explain such heterogeneity. Daw, Engelhard and their colleagues published the findings in 2019. That was a wake-up call, Daw says, particularly after he watched videos of what the mice actually experienced in the maze. “It’s just so much more complicated, and high dimensional, and richer” than expected, he says. The idea that this richness could be reduced to such a simple model seems ludicrous now, he adds. “I was just so blinded.” © 2024 Simons Foundation

Keyword: Attention; Drug Abuse
Link ID: 29479 - Posted: 09.14.2024

By Christina Caron Julianna McLeod, 26, had her first psychotic episode while taking Vyvanse for attention deficit hyperactivity disorder last year. Ms. McLeod, who lives in Ontario, Canada, had taken the drug before but paused while pregnant with her first child and didn’t start taking it again until six months postpartum. Although the dose was 40 milligrams, she often forgot when she had last taken a pill. So she took one whenever she remembered — and may have ended up taking more than her prescribed daily dose. The delusions that she experienced made her feel euphoric and highly energetic. “I felt like my brain was exploding with connections,” she said. In her mind, she was a “super detective” who was uncovering the people and organizations that were secretly engaging in child sex trafficking. She even began to believe that someone was drugging her and her baby. Psychosis and mania are each known side effects of stimulant medications, and the Food and Drug Administration has added warnings to the medications’ labels saying that they may cause symptoms like hallucinations, delusional thinking or mania. But these side effects are considered rare — experienced by an estimated 1 in 1,000 patients — and have not been extensively researched. It can take months for someone to fully recover. A new study published on Thursday in The American Journal of Psychiatry suggests that dosage may play a role. It found that among people who took high doses of prescription amphetamines such as Vyvanse and Adderall, there was a fivefold increased risk of developing psychosis or mania for the first time compared with those who weren’t taking stimulants. The researchers defined a high dose as more than 40 milligrams of Adderall, 100 milligrams of Vyvanse or 30 milligrams of dextroamphetamine. The medium dosage (20 to 40 milligrams of Adderall, 50 to 100 milligrams of Vyvanse or 16 to 30 milligrams of dextroamphetamine) was associated with a 3.5 times higher risk of psychosis or mania. There was no increased risk of psychosis or mania among those who used methylphenidate drugs, like Concerta or Ritalin, regardless of the dose. © 2024 The New York Times Company

Keyword: ADHD; Schizophrenia
Link ID: 29478 - Posted: 09.14.2024

By Ellen Barry A study of adolescent brain development that tested children before and after coronavirus pandemic lockdowns in the United States found that girls’ brains aged far faster than expected, something the researchers attributed to social isolation. The study from the University of Washington, published on Monday in the Proceedings of the National Academy of Sciences, measured cortical thinning, a process that starts in either late childhood or early adolescence, as the brain begins to prune redundant synapses and shrink its outer layer. Thinning of the cortex is not necessarily bad; some scientists frame the process as the brain rewiring itself as it matures, increasing its efficiency. But the process is known to accelerate in stressful conditions, and accelerated thinning is correlated with depression and anxiety. Scans taken in 2021, after shutdowns started to lift, showed that both boys and girls had experienced rapid cortical thinning during that period. But the effect was far more notable in girls, whose thinning had accelerated, on average, by 4.2 years ahead of what was expected; the thinning in boys’ brains had accelerated 1.4 years ahead of what was expected. “That is a stunning difference,” said Patricia K. Kuhl, a director of the Institute for Learning and Brain Sciences at the University of Washington and one of the study’s authors. The results, she added, suggested that “a girl who came in at 11, and then returned to the lab at age 14, now has a brain that looks like an 18-year-old’s.” Dr. Kuhl attributed the change to “social deprivation caused by the pandemic,” which she suggested had hit adolescent girls harder because they are more dependent on social interaction — in particular, talking through problems with friends — as a way to release stress. The difference between the genders “is just as clear as night and day,” Dr. Kuhl said. “In the girls, the effects were all over the brain — all the lobes, both hemispheres.” © 2024 The New York Times Company

Keyword: Stress; Development of the Brain
Link ID: 29477 - Posted: 09.11.2024

Alzheimer’s disease impairs a patient by destroying neurons, which otherwise live for decades, and by disrupting communication among the remaining brain cells. As neurons die, the areas of the brain they constitute begin to atrophy. A detailed picture of the progression is still under investigation, and the disease follows different tracks in different patients, but researchers have found brains afflicted with Alzheimer’s typically atrophy along the same basic pattern. A better understanding of that pattern may provide the foundation for methods to diagnose the disease earlier, which in turn would give medication and lifestyle changes the best chance of slowing dementia. In broad strokes, here’s how Alzheimer’s tends to change a brain. © 2024 SCIENTIFIC AMERICAN,

Keyword: Alzheimers
Link ID: 29476 - Posted: 09.11.2024

By Frieda Klotz For five years, Clare Dolman took lithium to manage her bipolar disorder. The medicine kept her happy and well with few side effects, and she described it as a wonder drug. But when she began to plan for a pregnancy, her psychiatrist advised her to go off the medication to protect the fetus. This was 1988, and it was the standard guidance at the time. While Dolman experienced some stresses during the pregnancy, her mood remained stable. But soon after giving birth, she began to experience mild hallucinations. “I thought, yes, there’s something wrong here,” she recalled. “But I had the insight still to see that I was getting ill, and my husband knew I was getting ill because he had seen me really bad.” She went on to spend five weeks in the hospital. Clare Dolman at the launch of the Bipolar Commission at the U.K. Parliament. Dolman, who has bipolar disorder, stopped taking lithium during her own pregnancies more than 30 years ago. She later became a mental health advocate and has studied the experiences of pregnant women with the illness. Visual: Courtesy of Clare Dolman Bipolar disorder involves extreme fluctuations in mood and is classified into different types according to symptoms and severity. For women with the condition, pregnancy can be a fraught endeavor as they balance the health of their growing fetus with their own mental state. Many, like Dolman, stop taking the medications that keep them well — which can lead to a recurrence of symptoms — and some avoid pregnancy altogether.

Keyword: Schizophrenia; Sexual Behavior
Link ID: 29475 - Posted: 09.11.2024

Anna Bawden Health and social affairs correspondent An epilepsy drug could help prevent the breathing of patients with sleep apnoea from temporarily stopping, according to research. Obstructive sleep apnoea is a common breathing problem that affects about one in 20 people, according to the National Institute for Health and Care Excellence in England. Patients often snore loudly, their breathing starts and stops during the night and they may wake up several times. Not only does this cause tiredness but it can also increase the risk of high blood pressure, stroke, heart disease and type 2 diabetes. An international study has identified that an epilepsy medication is associated with a marked reduction in sleep apnoea symptoms. The findings, presented at the European Respiratory Society Congress in Vienna, Austria, demonstrated there were possible options for those unable to use mechanical breathing aids such as continuous positive airway pressure (Cpap) machines. Prof Jan Hedner, from Sahlgrenska university hospital and the University of Gothenburg in Sweden, said: “The standard treatment for obstructive sleep apnoea is sleeping with a machine that blows air through a face mask to keep the airways open. Unfortunately, many people find these machines hard to use over the long term, so there is a need to find alternative treatments.” The researchers conducted a randomised controlled trial of almost 300 obstructive sleep apnoea patients in Belgium, the Czech Republic, France, Germany and Spain who did not use the Cpap machines. They were divided into four groups and given one of three strengths of sulthiame or a placebo. © 2024 Guardian News & Media Limited

Keyword: Sleep
Link ID: 29474 - Posted: 09.11.2024

By Christina Caron Patients and caregivers have struggled for two years to find stimulant medications like Adderall, Vyvanse and Concerta to treat attention deficit hyperactivity disorder. Some spend hours each month going from pharmacy to pharmacy to find a drug, while others are forced to switch to a different brand or formulation, or go without medication for weeks. This week the Drug Enforcement Administration announced a potential solution: It is raising the amount of lisdexamfetamine (Vyvanse) that can be produced by U.S. manufacturers this year by nearly 24 percent to meet demand in the United States and abroad. Vyvanse is an amphetamine that has been approved for use in children and adults with A.D.H.D. and has become commonly prescribed after the generic version was introduced last year. According to the D.E.A., the latest data shows that demand for the drug has been rising globally. But right now every manufacturer of generic Vyvanse listed on the Food and Drug Administration website is experiencing a shortage. Many health care providers who specialize in treating patients with A.D.H.D. said that the D.E.A.’s decision was a positive development but that it was unclear just how much of an effect it might have on the shortage. “Obviously it’s not going to solve the problem completely,” said Ami Norris-Brilliant, clinical director of the Division of A.D.H.D., Learning Disorders, and Related Disorders at the Icahn School of Medicine at Mount Sinai in New York City. “But I think anything that helps increase drug availability is a good thing.” It is not the first time that the D.E.A. has increased production quotas for A.D.H.D. drugs. Last year it announced a new 2023 limit for methylphenidate, which is used to make drugs like Ritalin and Concerta, raising the allotted amount by 27 percent for 2023. The drug remains in shortage, however, in the extended release formulation. © 2024 The New York Times Company

Keyword: ADHD
Link ID: 29473 - Posted: 09.11.2024

By Olivia Gieger Unlike traditional antidepressants, ketamine acts quickly to relieve depression symptoms, and its effects last long after the drug has cleared the system. Researchers have puzzled over what ketamine is doing in the brain to achieve these results. For one thing, the drug acts on N-methyl-D-aspartate (NMDA) glutamate receptors, which appear on neurons all over the brain. “Then the question is: Does the drug hit on all these brain regions simultaneously?” says Hailan Hu, professor of brain science at Zhejiang University. Or does it affect one region first, which sets off a series of downstream antidepressant effects? The answer is the latter, Hu and her colleagues report in a new study. Ketamine acts first on neurons in the lateral habenula, they found, in mice with depression-like symptoms. The structure—known as the “anti-reward” center—is hyperactive in people with depression and in mice modeling the condition, previous work has shown. That activity makes it highly susceptible to the drug’s effects, Hu and her colleagues discovered. Ketamine binds the NMDA receptors of cells in the lateral habenula and renders them inactive, which in turn interrupts downstream mechanisms of depression. The findings, published in Science in August, help explain how the known targets of ketamine are involved in such a rapid antidepressant response, explains Christophe Proulx, associate professor of psychiatry and neuroscience at Laval University. Proulx was not involved in the work but co-authored a Perspective article on it. Spotlighting the lateral habenula’s role also represents a new way of thinking about ketamine’s effects on depression—involving a shift away from a focus on weakened circuits and impaired plasticity, says Todd Gould, professor of psychiatry and neurobiology at the University of Maryland School of Medicine, who was not affiliated with the study. “[The work provides] additional strong evidence supporting a different view about how ketamine may be working.” Although ketamine inactivated NMDA receptors in the lateral habenula of the depressive-like mice, it had less impact in the CA1 region of the hippocampus, Hu and her colleagues observed using in-vitro slice electrophysiology and electrode recordings in awake animals. © 2024 Simons Foundation

Keyword: Depression
Link ID: 29472 - Posted: 09.11.2024

By Roni Caryn Rabin Move over, body mass index. Make room for roundness — to be precise, the body roundness index. The body mass index, or B.M.I., is a ratio of height to weight that has long been used as a medical screening tool. It is one of the most widely used health metrics but also one of the most reviled, because it is used to label people overweight, obese or extremely obese. The classifications have been questioned by athletes like the American Olympic rugby player Ilona Maher, whose B.M.I. of 30 technically puts her on the cusp of obesity. “But alas,” she said on Instagram, addressing online trolls who tried to shame her about her weight, “I’m going to the Olympics and you’re not.” Advocates for overweight individuals and people of color note that the formula was developed nearly 200 years ago and based exclusively on data from men, most of them white, and that it was never intended for medical screening. Even physicians have weighed in on the shortcomings of B.M.I. The American Medical Association warned last year that B.M.I. is an imperfect metric that doesn’t account for racial, ethnic, age, sex and gender diversity. It can’t differentiate between individuals who carry a lot of muscle and those with fat in all the wrong places. “Based on B.M.I., Arnold Schwarzenegger when he was a bodybuilder would have been categorized as obese and needing to lose weight,” said Dr. Wajahat Mehal, director of the Metabolic Health and Weight Loss Program at Yale University. “But as soon as you measured his waist, you’d see, ‘Oh, it’s 32 inches.’” So welcome a new metric: the body roundness index. B.R.I. is just what it sounds like — a measure of how round or circlelike you are, using a formula that takes into account height and waist, but not weight. © 2024 The New York Times Company

Keyword: Obesity
Link ID: 29471 - Posted: 09.07.2024

By Cassandra Willyard Megan Hodge’s first bout of intense pain arrived when she was in her mid-20s. Hodge and her husband were getting ready to visit family for Thanksgiving. Though Hodge had been dealing with a variety of chronic health issues, her workout had gone well that morning and she finally felt like she was getting a handle on her health. Hodge began packing. As she reached into her closet to grab a sweater, her back gave out. The pain was excruciating, so intense that she felt light-headed and thought she might vomit. As the years passed, Hodge had more frequent and more severe bouts of back pain. Any small movement could be a trigger — grabbing a towel from the linen closet, picking up a toy off the floor, sneezing. In 2021, Hodge experienced a particularly bad flare-up. None of the strategies she had previously used to help her manage seemed to be working. She was afraid to make any movement. She felt hopeless. “I just could not regain footing, metaphorically and physically,” she says. “I truly felt frozen in my chronic pain and chronic health journey.” Hodge is far from alone. In the United States, chronic pain affects tens of millions of people — about 1 in 5 adults and nearly 1 in 3 people ages 65 and older. “The amount of suffering from arthritis and aging that I’ve seen in my pain clinic, it’s overwhelming to me as a pain doctor,” says Antje Barreveld, an anesthesiologist at Mass General Brigham’s Newton-Wellesley Hospital in Massachusetts. What’s more, the mainstay therapy for severe acute and chronic pain — prescription opioids — has helped fuel an epidemic that kills tens of thousands of people each year. “We have to have some better alternatives,” she says. So researchers have doubled down in their quest to find new pain treatments that aren’t as addictive as opioids. “The pain field has really made very rapid and tremendous progress in the last decade,” says D.P. Mohapatra, a former pain scientist who now oversees research at the National Institute of Neurological Disorders and Stroke in Bethesda, Md. © Society for Science & the Public 2000–2024.

Keyword: Pain & Touch; Drug Abuse
Link ID: 29470 - Posted: 09.07.2024

By Daniela Hirschfeld Peter Mombaerts is a man of strong preferences. He likes Belgian beer — partly, but not entirely, for patriotic reasons. He likes classical music and observing the Earth from above while flying small planes with his amateur pilot’s license. He loves the feel of alpaca clothing during winter. But Mombaerts, who leads the Max Planck Research Unit for Neurogenetics in Frankfurt, Germany, says he has no favorite odor — even though he has been studying smells for more than 30 years. Mombaerts’s research has focused on how the brain processes odors, and on the impressive group of genes encoding odorant receptors in mammals. Humans have about 400 of these genes, which means that 2 percent of our roughly 20,000 genes help us to smell — the largest gene family known to date, as Mombaerts noted back in 2001 in the Annual Review of Genomics and Human Genetics. More than two decades later, it remains the record holder, and Mombaerts continues to delve into the genetics and neuroscience of how we smell the world around us. He spoke with Knowable Magazine about what’s been learned about the genes, receptors and neurons involved in sensing odors — and the mysteries that remain. This interview has been edited for length and clarity. Why did you start working on smell? When studying medicine in my native Belgium in the 1980s, I learned that I don’t really like to work so much with patients. But research interested me. I wanted to do neurobiology. I did my PhD in immunology with mice and genetics, and then moved to neuroscience. It was what I always wanted to do, but I had to find the right topic, the right lab and the right mentor — and all that came together when Linda Buck and Richard Axel published their paper about their discovery of the genes for odorant receptors. This paper came out in the journal Cell on April 5, 1991, and when I read the first few sentences I thought, “That’s what I want to work on.” Axel became my postdoc mentor. When Buck and Axel won the Nobel Prize in Physiology or Medicine in 2004, I wrote a Perspective piece for the New England Journal of Medicine  that I titled “Love at First Smell.” © 2024 Annual Reviews

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29469 - Posted: 09.07.2024

Nicola Davis Science correspondent Researchers have gained new insight into how and why some people experience depression after finding a particular brain network is far bigger in people living with the condition. The surface of the brain is a communication junction box at which different areas talk to each other to carry out particular processes. But there is a finite amount of space for these networks to share. Now researchers say that in people with depression, a larger part of the brain is involved in the network that controls attention to rewards and threats than in those without depression. “It’s taking up more real estate on the brain surface than we see is typical in healthy controls,” said Dr Charles Lynch, a co-author of the research, from Weill Cornell Medicine in New York. He added that expansion meant the size of other – often neighbouring – brain networks were smaller. Writing in the journal Nature, Lynch and colleagues report how they used precision functional mapping, a new approach to brain imaging that analyses a host of fMRI (functional MRI) scans from each individual. The team applied this method to 141 people with depression and 37 people without it, enabling them to measure accurately the size of each participant’s brain networks. They then took the average size for each group. They found that a part of the brain called the frontostriatal salience network was expanded by 73% on average in participants with depression compared with healthy controls. © 2024 Guardian News & Media Limited

Keyword: Depression; Brain imaging
Link ID: 29468 - Posted: 09.07.2024

By Christina Jewett The number of teenagers who reported using e-cigarettes in 2024 has tumbled from a worrisome peak reached five years ago, raising hopes among public health officials for a sustained reversal in vaping trends among adolescents. In an annual survey conducted from January through May in schools across the nation, fewer than 8 percent of high school students reported using e-cigarettes in the past month, the lowest level in a decade. That’s far lower than the apex, in 2019, when more than 27 percent of high school students who took the survey reported that they vaped — and an estimated 500,000 fewer adolescents than last year. The data is from the National Youth Tobacco Survey, a questionnaire filled out by thousands of middle and high school students that is administered each year by the Food and Drug Administration and the Centers for Disease Control and Prevention. Overall, it found that just under 6 percent of middle and high school students reported vaping in the last month, down from nearly 8 percent among those surveyed last year. Use among high school students largely accounted for this year’s decline; middle school use stayed fairly steady with 3.5 percent reporting they had vaped compared to 4.6 percent the year before. “I want to be unequivocally clear that this continued decline in e-cigarette use among our nation’s youth is a monumental public health win,” Brian King, the director of the F.D.A.’s tobacco division, said during a news briefing on Wednesday. Public health experts said several factors may have contributed to the decline in teenage vaping, including city and state flavored tobacco bans, a blitz of enforcement against sellers of flavored vapes and three public messaging campaigns aimed at young people about the dangers of vaping. © 2024 The New York Times Company

Keyword: Drug Abuse
Link ID: 29467 - Posted: 09.07.2024

Does a whiff of pollen trigger a sneeze or a cough? Scientists have discovered nerve cells that cause one response versus another: ‘sneeze neurons’ in the nasal passages relay sneeze signals to the brain, and separate neurons send cough messages, according to a study1 performed in mice. The findings could lead to new and improved treatments for conditions such as allergies and chronic coughs. That’s welcome news because these conditions can be “incredibly frustrating” and the side effects of current treatments can be “incredibly problematic”, says pulmonologist Matthew Drake at Oregon Health & Science University in Portland, who was not involved in the work. The study was published today in Cell. Previous work2 categorized neurons in the mouse airway on the basis of the proteins complexes, called ion channels, that are carried on the cell surfaces. To work out which nose neurons cause sneezing, researchers exposed mice to various compounds, each known to activate specific types of ion channel. They struck gold when a substance called BAM 8-22 left the mice sneezing. The compound is known to activate an ion channel called MrgprC11, leading the researchers to suspect that neurons carrying MrgprC11 cause sneezing. Indeed, when the researchers deleted MrgprC11 from the suspected sneeze neurons and then gave mice the flu, they found themselves with sick, but sneezeless, mice. Even with the sneeze neurons out of the picture, the sick mice continued to have cough-like reactions to influenza infection. Using methods similar to those that homed in on the sneeze neurons, the researchers tracked the cough response to a set of neurons in the trachea that express a signalling chemical called somatostatin. Viruses “evolve very quickly”, says neuroscientist and study co-author Qin Liu at Washington University in St. Louis, Missouri. That could explain why there are two separate systems capable of detecting and clearing them from the airways. © 2024 Springer Nature Limited

Keyword: Neuroimmunology
Link ID: 29466 - Posted: 09.07.2024

By Rodrigo Pérez Ortega Names can be deceiving. One might think “cerebrospinal fluid” only lives in the brain and spinal cord. Indeed, that’s what scientists and doctors have largely believed for centuries. But the clear liquid—which cleans, feeds, and protects the organs it surrounds—also bathes the body’s nerves, researchers report today in Science Advances. “This is one of the [most] important papers in this area,” says Karl Bechter, a clinical neurologist at Ulm University who was not involved in the study. In the past, he and others have suggested instances in which cerebrospinal fluid (CSF) permeates nerves, but he says this is the first study that shows it can travel far throughout the body. The finding could open new ways to deliver drugs to some of the most inaccessible parts of the body. The human body is a bundle of nerves. Besides the head honchos that make up the central nervous system—the brain and spinal cord—kilometers of spindly fibers snake their way throughout our anatomy. Here, they form a peripheral nervous system that fires the signals that allow us to do everything from walking to feeling pain. Yet even though the two systems interface, previous anatomy studies indicated CSF was restricted to the central nervous system. Things changed 2.5 years ago when Edward Scott, a stem cell biologist at the University of Florida, and his surgeon colleague Joe Pessa noticed something strange during a plastic surgery study. Pessa was researching ways to avoid damaging CSF-containing structures and nerves during surgical procedures. When the scientists injected saline into the brain chambers of human cadavers that contained CSF, a peripheral nerve in the wrist swelled up. They then decided to explore further, injecting a fluorescent liquid in live mice’s brain chambers to track where the liquid went. The dye somehow made its way to the sciatic nerve, which runs throughout the back of the leg. Intrigued, the team decided to repeat the experiment in mice using a much finer tracer: nanoparticles of gold. These tiny particles can be detected through both light and electron microscopy and can be tailored to specific sizes.

Keyword: Brain imaging; Biomechanics
Link ID: 29465 - Posted: 09.07.2024

By Jessica Silver-Greenberg and Katie Thomas Acadia Healthcare is one of America’s largest chains of psychiatric hospitals. Since the pandemic exacerbated a national mental health crisis, the company’s revenue has soared. Its stock price has more than doubled. But a New York Times investigation found that some of that success was built on a disturbing practice: Acadia has lured patients into its facilities and held them against their will, even when detaining them was not medically necessary. In at least 12 of the 19 states where Acadia operates psychiatric hospitals, dozens of patients, employees and police officers have alerted the authorities that the company was detaining people in ways that violated the law, according to records reviewed by The Times. In some cases, judges have intervened to force Acadia to release patients. Some patients arrived at emergency rooms seeking routine mental health care, only to find themselves sent to Acadia facilities and locked in. A social worker spent six days inside an Acadia hospital in Florida after she tried to get her bipolar medications adjusted. A woman who works at a children’s hospital was held for seven days after she showed up at an Acadia facility in Indiana looking for therapy. And after police officers raided an Acadia hospital in Georgia, 16 patients told investigators that they had been kept there “with no excuses or valid reason,” according to a police report. Acadia held all of them under laws meant for people who pose an imminent threat to themselves or others. But none of the patients appeared to have met that legal standard, according to records and interviews. Most doctors agree that people in the throes of a psychological crisis must sometimes be detained against their will to stabilize them and prevent harm. These can be tough calls, balancing patients’ safety with their civil rights. But at Acadia, patients were often held for financial reasons rather than medical ones, according to more than 50 current and former executives and staff members. © 2024 The New York Times Company

Keyword: Schizophrenia; Depression
Link ID: 29464 - Posted: 09.04.2024

By Kerri Smith The smell in the laboratory was new. It was, in the language of the business, tenacious: for more than a week, the odour clung to the paper on which it had been blotted. To researcher Alex Wiltschko, it was the smell of summertime in Texas: watermelon, but more precisely, the boundary where the red flesh transitions into white rind. “It was a molecule that nobody had ever seen before,” says Wiltschko, who runs a company called Osmo, based in Cambridge, Massachusetts. His team created the compound, called 533, as part of its mission to understand and digitize smell. His goal — to develop a system that can detect, predict or create odours — is a tall order, as molecule 533 shows. “If you looked at the structure, you would never have guessed that it smelled this way.” That’s one of the problems with understanding smell: the chemical structure of a molecule tells you almost nothing about its odour. Two chemicals with very similar structures can smell wildly different; and two wildly different chemical structures can produce an almost identical odour. And most smells — coffee, Camembert, ripe tomatoes — are mixtures of many tens or hundreds of aroma molecules, intensifying the challenge of understanding how chemistry gives rise to olfactory experience. Another problem is working out how smells relate to each other. With vision, the spectrum is a simple colour palette: red, green, blue and all their swirling intermediates. Sounds have a frequency and a volume, but for smell there are no obvious parameters. Where does an odour identifiable as ‘frost’ sit in relation to ‘sauna’? It’s a real challenge to make predictions about smell, says Joel Mainland, a neuroscientist at the Monell Chemical Senses Center, an independent research institute in Philadelphia, Pennsylvania. © 2024 Springer Nature Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29463 - Posted: 09.04.2024