By Dave Philipps A van full of U.S. Special Operations veterans crossed the border into Mexico on a sunny day in July to execute a mission that, even to them, sounded pretty far out. Listen to this article with reporter commentary Over a period of 48 hours, they planned to swallow a psychedelic extract from the bark of a West African shrub, fall into a void of dark hallucinations and then have their consciousness shattered by smoking the poison of a desert toad. The objective was to find what they had so far been unable to locate anywhere else: relief from post-traumatic stress disorder and traumatic brain injury symptoms. “It does sound a little extreme, but I’ve tried everything else, and it didn’t work,” said a retired Army Green Beret named Jason, who, like others in the van, asked that his full name not be published because of the stigma associated with using psychedelics. A long combat career exposed to weapons blasts had left him struggling with depression and anger, a frayed memory and addled concentration. He was on the verge of divorce. Recently, he said, he had put a gun to his head. “I don’t know if this will work,” Jason said of psychedelic therapy. “But at this point, I have nothing to lose.” Psychedelic therapy trips like this are increasingly common among military veterans. For years, psychedelic clinics in Mexico were a little-known last-ditch treatment for people struggling with drug addiction. More recently, veterans have found that they also got lasting relief from mental health issues they had struggled with since combat. No one tracks how many veterans seek psychedelic treatment in Mexico. Clinic owners estimate they now treat a few thousand American veterans a year, and say the number is steadily growing. Many of the veterans have free access to the U.S. veterans’ health care system but find standard treatments for combat-related mental health issues to be ineffective. The Department of Veterans Affairs announced this month that, for the first time in more than 50 years, it would fund research into psychedelic therapy. But while the research is conducted, the treatments will remain inaccessible to most veterans, perhaps for years. © 2024 The New York Times Company

Keyword: Stress; Drug Abuse
Link ID: 29608 - Posted: 12.21.2024

By Mitch Leslie It’s a dismaying thought during a holiday season full of cookies and big meals, but severely restricting calories consumed is one of the best supported strategies for a healthier, longer life. Slicing food consumption stretches the lives of animals in lab experiments, and similar deprivation seems to improve health in people, although almost no one can sustain such a calorie-depleted diet for long. Now, researchers in China studying animals on lean rations have identified a molecule made by gut bacteria that delivers some of the same benefits. When given on its own, the molecule makes flies and worms live longer and refurbishes age-weakened muscles in mice, all without leaving the animals hungry. Although the molecule’s effects in people remain unclear, the discovery is “a really important step forward,” says gerontologist Richard Miller of the University of Michigan, who wasn’t connected to the research. The work, reported in two studies today in Nature, “is very thorough.” Research over the past 90 years has shown that calorie restriction—which to scientists typically means a diet with between 10% and 50% fewer calories than normal—can extend longevity in organisms as diverse as yeast, nematodes, and mice. One experiment also found an effect in monkeys. Trials to test whether calorie restriction increases human life span would take too long, but participants in the 2-year CALERIE trial, which ran from 2007 to 2010 and aimed to cut calorie intake by 25%, enjoyed a slew of improvements, including lower levels of low-density lipoprotein cholesterol, increased sensitivity to insulin, and a 10% reduction in weight. However, the trial also illustrates what makes calorie restriction so challenging: Participants on average cut their caloric intake by only half the experiment’s goal. So, scientists have been hunting for molecules that trigger health-promoting, longevity-stretching effects without privation. To identify new candidates, molecular biologist and biochemist Sheng-Cai Lin of Xiamen University and colleagues took a systematic approach, analyzing the levels of more than 1200 metabolic molecules in blood samples from calorically restricted mice and from counterparts with no dietary limits. They discovered that just over 200 molecules became more abundant when food was in short supply.

Keyword: Obesity
Link ID: 29607 - Posted: 12.21.2024

By Terence Monmaney The road switches back and forth again and again as it climbs into Montchavin, perched in the French Alps at 4,100 feet above sea level. The once-sleepy mountainside village, developed into a ski resort in the 1970s, is dotted with wooden chalet-style condo buildings and situated in the midst of a vast downhill complex known as Paradiski, one of the world’s largest. Well known to skiers and alpinistes, Montchavin also has grabbed the attention of medical researchers as the site of a highly unusual cluster of a devastating neurological disease, amyotrophic lateral sclerosis. ALS, brought about by the progressive loss of nerve function in the brain, spinal cord and motor neurons in the limbs and chest, leading to paralysis and death, is both rare and rather evenly distributed across the globe: It afflicts two to three new people out of 100,000 per year. Though Montchavin is flooded with visitors in winter and summer, the year-round resident population is only a couple hundred, and neighboring villages aren’t much bigger, so the odds are strongly against finding more than just a few ALS patients in the immediate area. Yet physicians have reported 14. The first of the village patients to arouse suspicion in Emmeline Lagrange, the neurologist who has led the investigation into the problem, was a woman in her late thirties, a ski instructor and ski lift ticket-checker originally from Poland who worked in the offseason at the local tourism office. It was 2009. A physician in Montchavin had referred the woman to Lagrange, who practices at Grenoble University Hospital, 84 miles southwest of the village. Lagrange diagnosed ALS and recalls phoning the Montchavin physician to explain the consequences: “The first thing she said was, ‘I certainly know what it is. It’s the fourth case in the village. My neighbor died of ALS 20 years ago and two friends of hers are still victims of the disease.’”

Keyword: ALS-Lou Gehrig's Disease ; Neurotoxins
Link ID: 29606 - Posted: 12.21.2024

By Calli McMurray, Angie Voyles Askham, Claudia López Lloreda, Shaena Montanari Neuroscience can sometimes feel like an old mouse club—but it wasn’t always that way. In the 1960s and ’70s, neuroscientists routinely put on their field boots to search for the “animal that was expert at doing the task that you were interested in studying,” says Eve Marder, university professor of biology at Brandeis University. “People studied insects and annelids and mollusks and every kind of animal imaginable. And if they could have studied elephants, they would have.” Many fundamental—and Nobel-prize-winning—discoveries emerged from this approach. Recording from the squid’s giant axon, for example, revealed how action potentials work; experiments in sea slugs illuminated the molecular changes that drive learning and memory; work in barn owls unraveled sound localization; and studies in horseshoe crabs first exposed lateral inhibition in photoreceptors. But by the end of the 20th century, model diversity had fallen out of vogue. A small band of neuroethologists continued to explore animals off the beaten path, but the majority of neuroscientists soon jumped over to standard animal models, Marder says. Many of today’s common model organisms—including the mouse, zebrafish, roundworm and fruit fly—soared in popularity because they are cheap, easy to work with and quick to raise in a lab. The invention of molecular and genetic tools tailored to these species only increased their appeal, as did attention from the U.S. federal government. In 1999, the National Institutes of Health (NIH) published a list of 13 canonical model organisms for biomedical research, and in 2004 the organization’s “road map” encouraged the use of research animals for which genetic tools were available. Now, two decades later, a non-model organism “renaissance” is underway, says Ishmail Abdus-Saboor, associate professor of biological sciences at Columbia University, as a growing number of neuroscientists step outside of the model organism box. This shift is largely due to cost reductions and technological advances in “species-neutral” techniques, says Sam Reiter, assistant professor of computational neuroethology at the Okinawa Institute of Science and Technology, such as high-throughput extracellular recordings, machine-learning-based behavioral tracking, genome and transcriptome sequencing, and gene-editing tools. “This lets researchers quickly reach close to the cutting edge, even if working on an animal where little is known.” © 2024 Simons Foundation

Keyword: Evolution
Link ID: 29605 - Posted: 12.21.2024

By Emily McLaughlin Three days after our baby was born, my husband and I brought our newborn daughter home to our house in Tarrytown, New York. I was 32, fit and healthy, and had had an uneventful pregnancy. But on the second afternoon back home, while nursing, a thunderclap headache struck. The pounding in my temple literally brought me to my knees. I tried to tough it out, but it didn’t go away. That evening, I called my doctor. Since I was low-risk with normal blood pressure, she suggested rest and hydration. Then in the middle of that night, while I was still in debilitating pain, dark spots started to float across my vision. As my husband rushed me to the hospital, he asked me a few simple questions as he drove: Did you page the doctor? How’s your nausea? My answers came out in slow motion at first, then turned into a stutter, before they finally stopped. At the hospital, an emergency brain scan showed an intracerebral hemorrhage in the right frontal lobe — the site of executive functioning, creativity and emotion. The next thing I remember is waking in the Neuro-ICU of a nearby hospital — paralyzed on the left side, unable to smile, process time or even read the sign telling nurses I wasn’t allowed to swallow in case the muscles in my mouth were affected and I choked. I couldn’t get the words out to ask if I’d be trapped in my head for good. Ten days later, on blood pressure and antiseizure meds, I was finally allowed to go home to my newborn. It felt like I needed more care than she did. With only one strong, normally working arm, I couldn’t cradle my baby. A constant headache made it impossible to stand. Doctors said the headaches might last a year, until the blood in my brain reabsorbed. My left leg worked, but poor balance made even walking around the house difficult. The left half of my face couldn’t move, and my speech came out weak and slowly. I could not connect emotion to the rhythm of my words. I delivered questions as flat, imperative statements.

Keyword: Stroke; Hormones & Behavior
Link ID: 29604 - Posted: 12.21.2024

By Marla Broadfoot Everyone has heard that it’s vital to get seven to nine hours of sleep a night, a recommendation repeated so often it has become gospel. Get anything less, and you are more likely to suffer from poor health in the short and long term — memory problems, metabolic issues, depression, dementia, heart disease, a weakened immune system. But in recent years, scientists have discovered a rare breed who consistently get little shut-eye and are no worse for wear. Natural short sleepers, as they are called, are genetically wired to need only four to six hours of sleep a night. These outliers suggest that quality, not quantity, is what matters. If scientists could figure out what these people do differently it might, they hope, provide insight into sleep’s very nature. “The bottom line is, we don’t understand what sleep is, let alone what it’s for. That’s pretty incredible, given that the average person sleeps a third of their lives,” says Louis Ptáček, a neurologist at the University of California San Francisco. Scientists once thought sleep was little more than a period of rest, like powering down a computer in preparation for the next day’s work. Thomas Edison called sleep a waste of time — “a heritage from our cave days” — and claimed to never sleep more than four hours a night. His invention of the incandescent lightbulb encouraged shorter sleep times in others. Today, a historically high number of US adults are sleeping less than five hours a night. But modern sleep research has shown that sleep is an active, complicated process we don’t necessarily want to cut short. During sleep, scientists suspect that our bodies and brains are replenishing energy stores, flushing waste and toxins, pruning synapses and consolidating memories. As a result, chronic sleep deprivation can have serious health consequences.

Keyword: Sleep; Genes & Behavior
Link ID: 29603 - Posted: 12.14.2024

By Calli McMurray A strong, long-lasting sensory stimulus—be it visual, auditory, olfactory or tactile—triggers plasticity in the neurons that respond to it. But as a scientist long interested in temperature, Jan Siemens wondered: Does the same principle apply to prolonged heat? In mammals, the body changes when temperatures soar—blood vessels dilate, heat-generating brown adipose tissue shuts off, the heart rate lowers, locomotion slows—but it wasn’t clear if the brain played a role in these changes, or even changed itself, says Siemens, professor of pharmacology at the University of Heidelberg. Siemens and his team started a search for heat-induced neuronal plasticity in the ventromedial preoptic area of the hypothalamus (VMPO) in mice. They chose the region because of its involvement in regulating body temperature and generating fever; neurons there receive temperature information downstream from cells innervating the skin, whereas others are themselves warm-sensitive. They identified cells to target by measuring the expression of c-FOS, a gene that is activated by neuronal activity, after housing the mice at 36 degrees Celsius for up to eight hours. At first, however, their investigative trail went cold. In brain slices, those warm-responding cells showed only slight and inconsistent changes in synaptic plasticity. “That was actually quite humbling and disappointing,” Siemens says. But then they made a “serendipitous observation,” he says: A subgroup of neurons expressing the leptin receptor became almost constantly active after four weeks of heat acclimation. The firing was so synchronized and regular that Wojciech Ambroziak, a postdoctoral scholar in the lab at the time, described it as “soldiers marching in a line,” Siemens recalls. © 2024 Simons Foundation

Keyword: Obesity
Link ID: 29602 - Posted: 12.14.2024

Jon Hamilton Not all brain cells are found in the brain. For example, a team at Caltech has identified two distinct types of neurons in the abdomens of mice that appear to control different aspects of digestion. The finding, reported in the journal Nature, helps explain how clusters of neurons in the body play a key role in the gut-brain connection, a complex two-way communication system between the brain and digestive system. It also adds to the evidence that neurons in the body can take on specialized functions, "just like in the brain," says Yuki Oka, an author of the study. "The peripheral nervous system is smart," says Frank Duca of the University of Arizona, who was not involved in the study. "You have specific neurons within this system that are performing a wide variety of functions, either with the brain's help or sometimes even without the brain's input," he says. The study focused on a subset of the peripheral nervous system called the sympathetic nervous system, which becomes active when the brain detects danger. "Your adrenaline goes up and your glucose level in the blood is really high because you need to fight or flight," Oka says. At the same time, the sympathetic nervous system dials back functions that are less urgent, like digestion and moving food through the gut. © 2024 npr

Keyword: Obesity
Link ID: 29601 - Posted: 12.14.2024

By Max Kozlov A popular weight-loss regimen stunts hair growth, data collected from mice and humans suggest1. The study’s findings show that intermittent fasting, which involves short bouts of food deprivation, triggers a stress response that can inhibit or even kill hair-follicle stem cells, which give rise to hair. The results, published in today in Cell, suggest that although short-term fasting can provide health benefits, such as increased lifespan in mice, not all tissue and cell types benefit. “I was shocked to hear these results,” says Ömer Yilmaz, a stem-cell biologist at the Massachusetts Institute of Technology in Cambridge who was not involved in the study. “We’ve come to expect that fasting is going to be beneficial for most, if not all cell types and good for stem cells. This is the inverse of what we expected, and the finding seems to hold true in humans.” Deliberate deprivation During the past decade, intermittent fasting has become one of the most popular dieting regimens; by one count, about 12% of adults in the United States practised it in 2023. One of the most common forms is time-restricted eating, which involves eating only within a limited time frame each day. Stem cells seem to be particularly vulnerable to changes in diet. For example, Yilmaz and his colleagues reported2 in August that stem cells in the guts of mice showed a burst of activity during post-fast feasting. This activity helped to repair damage in the animals’ intestines. To learn whether dieting affects hair regrowth, which can be affected by stress, Bing Zhang, a regenerative biologist at Westlake University in Zhejiang, China, and his colleagues shaved mice and subjected them to one of two intermittent-fasting regimens: time-restricted eating and alternate-day fasting, in which animals fasted for 24 hours and then ate their normal diet for the following 24 hours. By the end of the three-month study, the dieting mice had not regrown as much hair as control animals that ate a similar number of calories, the authors found. © 2024 Springer Nature Limited

Keyword: Obesity
Link ID: 29600 - Posted: 12.14.2024

By Jason Bittel Have you ever felt like there was a pit in your stomach? What about a flutter in your heart? It turns out that the anatomical connections we make with certain emotions and feelings — what researchers call embodied emotions — may be more universal than you’d think. In fact, people have been making very similar statements about their bodies for about 3,000 years. In a new study published in iScience, researchers catalogued words for body parts and emotions used by people who lived in Mesopotamia between 934 and 612 BCE, in what is now a region that includes Egypt, Iraq, and Türkiye. Then, they compared those ancient ideas etched on clay tablets and other artifacts to commonly used modern-day links between emotions and body parts, using bodily maps to visualize the similarities and differences. “We see certain body areas that are still used in similar contexts in modern times,” says Juha Lahnakoski, lead author of the study and a cognitive neuroscientist at Germany’s LVR Clinic Düsseldorf, in an email. “For example, the heart was often mentioned together with positive emotions such as love, pride, and happiness, as we might still say ‘my heart swelled’ with joy or pride.” © Society for Science & the Public 2000–2024.

Keyword: Emotions
Link ID: 29599 - Posted: 12.14.2024

By Alissa Wilkinson There’s a moment in “Theater of Thought” (in theaters) when Darío Gil, the director of research at IBM, is explaining quantum computing to Werner Herzog, the movie’s director. Standing before a whiteboard, Gil draws some points on spheres to illustrate how qubits work, then proceeds to define the Schrödinger equation. As he talks and writes, the audio grows quieter, and Herzog’s distinctive resonant German accent takes over. “I admit that I literally understand nothing of this, and I assume most of you don’t either,” he intones in voice-over. “But I found it fascinating that this mathematical formula explains the law that draws the subatomic world.” It’s a funny moment, a playful way to keep us from glazing over when presented with partial differential equations. Herzog may be a world-renowned filmmaker, but he’s hardly a scientist, and that makes him the perfect director for “Theater of Thought,” a documentary about, as he puts it, the “mysteries of our brain.” Emphasis on mysteries. Herzog interviews a dizzying array of scientists, researchers, and even a Nobel Prize winner or two. He asks them about everything: how the brain works, what consciousness means, what the tiniest organisms in the world are, whether parrots understand human speech, whether rogue governments can control thoughts, whether we’re living in an elaborate simulation, how telepathy and psychedelics work, and, at several points, what thinking even is. Near the end of the film he notes that not one of the scientists could explain what a thought is, or what consciousness is, but “they were all keenly alive to the ethical questions in neuroscience.” In other words, they’re immersed in both the mystery and what their field of study implies about the future of humanity. There’s a boring way to make this movie, with talking-head interviews that are arranged to form a coherent argument. Herzog goes another direction, starting off by narrating why he’s making it, then talking about his interviewees as we are introduced to them in their labs or in their favorite outdoor settings. (He also visits Philippe Petit, the Twin Towers tightrope walker, as he practices in his Catskills backyard.) Herzog’s constant verbal presence brings us into his own head space — his own brain, if you will — and gives us the sense that we’re following his patterns of thought. © 2024 The New York Times Company

Keyword: Consciousness
Link ID: 29598 - Posted: 12.14.2024

By Miryam Naddaf Researchers have identified 13 proteins in the blood that predict how quickly or slowly a person’s brain ages compared with the rest of their body. Their study1, published in Nature Aging on 9 December, used a machine-learning model to estimate ‘brain ages’ from scans of more than 10,000 people. The authors then analysed thousands of scans alongside blood samples and found eight proteins that were associated with fast brain ageing, and five linked to slower brain ageing. “Previous studies mainly focused on the association between the proteins and the chronological age, that means the real age of the individual,” says study co-author Wei-Shi Liu, a neurologist at Fudan University in Shanghai, China. However, studying biomarkers linked to a person’s brain age could help scientists to identify molecules to target in future treatments for age-related brain diseases. “These proteins are all promising therapeutic targets for brain disorders, but it may take a long time to validate them,” says Liu. Using machine learning to analyse brain-imaging data from 10,949 people, Liu and his colleagues created a model to calculate a person’s brain age, on the basis of features such as the brain’s volume, surface area and distribution of white matter. They wanted to identify proteins that are associated with a large brain age gap — the difference between brain age and chronological age. To do this, the researchers analysed levels of 2,922 proteins in blood samples from 4,696 people, more than half of whom were female, and compared them with the same people’s brain ages derived from the scans. They identified 13 proteins that seemed to be connected with large brain age gaps, some of which are known to be involved in movement, cognition and mental health.

Keyword: Development of the Brain
Link ID: 29597 - Posted: 12.11.2024

By Grace Huckins Genes on the X and Y chromosomes—and especially those on the Y—appear to be associated with autism likelihood, according to a study focused on people who have missing or extra sex chromosomes. The findings add to the ongoing debate about whether autism’s sex bias reflects a male vulnerability, a female protective effect or other factors. “The Y chromosome is often left out of genetic discovery studies. We really have not interrogated it in [autism] studies very much,” says Matthew Oetjens, assistant professor of human genetics at Geisinger Medical Center’s Autism and Developmental Medicine Institute, who led the new work. There is a clear sex difference in autism prevalence: Men are about four times as likely as women to have a diagnosis. But uncovering the reasons for that discrepancy has proved challenging and contentious. Multiple biological factors may play a role, in addition to social factors—such as the difficult-to-measure gulfs between how boys and girls are taught to behave. Add on the possibility of diagnostic bias and the question starts to look less like a scientific problem and more like a politically toxic Gordian knot. But there are some threads that researchers can pull to disentangle these effects, as the new study illustrates. People with sex chromosome aneuploidies—or unusual combinations of sex chromosomes, such as XXY in those with Klinefelter syndrome or a single X in Turner syndrome—provide a unique opportunity to examine how adding or taking away chromosomes can affect biology and behavior. Previous studies noted high rates of autism in people with sex chromosome aneuploidies, but those analyses were subject to ascertainment bias; perhaps those people found out about their aneuploidies only after seeking support for their neurodevelopmental conditions. © 2024 Simons Foundation

Keyword: Autism; Sexual Behavior
Link ID: 29596 - Posted: 12.11.2024

By Derek Thompson At 3 a.m. I’m jolted awake. The room is dark and still. I grab my phone and scan sports scores and Twitter. Still awake. A faceless physician whispers in my mind: To overcome middle-of-the-night insomnia, experts say you ought to get out of bed … I get out of bed. I pour a glass of water and drink it. I go back to bed. Still awake. Perhaps you know the feeling. Like millions of Americans and hundreds of millions of people around the world, I suffer from so-called mid-sleep awakenings that can keep me up for hours. One day, I was researching my nocturnal issues when I discovered a cottage industry of writers and sleep hackers who claim that sleep is a nightmare because of the industrial revolution, of all things. Essays in The Guardian, CNN, The New York Times, and The New York Times Magazine recommended an old fix for restlessness called “segmented sleep.” In premodern Europe, and perhaps centuries earlier, people routinely went to sleep around nightfall and woke up around midnight—only to go back to sleep a few hours later, until morning. They slept sort of like I do, but they were Zen about it. Then, the hackers claim, modernity came along and ruined everything by pressuring everybody to sleep in one big chunk. The romanticization of preindustrial sleep fascinated me. It also snapped into a popular template of contemporary internet analysis: If you experience a moment’s unpleasantness, first blame modern capitalism. So I reached out to Roger Ekirch, the historian whose work broke open the field of segmented sleep more than 20 years ago. In the 1980s, Ekirch was researching a book about nighttime before the industrial revolution. One day in London, wading through public records, he stumbled on references to “first sleep” and “second sleep” in a crime report from the 1600s. He had never seen the phrases before. When he broadened his search, he found mentions of first sleep in Italian (primo sonno), French (premier sommeil), and even Latin (primo somno); he found documentation in Africa, the Middle East, South Asia, and Latin America. © 2024 The Atlantic Monthly Group.

Keyword: Sleep
Link ID: 29595 - Posted: 12.11.2024

By Joshua Cohen Earlier this fall, the Centers for Disease Control and Prevention reported data showing that adult obesity rates — long trending upwards — had fallen modestly over the past few years, from 41.9 to 40.3 percent. The decline sparked discussion on social media and in major news outlets about whether the U.S. has passed so-called “peak obesity” — and whether the growing use of certain weight-loss drugs might account for the shift. An opinion piece in the Financial Times suggested that the public health world might look back on the current moment in much the same way that it now reflects on 1963, when cigarette sales hit their high point and then dropped dramatically over the following decades. The article’s author, John Burn-Murdoch, speculated that the dip is “highly likely” to be caused by the use of glucagon-like peptide-1 receptor agonists, or GLP-1s, for weight loss. It’s easy to see why one might make that connection. Although GLP-1s have been used for nearly two decades in the treatment of type 2 diabetes, their use for obesity only took off more recently. In 2014, the Food and Drug Administration approved a GLP-1 agonist named Saxenda specifically for this purpose. Then in the late 2010s, a GLP-1 drug named Ozempic, made from the active ingredient semaglutide, began to be used off-label. The FDA also authorized Wegovy, another semaglutide-based GLP-1 medication, explicitly for weight loss in 2021. Still, it is premature to declare that GLP-1s have caused overall declining obesity rates in the U.S. There are a number of ways to interpret the CDC data, and not all of them suggest that obesity rates have actually fallen. Further, recent evidence indicates that GLP-1s might not be as effective for weight loss as initially thought. And there are reasons to question the comparison to cigarette sales. Taken together, all of this suggests that we may need to wait to understand how this new class of drugs affects weight loss at the population level.

Keyword: Obesity
Link ID: 29594 - Posted: 12.11.2024

7 Things Everyone Should Know About Antidepressants By Christina Caron Even if you’ve never taken an antidepressant, you’re probably familiar with the criticism and controversy that surrounds these drugs. It’s not uncommon to hear things like: “Those pills are just a placebo.” “You’ll definitely gain weight.” “Once you start, you’ll become dependent on them.” Is any of this true? Some of these statements have “a kernel of truth,” said Dr. Gerard Sanacora, a professor of psychiatry at the Yale School of Medicine. And it’s important to set the record straight because the expectations people have about their treatment — whether good or bad — “really do play a large role in how the treatment actually unfolds,” he added. Dr. Sanacora and other experts addressed some common questions and misconceptions about antidepressants. Will antidepressants change who I am? When an antidepressant starts to work, you may feel like a different person in some ways, said Naomi Torres-Mackie, a clinical psychologist in New York City. “Picture this giant, dark cloud weighing you down — as that lifts, the world is going to look different,” she said, adding: “But as you get used to it, you may see that it actually allows you to have more joy in your life.” On the other hand, up to half of people who take antidepressants may experience some degree of emotional blunting or numbed emotions, and research suggests that the blunting is more likely to happen with a higher medication dosage. When antidepressants are working correctly, patients should still feel a range of emotions, even if the sadness they used to feel every day is gone, said Dr. Laine Young-Walker, chair of the department of psychiatry at the University of Missouri School of Medicine. © 2024 The New York Times Compan

Keyword: Depression
Link ID: 29593 - Posted: 12.11.2024

By Max Kozlov Joylessness triggered by stress creates a distinct brain signature, according to research in mice1. The study also reveals one brain pattern that seems to confer resilience to stress — and another that makes stressed animals less likely to feel pleasure, a core symptom of depression. These findings, published today in Nature, offer clues as to how the brain gives rise to anhedonia, a resistance to enjoyment and pleasure. The results also provide a new avenue for treating the condition — if the findings are validated in humans. “Their approach in this study is spot on,” says Conor Liston, a neuroscientist at Weill Cornell Medicine in New York City, who was not involved in the work. The experiments fill “a big gap”, he says. “Anhedonia is something we don’t understand very well.” More than 70% of people with severe depression experience anhedonia, which is also common in those with schizophrenia, Parkinson’s disease and other neurological and psychiatric conditions. The symptom is notoriously difficult to treat, even in those taking medication, Liston says. “Anhedonia is something that patients care about the most, and feel like it’s least addressed by current treatments,” he says. To understand how the brain gives rise to anhedonia, Mazen Kheirbek, a systems neuroscientist at the University of California, San Francisco, and his colleagues studied mice that had been placed under stress by exposure to larger, more aggressive mice. Typically, mice have a sweet tooth and prefer sugar water over plain water if given the option. But some stressed mice instead preferred plain water — which Kheirbek and his colleagues interpreted as a rodent version of anhedonia. Other mice subjected to the same stress preferred the sugar water. The authors labelled these animals ‘resilient’. © 2024 Springer Nature Limited

Keyword: Stress; Depression
Link ID: 29592 - Posted: 12.07.2024

By Steven Strogatz Death might seem like a pure loss, the disappearance of what makes a living thing distinct from everything else on our planet. But zoom in closer, to the cellular level, and it takes on a different, more nuanced meaning. There is a challenge in simply defining what makes an individual cell alive or dead. Scientists today are working to understand the various ways and reasons that cells disappear, and what these processes mean to biological systems. In this episode, cellular biologist Shai Shaham talks to Steven Strogatz about the different forms of cell death, their roles in evolution and disease, and why the right kinds and patterns of cell death are essential to our development and well-being. STEVE STROGATZ: In the second that it took you to hit play on this episode, a million cells in your body died. Some were programmed to expire in natural, regulated processes, such as apoptosis. Some terminated their own lives after infection, to stop viral invaders from spreading. Others suffered physical damage and went through necrosis, their membranes splitting open and their contents spilling out. We know there are nearly a dozen different ways for our cells to kick the bucket. And learning how to control these processes can make all the difference in the world to a sick patient. In this episode, we ask cellular biologist Shai Shaham (opens a new tab), how can the death of a cell help other cells around it? And how do these insights help us understand life itself? Shai is a professor at The Rockefeller University (opens a new tab), where he studies programmed cell death during animal development and the complex role that glial cells play in the nervous system. There was an example near and dear to my heart, since we work on C. elegans, which is a nematode worm. And there was a recent description of a nematode that was extracted from permafrost in Siberia where it froze about 40,000 years ago and was revived back in the lab. And so you ask yourself, was that whole organism alive or dead for 40,000 years? © 2024 Simons Foundation

Keyword: Apoptosis; Development of the Brain
Link ID: 29591 - Posted: 12.07.2024

Aswathy Ammothumkandy, Charles Liu, Michael A. Bonaguidi Your brain can still make new neurons when you’re an adult. But how does the rare birth of these new neurons contribute to cognitive function? Neurons are the cells that govern brain function, and you are born with most of the neurons you will ever have during your lifetime. While the brain undergoes most of its development during early life, specific regions of the brain continue to generate new neurons throughout adulthood, although at a much lower rate. Whether this process of neurogenesis actually happens in adults and what function it serves in the brain is still a subject of debate among scientists. Past research has shown that people with epilepsy or Alzheimer’s disease and other dementias develop fewer neurons as adults than people without these conditions. However, whether the absence of new neurons contributes to the cognitive challenges patients with these neurological disorders face is unknown. We are part of a team of stem cell researchers, neuroscientists, neurologists, neurosurgeons and neuropsychologists. Our newly published research reveals that the new neurons that form in adults’ brains are linked to how you learn from listening to other people. Researchers know that new neurons contribute to memory and learning in mice. But in humans, the technical challenges of identifying and analyzing new neurons in adult brains, combined with their rarity, had led scientists to doubt their significance to brain function. To uncover the relationship between neurogenesis in adults and cognitive function, we studied patients with drug-resistant epilepsy. These patients underwent cognitive assessments prior to and donated brain tissue during surgical procedures to treat their seizures. To see whether how many new neurons a patient had was associated with specific cognitive functions, we looked under the microscope for markers of neurogenesis. © 2010–2024, The Conversation US, Inc.

Keyword: Neurogenesis; Learning & Memory
Link ID: 29590 - Posted: 12.07.2024

By Shane O’Neill In 2018, Matt Christensen kicked heroin by replacing drugs with drinking. When he stopped drinking in 2022, he turned to food. He put on 95 pounds. His doctor recommended he try Wegovy, part of a class of drugs known as GLP-1 receptor agonists, to help him lose weight. Eventually he switched to a different drug called Zepbound, which targets both GLP-1 and GIP agonists. The drugs worked. Get concise answers to your questions. Try Ask The Post AI. But a funny thing happened on his weight-loss journey: His cravings for food had diminished but so had his cravings for drugs and alcohol. Christensen, 42, started drinking at age 9 and using heroin at 17. For decades, catching a cold meant reaching for a hot toddy. Work stress meant numbing out with Xanax. Even passing through certain neighborhoods in Chicago where he used to buy drugs would lead to cravings. But after he started taking GLP-1 agonists, those triggers became, well, less triggering. “It was the weirdest thing,” he said. “It was just quiet. I just found it really easy all of a sudden.” More than that, Christensen noticed that an unease he had always felt in his body — a discomfort he perpetually tried to quell with fidgeting, food or drugs — was diminishing. “That’s a feeling that I’ve had my entire life,” he said. “Taking these drugs has toned that down. “There’s no silver bullet for addiction or mental illness, but for me, in concert with the other treatments, it has been an absolute game changer,” he said. Matt Christensen says weight-loss drugs like Ozempic and Zepbound have been “an absolute game changer” when it comes to his addiction struggles.

Keyword: Drug Abuse; Obesity
Link ID: 29589 - Posted: 12.07.2024