By Frieda Klotz Up until a couple years ago, an attorney in his late 30s used to repeatedly check his vehicle for signs that he might have injured a pedestrian. The man had no reason to think he had actually hit someone, but his obsessive-compulsive disorder made him fearful. “I spent hours examining the car,” he said. He’d feel the body for dents, take photos, and was never quite done. At its worst, the condition consumed up to 17 hours of his day. “My mind was hijacked for 25 years by a devil that was OCD,” said the man, who asked that his name not be used due to the stigma surrounding mental health disorders and the treatment he’s undergone. He was first diagnosed with the disorder, which is characterized by obsessive preoccupations that interfere with daily life, when he was 15, shortly after his mother died. In the intervening years, he tried numerous forms of therapy, medication, brain stimulation, and residential treatments — all of which, he estimated, cost him hundreds of thousands of dollars. None of them helped long-term. In 2022, his father heard about a brain surgery intended to relieve OCD symptoms and found it was offered by two hospitals affiliated with Brown University. In December 2023, a neurosurgeon created a small hole in the man’s skull and deployed heat to burn away brain tissue. The resulting lesion is thought to disrupt the interaction between parts of the brain associated with OCD symptoms. “I didn’t think it would work at all, because nothing had worked on me,” he told Undark on a Zoom call with his neuropsychologist at Brown, Nicole McLaughlin, and a communications officer from the health system where the attorney had his surgery. “It was a complete miracle.” He added that he was still aware of his repeating thoughts after the surgery, but they no longer bothered him: “It was unbelievable.”

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 29748 - Posted: 04.16.2025

The devastating stimulant has been hitting Portland, Maine hard, even competing with fentanyl as the street drug of choice. Although a fentanyl overdose can be reversed with Narcan, no medicine can reverse a meth overdose. Nor has any been approved to treat meth addiction. Unlike fentanyl, which sedates users, meth can make people anxious and violent. Its effects can overwhelm not just users but community residents and emergency responders. John once fielded customer complaints for a telecommunications company. Now he usually hangs out with friends in the courtyard of a center offering services to help people who use drugs, hitting his pipe, or as he calls it, “getting methicated.” He usually lives outdoors, though he can sometimes handle a few days at a shelter. By noon, he tries to stop smoking meth, so he can get to sleep later that night. Quitting is not on his radar: meth rules his life. “We cannot ride on the railroad, the railroad rides upon us,” he said, with a nod to Henry David Thoreau. Most weekdays, Bill Burns, an addiction and mental health specialist with the Portland police, walks the Bayside neighborhood, checking in on folks. On Thursdays, he rewards the regulars he drives to addiction treatment clinics with his own homemade jolts of dopamine: sugar-dense, Rice Krispie-style treats. Recently, he encountered a young man in full meth psychosis, wild-eyed, bare-chested and bleeding, flinging himself against concrete barriers in an alley. Mr. Burns slipped between the man and a brick wall and wrapped his arms protectively around him. Even as the man flailed uncontrollably, smacking Mr. Burns and smearing blood on his shirt, he managed to stammer, “Sorry!” Speaking softly, Mr. Burns kept repeating, “You’re going to be safe. You’re OK. We’re here because we just want to make sure you’re safe. No, you’re not in trouble. Nobody wants to hurt you. ” © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29747 - Posted: 04.16.2025

By Rachel Brazil Drugs that mimic glucagonlike peptide-1 (GLP-1), such as semaglutide—marketed as Ozempic or Wegovy—have revolutionized the treatment of obesity and type 2 diabetes, but they have major drawbacks. “[They] are expensive to manufacture, they have to be refrigerated, and they often have to be injected because they cannot go through the gastrointestinal tract without being degraded,” explains Alejandra Tomas, a cell biologist at Imperial College London who studies the cellular receptor GLP-1 drugs target. That’s all because they consist of peptides, or long chains of amino acids. A small-molecule version of the therapy, on the other hand, could be given as a daily pill and would be much cheaper to produce. Companies including Eli Lilly, Pfizer, and Roche have launched clinical trials of such compounds. Results from Lilly’s first phase 3 trial of its oral drug are expected later this year. But Pfizer announced this week it was halting development of its candidate after signs of liver injury in a trial participant. The candidates furthest along in development activate the same receptors as peptide drugs do, in much the same way. But several firms are exploring more innovative small molecules that target different sites on those receptors—and could lead to even more effective treatments with fewer side effects. “In the next 4 or 5 years, this field will mature and more patients ultimately should be able to get these medicines,” says Kyle Sloop, a molecular biologist at Lilly Research Laboratories. By mimicking a natural hormone, semaglutide and other drugs in its class help regulate blood sugar by increasing insulin secretion from the pancreas in response to glucose, and suppress appetite by slowing down digestion. The first generation of peptide drugs were essentially copies of GLP-1, with modifications to prevent the peptide from quickly degrading once in the body. Novo Nordisk first won U.S. approval for semaglutide to treat type 2 diabetes in 2017. It needed to be injected, but in 2019 the company added a pill form, which includes an absorption-enhancing ingredient that allows the peptide to penetrate the stomach wall. However, it requires a high dose and has to be taken while fasting, with minimal liquid.

Keyword: Obesity
Link ID: 29746 - Posted: 04.16.2025

By Roni Caryn Rabin Middle-aged and older adults who sought hospital or emergency room care because of cannabis use were almost twice as likely to develop dementia over the next five years, compared with similar people in the general population, a large Canadian study reported on Monday. When compared with adults who sought care for other reasons, the risk of developing dementia was still 23 percent higher among users of cannabis, the study also found. The study included the medical records of six million people in Ontario from 2008 to 2021. The authors accounted for health and sociodemographic differences between comparison groups, some of which play a role in cognitive decline. The data do not reveal how much cannabis the subjects had been using, and the study does not prove that regular or heavy cannabis use plays a causal role in dementia. But the finding does raise serious concerns that require further exploration, said Dr. Daniel T. Myran, the first author of the study, which was published in JAMA Neurology. “Figuring out whether or not cannabis use or heavy regular chronic use causes dementia is a challenging and complicated question that you don’t answer in one study,” said Dr. Myran, an assistant professor of family medicine at University of Ottawa. “This contributes to the literature and to a sign, or signal, of concern.” Dr. Myran’s previous research has found that patients with cannabis use disorder died at almost three times the rate of individuals without the disorder over a five-year period. He has also reported that more cases of schizophrenia and psychosis in Canada have been linked to cannabis use disorder since the drug was legalized. © 2025 The New York Times Company

Keyword: Alzheimers; Drug Abuse
Link ID: 29745 - Posted: 04.16.2025

By Azeen Ghorayshi The percentage of American children estimated to have autism spectrum disorder increased in 2022, continuing a long-running trend, according to data released on Tuesday by the Centers for Disease Control and Prevention. Among 8-year-olds, one in 31 were found to have autism in 2022, compared with 1 in 36 in 2020. That rate is nearly five times as high as the figure in 2000, when the agency first began collecting data. The health agency noted that the increase was most likely being driven by better awareness and screening, not necessarily because autism itself was becoming more common. That diverged sharply from the rhetoric of the nation’s health secretary, Robert F. Kennedy Jr., who on Tuesday said, “The autism epidemic is running rampant.” Mr. Kennedy has repeatedly tried to connect rising autism rates with vaccines, despite dozens of studies over decades that failed to establish such a link. The health secretary nonetheless has initiated a federal study that will revisit the possibility and has hired a well-known vaccine skeptic to oversee the effort. Mr. Kennedy recently announced an effort by the Department of Health and Human Services to pinpoint the “origins of the epidemic” by September, an initiative that was greeted with skepticism by many autism experts. “It seems very unlikely that it is an epidemic, in the way that people define epidemics,” said Catherine Lord, a psychologist and autism researcher at the David Geffen School of Medicine at the University of California, Los Angeles. A significant part of the increase instead can be attributed to the expansion of the diagnosis over the years to capture milder cases, Dr. Lord said, as well as decreased stigma and greater awareness of support services. Still, she left open the possibility that other factors are contributing to more children developing autism. “We can account for a lot of the increase but perhaps not all of it,” Dr. Lord said. “But whatever it is, it’s not vaccines,” she added. © 2025 The New York Times Company

Keyword: Autism
Link ID: 29744 - Posted: 04.16.2025

By Carl Zimmer The human brain is so complex that scientific brains have a hard time making sense of it. A piece of neural tissue the size of a grain of sand might be packed with hundreds of thousands of cells linked together by miles of wiring. In 1979, Francis Crick, the Nobel-prize-winning scientist, concluded that the anatomy and activity in just a cubic millimeter of brain matter would forever exceed our understanding. “It is no use asking for the impossible,” Dr. Crick wrote. Forty-six years later, a team of more than 100 scientists has achieved that impossible, by recording the cellular activity and mapping the structure in a cubic millimeter of a mouse’s brain — less than one percent of its full volume. In accomplishing this feat, they amassed 1.6 petabytes of data — the equivalent of 22 years of nonstop high-definition video. “This is a milestone,” said Davi Bock, a neuroscientist at the University of Vermont who was not involved in the study, which was published Wednesday in the journal Nature. Dr. Bock said that the advances that made it possible to chart a cubic millimeter of brain boded well for a new goal: mapping the wiring of the entire brain of a mouse. “It’s totally doable, and I think it’s worth doing,” he said. More than 130 years have passed since the Spanish neuroscientist Santiago Ramón y Cajal first spied individual neurons under a microscope, making out their peculiar branched shapes. Later generations of scientists worked out many of the details of how a neuron sends a spike of voltage down a long arm, called an axon. Each axon makes contact with tiny branches, or dendrites, of neighboring neurons. Some neurons excite their neighbors into firing voltage spikes of their own. Some quiet other neurons. Human thought somehow emerges from this mix of excitation and inhibition. But how that happens has remained a tremendous mystery, largely because scientists have been able to study only a few neurons at a time. In recent decades, technological advances have allowed scientists to start mapping brains in their entirety. In 1986, British researchers published the circuitry of a tiny worm, made up of 302 neurons. In subsequent years, researchers charted bigger brains, such as the 140,000 neurons in the brain of a fly. © 2025 The New York Times Company

Keyword: Brain imaging; Development of the Brain
Link ID: 29743 - Posted: 04.12.2025

Dyani Lewis Human brain cells engineered to evade detection by the immune system have successfully restored muscle control in a rat model of Parkinson’s disease1. The study is a step towards the development of a ‘universal’ cell line that can be transplanted into anyone, to cure a raft of diseases without the need for anti-rejection drugs. “It’s a one-cell-fits-all proposal,” says Clare Parish, a stem-cell biologist at the Florey Institute of Neuroscience and Mental Health in Melbourne, Australia, and a co-author of the study. The work, published today in Cell Stem Cell, builds on earlier efforts to ‘cloak’ cells from the immune system. Cloaking is a key goal for cell-replacement therapies being tested for conditions ranging from type 2 diabetes and Parkinson’s disease to heart failure and blindness. It would eliminate the need for immunosuppressant drugs, which increase the risk of infection and cancer, and cause tissue damage that ultimately shortens the life of a recipient. To help cells to evade the immune system, the researchers created a cell line with eight genes altered to increase their activity so they acted as an immune invisibility cloak. All of the genes have been shown to assist the placenta and cancer cells in naturally evading immune surveillance. For example, mouse embryonic stem cells engineered with the same set of genes were able to evade detection when transplanted into mice2. Instead of mouse embryonic cells, Parish and her team used human pluripotent stem cells, which can develop into most types of cell found in the body. After being engineered with the cloaking genes, the cells differentiated into nerve cells suitable for treating Parkinson’s disease. The researchers injected the neurons into mice whose immune systems had been replaced with human immune cells, and the neurons were not rejected, suggesting that they were able to evade detection. © 2025 Springer Nature Limited

Keyword: Parkinsons
Link ID: 29742 - Posted: 04.12.2025

By Gayoung Lee edited by Allison Parshall Crows sometimes have a bad rap: they’re said to be loud and disruptive, and myths surrounding the birds tend to link them to death or misfortune. But crows deserve more love and charity, says Andreas Nieder, a neurophysiologist at the University of Tübingen in Germany. They not only can be incredibly cute, cuddly and social but also are extremely smart—especially when it comes to geometry, as Nieder has found. In a paper published on Friday in Science Advances, Nieder and his colleagues report that crows display an impressive aptitude at distinguishing shapes by using geometric irregularities as a cognitive cue. These crows could even discern quite subtle differences. For the experiment, the crows perched in front of a digital screen that, almost like a video game, displayed progressively more complex combinations of shapes. First, the crows were taught to peck at a certain shape for a reward. Then they were presented with that same shape among five others—for example, one star shape placed among five moon shapes—and were rewarded if they correctly picked the "outlier." “Initially [the outlier] was very obvious,” Nieder says. But once the crows appeared to have familiarized themselves with how the “game” worked, Nieder and his team introduced more similar quadrilateral shapes to see if the crows would still be able to identify outliers. “And they could tell us, for instance, if they saw a figure that was just not a square, slightly skewed, among all the other squares,” Nieder says. “They really could do this spontaneously [and] discriminate the outlier shapes based on the geometric differences without us needing them to train them additionally.” Even when the researchers stopped rewarding them with treats, the crows continued to peck the outliers. © 2024 SCIENTIFIC AMERICAN,

Keyword: Evolution; Intelligence
Link ID: 29741 - Posted: 04.12.2025

By Michael Schulson Two years ago, at a Stop & Shop in Rhode Island, the Danish neuroscientist and physician Henriette Edemann-Callesen visited an aisle stocked with sleep aids containing melatonin. She looked around in amazement. Then she took out her phone and snapped a photo to send to colleagues back home. “It was really pretty astonishing,” she recalled recently. In Denmark, as in many countries, the hormone melatonin is a prescription drug for treating sleep problems, mostly in adults. Doctors are supposed to prescribe it to children only if they have certain developmental disorders that make it difficult to sleep — and only after the family has tried other methods to address the problem. But at the Rhode Island Stop & Shop, melatonin was available over the counter, as a dietary supplement, meaning it receives slightly less regulatory scrutiny, in some respects, than a package of Skittles. Many of the products were marketed for children, in colorful bottles filled with liquid drops and chewable tablets and bright gummies that look and taste like candy. A quiet but profound shift is underway in American parenting, as more and more caregivers turn to pharmacological solutions to help children sleep. What makes that shift unusual is that it’s largely taking place outside the traditional boundaries of health care. Instead, it’s driven by the country’s sprawling dietary supplements industry, which critics have long said has little regulatory oversight — and which may get a boost from Secretary of Health and Human Services Robert F. Kennedy Jr., who is widely seen as an ally to supplement makers. Thirty years ago, few people were giving melatonin to children, outside of a handful of controlled experiments. Even as melatonin supplements grew in popularity among adults in the late 1990s in the United States and Canada, some of those products carried strict warnings not to give them to younger people. But with time, the age floor dropped, and by the mid-2000s, news reports and academic surveys suggest some early adopters were doing just that. (Try it for ages 11-and-up only, one CNN report warned at the time.) By 2013, according to a Wall Street Journal article, a handful of companies were marketing melatonin products specifically for kids.

Keyword: Biological Rhythms; Development of the Brain
Link ID: 29740 - Posted: 04.12.2025

Jon Hamilton Researchers created an assembloid by integrating four organoids that represent the four components of the human sensory pathway, along which pain stimuli signals are conveyed to the brain. Stimulation of the sensory organoid (top) by pain-inducing substances, such as capsaicin, triggers neuronal activity in that organoid which is then transmitted to the adjacent spinal-cord organoid, the thalamic organoid and, finally, to the cortical organoid (bottom) Researchers integrated four organoids that represent the four components of the human sensory pathway, along which pain signals are conveyed to the brain. Stimulation of the sensory organoid (top) by substances, such as capsaicin, triggers neuronal activity that is then transmitted throughout the rest of the organoids. Pasca lab/Stanford Medicine Scientists have re-created a pain pathway in the brain by growing four key clusters of human nerve cells in a dish. This laboratory model could be used to help explain certain pain syndromes, and offer a new way to test potential analgesic drugs, a Stanford team reports in the journal Nature. "It's exciting," says Dr. Stephen Waxman, a professor at Yale School of Medicine who was not involved in the research. © 2025 npr

Keyword: Pain & Touch; Development of the Brain
Link ID: 29739 - Posted: 04.12.2025

By Yasemin Saplakoglu Humans tend to put our own intelligence on a pedestal. Our brains can do math, employ logic, explore abstractions and think critically. But we can’t claim a monopoly on thought. Among a variety of nonhuman species known to display intelligent behavior, birds have been shown time and again to have advanced cognitive abilities. Ravens plan (opens a new tab) for the future, crows count and use tools (opens a new tab), cockatoos open and pillage (opens a new tab) booby-trapped garbage cans, and chickadees keep track (opens a new tab) of tens of thousands of seeds cached across a landscape. Notably, birds achieve such feats with brains that look completely different from ours: They’re smaller and lack the highly organized structures that scientists associate with mammalian intelligence. “A bird with a 10-gram brain is doing pretty much the same as a chimp with a 400-gram brain,” said Onur Güntürkün (opens a new tab), who studies brain structures at Ruhr University Bochum in Germany. “How is it possible?” Researchers have long debated about the relationship between avian and mammalian intelligences. One possibility is that intelligence in vertebrates — animals with backbones, including mammals and birds — evolved once. In that case, both groups would have inherited the complex neural pathways that support cognition from a common ancestor: a lizardlike creature that lived 320 million years ago, when Earth’s continents were squished into one landmass. The other possibility is that the kinds of neural circuits that support vertebrate intelligence evolved independently in birds and mammals. It’s hard to track down which path evolution took, given that any trace of the ancient ancestor’s actual brain vanished in a geological blink. So biologists have taken other approaches — such as comparing brain structures in adult and developing animals today — to piece together how this kind of neurobiological complexity might have emerged. © 2025 Simons Foundation

Keyword: Intelligence; Evolution
Link ID: 29738 - Posted: 04.09.2025

By Matt Richtel So sharp are partisan divisions these days that it can seem as if people are experiencing entirely different realities. Maybe they actually are, according to Leor Zmigrod, a neuroscientist and political psychologist at Cambridge University. In a new book, “The Ideological Brain: The Radical Science of Flexible Thinking,” Dr. Zmigrod explores the emerging evidence that brain physiology and biology help explain not just why people are prone to ideology but how they perceive and share information. What is ideology? It’s a narrative about how the world works and how it should work. This potentially could be the social world or the natural world. But it’s not just a story: It has really rigid prescriptions for how we should think, how we should act, how we should interact with other people. An ideology condemns any deviation from its prescribed rules. You write that rigid thinking can be tempting. Why is that? Ideologies satisfy the need to try to understand the world, to explain it. And they satisfy our need for connection, for community, for just a sense that we belong to something. There’s also a resource question. Exploring the world is really cognitively expensive, and just exploiting known patterns and rules can seem to be the most efficient strategy. Also, many people argue — and many ideologies will try to tell you — that adhering to rules is the only good way to live and to live morally. I actually come at it from a different perspective: Ideologies numb our direct experience of the world. They narrow our capacity to adapt to the world, to understand evidence, to distinguish between credible evidence and not credible evidence. Ideologies are rarely, if ever, good. Q: In the book, you describe research showing that ideological thinkers can be less reliable narrators. Can you explain? Remarkably, we can observe this effect in children. In the 1940s, Else Frenkel-Brunswik, a psychologist at the University of California, Berkeley, interviewed hundreds of children and tested their levels of prejudice and authoritarianism, like whether they championed conformity and obedience or play and imagination. When children were told a story about new pupils at a fictional school and asked to recount the story later, there were significant differences in what the most prejudiced children remembered, as opposed to the most liberal children. © 2025 The New York Times Company

Keyword: Emotions; Attention
Link ID: 29737 - Posted: 04.09.2025

By Rodrigo Pérez Ortega It’s clear a child’s early experiences can leave a lasting imprint on how their brain forms and functions. Now, a new study reveals how various environmental factors, including financial struggles and neighborhood safety, affect the quality of the brain’s white matter—the wiring that connects different brain regions—and in turn, a child’s cognitive abilities. The work, published today in the Proceedings of the National Academy of Sciences, also points to social factors that can boost resilience in a young brain. “It’s a really impressive, compelling paper about the long-term consequences of growing up in undersupported environments,” says John Gabrieli, a neuroscientist at the Massachusetts Institute of Technology who was not involved in the study. White matter consists of nerve fibers facilitating communication between brain regions. They are sheathed in an insulating material called myelin that gives white matter its color. Much of the research to date on how the brain supports cognition has focused on gray matter, tissue mostly made of the cell bodies of neurons that process information, which shows up as gray on brain scans. But complex cognitive tasks are “a symphony of a network” formed by multiple brain areas, Gabrieli says. “And the white matter is what mediates that communication.” Previous studies have linked poverty and childhood trauma—among other adverse environments—with a lower quality of white matter in children and lower scores on cognitive tests. However, these studies included a small number or participants and only looked at one or a few environmental variables at a time. For a more complete picture, developmental neuroscientist Sofia Carozza at Brigham and Women’s Hospital and colleagues analyzed data from more than 9000 participants in the Adolescent Brain Cognitive Development (ABCD) Study. Funded by the National Institutes of Health and established in 2015, ABCD is the largest longitudinal study of brain development in a representative group of U.S. children. Surveys of participants and their parents provide data on their home environment, including household income and parents’ level of education. At age 9 or 10, ABCD participants got a form of magnetic resonance imaging that measures the movement of water in the brain. From the strength of this directional signal, researchers can infer how robust and organized the bundles of white matter fibers are, and whether they have signs of deterioration or damage. © 2025 American Association for the Advancement of Science.

Keyword: Development of the Brain; Learning & Memory
Link ID: 29736 - Posted: 04.09.2025

Avram Holmes. Human thought and behavior emerge through complex and reciprocal interactions that link microscale molecular and cellular processes with macroscale functional patterns. Functional MRI (fMRI), one of the most common methods for studying the human brain, detects these latter patterns through the “blood oxygen level dependent,” or BOLD, signal, a composite measure of both neural and vascular signals that reflects an indirect measure of brain activity. Despite an enormous investment by scientific funders and the research community in the use of fMRI, though, researchers still don’t fully understand the underlying mechanisms that drive individual or population-level differences measured via in-vivo brain imaging, which limits our ability to interpret those data. For fMRI to meaningfully contribute to progress in neuroscience, we need to develop research programs that link phenomena across levels, from genes and molecules to cells, circuits, networks and behavior. Without a concerted effort in this direction, fMRI will remain a methodological spandrel, a byproduct of technological development rather than a tool explicitly designed to reveal neural mechanisms, generating isolated datapoints that are left unintegrated with broader scientific theory or progress. Recently, the human functional neuroimaging community has turned a critical eye toward its own methods and findings. These debates have led to field-wide initiatives calling for larger and more diverse study samples, better phenotypic reliability and findings that generalize across populations. But researchers have put relatively little emphasis on contextualizing the resulting work across levels of analysis or on deciphering the biological mechanism that may underpin changes to the BOLD signal across groups and individual people or over the lifespan. Appeals to better integrate the different levels of neuroscience are not new. But despite persuasive arguments, fMRI researchers have largely remained scientifically siloed, isolated by a nearly ubiquitous focus on a single level of analysis and a rigid adherence to a select set of imaging methods. Our work is typically presented inside of field-specific echo chambers—departmental or group seminars, topic-specific journals and society meetings—where our methodological and analytic choices go unchallenged. What progress can we expect to make if we remain isolated from other fields of study? © 2025 Simons Foundation

Keyword: Brain imaging
Link ID: 29735 - Posted: 04.09.2025

Alexandra Topping The benefits of taking drugs for attention deficit hyperactivity disorder outweigh the impact of increases in blood pressure and heart rate, according to a new study. An international team of researchers led by scientists from the University of Southampton found the majority of children taking ADHD medication experienced small increases in blood pressure and pulse rates, but that the drugs had “overall small effects”. They said the study’s findings highlighted the need for “careful monitoring”. Prof Samuele Cortese, the senior lead author of the study, from the University of Southampton, said the risks and benefits of taking any medication had to be assessed together, but for ADHD drugs the risk-benefit ratio was “reassuring”. “We found an overall small increase in blood pressure and pulse for the majority of children taking ADHD medications,” he said. “Other studies show clear benefits in terms of reductions in mortality risk and improvement in academic functions, as well as a small increased risk of hypertension, but not other cardiovascular diseases. Overall, the risk-benefit ratio is reassuring for people taking ADHD medications.” About 3 to 4% of adults and 5% of children in the UK are believed to have ADHD, a neurodevelopmental disorder with symptoms including impulsiveness, disorganisation and difficulty focusing, according to the National Institute for Health and Care Excellence (Nice). Doctors can prescribe stimulants, such as methylphenidate, of which the best-known brand is Ritalin. Other stimulant medications used to treat ADHD include lisdexamfetamine and dexamfetamine. Non-stimulant drugs include atomoxetine, an sNRI (selective norepinephrine reuptake inhibitor), and guanfacine. © 2025 Guardian News & Media Limited

Keyword: ADHD; Drug Abuse
Link ID: 29734 - Posted: 04.09.2025

is a psychologist, writer and professor in the history and philosophy of science programme at the University of Melbourne. She is the author of Delusions of Gender: How Our Minds, Society, and Neurosexism Create Difference (2010), Testosterone Rex: Myths of Sex, Science, and Society (2017) and Patriarchy Inc.: What We Get Wrong About Gender Equality – and Why Men Still Win at Work (2025). She lives in Melbourne, Australia. Carole Hooven is a human evolutionary biologist with a focus on behavioural endocrinology. She is a nonresident senior fellow at the American Enterprise Institute, an associate in Harvard’s Department of Psychology, and the author of T: The Story of Testosterone, the Hormone That Dominates and Divides Us (2021). She lives in Cambridge, Massachusetts. Does biology determine destiny, or is society the dominant cause of masculine and feminine traits? In this spirited exchange, the psychologist Cordelia Fine and the evolutionary biologist Carole Hooven unpack the complex relationship between testosterone and human behaviour. Fine emphasises variability, flexibility and context – seeing gender as shaped by social forces as much as it is by hormones. By contrast, Hooven stresses consistent patterns; while acknowledging the influence of culture and the differences between individuals, she maintains that biology explains why certain sex-linked behaviours persist across cultures. © Aeon Media Group Ltd. 2012-2025.

Keyword: Sexual Behavior; Evolution
Link ID: 29733 - Posted: 04.09.2025

Ian Sample Science editor Researchers who tracked cases of dementia in Welsh adults have uncovered the strongest evidence yet that the shingles vaccination reduces the risk of developing the devastating brain disease. Health records of more than 280,000 older adults revealed that those who received a largely discontinued shingles vaccine called Zostavax were 20% less likely to be diagnosed with dementia over the next seven years than those who went without. Pascal Geldsetzer, at Stanford University, said: “For the first time we are able to say much more confidently that the shingles vaccine causes a reduction in dementia risk. If this truly is a causal effect, we have a finding that’s of tremendous importance.” The researchers took advantage of a vaccination rollout that took place in Wales more than a decade ago. Public health policy dictated that from 1 September 2013, people born on or after 2 September 1933 became eligible for the Zostavax shot, while those who were older missed out. The policy created a natural experiment where the older population was sharply divided into two groups depending on their access to the vaccine. This allowed the researchers to compare dementia rates in older people born weeks apart but on either side of the vaccine eligibility divide. After accounting for the fact that not all those eligible for the vaccine received it, the researchers found vaccination led to a 20% reduction in dementia risk, with the strongest effect in women. Anupam Jena, a professor of healthcare policy at Harvard Medical School, said the implications were profound. © 2025 Guardian News & Media Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 29732 - Posted: 04.05.2025

By Smriti Mallapaty Neuroscientists have observed for the first time how structures deep in the brain are activated when the brain becomes aware of its own thoughts, known as conscious perception1. The brain is constantly bombarded with sights, sounds and other stimuli, but people are only ever aware of a sliver of the world around them — the taste of a piece of chocolate or the sound of someone’s voice, for example. Researchers have long known that the outer layer of the brain, called the cerebral cortex, plays a part in this experience of being aware of specific thoughts. The involvement of deeper brain structures has been much harder to elucidate, because they can be accessed only with invasive surgery. Designing experiments to test the concept in animals is also tricky. But studying these regions would allow researchers to broaden their theories of consciousness beyond the brain’s outer wrapping, say researchers. “The field of consciousness studies has evoked a lot of criticism and scepticism because this is a phenomenon that is so hard to study,” says Liad Mudrik, a neuroscientist at Tel Aviv University in Israel. But scientists have increasingly been using systematic and rigorous methods to investigate consciousness, she says. Aware or not In a study published in Science today1, Mingsha Zhang, a neuroscientist at Beijing Normal University, focused on the thalamus. This region at the centre of the brain is involved in processing sensory information and working memory, and is thought to have a role in conscious perception. Participants were already undergoing therapy for severe and persistent headaches, for which they had thin electrodes injected deep into their brains. This allowed Zhang and his colleagues to study their brain signals and measure conscious awareness. © 2025 Springer Nature Limited

Keyword: Consciousness
Link ID: 29731 - Posted: 04.05.2025

By Carl Zimmer After listening to hundreds of hours of ape calls, a team of scientists say they have detected a hallmark of human language: the ability to put together strings of sounds to create new meanings. The provocative finding, published Thursday in the journal Science, drew praise from some scholars and skepticism from others. Federica Amici, a primatologist at the University of Leipzig in Germany, said that the study helped place the roots of language even further back in time, to millions of years before the emergence of our species. “Differences between humans and other primates, including in communication, are far less distinct and well-defined than we have long assumed,” Dr. Amici said. But other researchers said that the study, which had been conducted on bonobos, close relatives of chimpanzees, had little to reveal about how we use words. “The present findings don’t tell us anything about the evolution of language,” said Johan Bolhuis, a neurobiologist at Utrecht University in the Netherlands. Many species can communicate with sounds. But when an animal makes a sound, it typically means just one thing. Monkeys, for instance, can make one warning call in reference to a leopard and a different one for an incoming eagle flying. In contrast, we humans can string words together in ways that combine their individual meanings into something new. Suppose I say, “I am a bad dancer.” When I combine the words “bad” and “dancer,” I no longer mean them independently; I’m not saying, “I am a bad person who also happens to dance.” Instead, I mean that I don’t dance well. Linguists call this compositionality, and have long considered it an essential ingredient of language. “It’s the force behind language’s creativity and productivity,” said Simon Townsend, a comparative psychologist at the University of Zurich in Switzerland. “Theoretically, you can come up with any phrase that has never been uttered before.” © 2025 The New York Times Company

Keyword: Language; Evolution
Link ID: 29730 - Posted: 04.05.2025

By Mitch Leslie Unlike the combative immune cells that protect us from pathogens, regulatory T cells (Tregs) are nurturers. They salve inflammation, promote healing of injured tissue, and rein in immune attacks to curb self-inflicted damage. Now, a study of mice reported today in Science suggests some Tregs also act on nerve cells to quell a specific type of pain—but only in females. Why only female rodents seem to benefit remains unclear, but researchers hope they might someday enlist these Tregs to address pain conditions, many of which disproportionately affect women. “It’s a very impressive paper,” says neuroscientist Gila Moalem-Taylor of the University of New South Wales Sydney, who wasn’t connected to the research. The study “uses elegant, sophisticated methods to conclusively demonstrate the mechanisms” by which the cells reduce one kind of sensitivity to pain, she says. Tregs, a type of white blood cell, are best known for their role in keeping the immune system in balance and preventing autoimmunity. But researchers have recently found that they also help control pain. For example, a 2021 study by neuroscientist Allan Basbaum of the University of California San Francisco (UCSF) and colleagues showed that Tregs reduce mice’s sensitivity to pain triggered by other immune cells that reside in the brain and spinal cord. That research and additional work suggested Tregs influence pain by targeting various immune cells and tamping down inflammation. But these studies left open the possibility that Tregs might also directly affect pain-sensing nerve cells. Basbaum, his postdoc Élora Midavaine, UCSF dermatologist Sakeen Kashem, and their colleagues launched the new study to nail down how the regulatory cells curb pain. They focused on Tregs that dwell in the meninges—the membranes that sheathe the brain and spinal cord—and in similar nearby membranes. The cells are much more abundant in these structures than elsewhere in the nervous system. To find out whether the cells affect pain perception, the scientists used genetically engineered mice whose Tregs are vulnerable to a toxin produced by the bacteria that cause diphtheria. Injecting this toxin into the meninges in the lower back killed about 90% of the Tregs in the membranes without harming Tregs in the rest of the body.

Keyword: Pain & Touch; Glia
Link ID: 29729 - Posted: 04.05.2025