By Rachel Nuwer No one knows why magic mushrooms evolved to produce psilocybin, a powerful psychedelic molecule. But this trait was apparently so beneficial for fungi that it independently evolved in two distantly related types of mushrooms. An even greater surprise to biologists was that rather than arriving at the same solution for producing psilocybin, the two groups pursued completely different biochemical pathways, according to a study published last month in the journal Angewandte Chemie International Edition. “This finding reminds us that nature finds more than one way to make important molecules,” said Dirk Hoffmeister, a pharmaceutical microbiologist at Friedrich Schiller University Jena in Germany and an author of the study. He added that it was also evidence that mushrooms were “brilliant chemists.” Practically speaking, Dr. Hoffmeister said, the research also suggested a possible new path for synthesizing psilocybin for use in scientific research and therapies. “We can expand our toolbox,” he said. Psilocybe and Inocybe mushrooms occur in some of the same habitats, but they follow different lifestyles. Psilocybe, the group that includes what are traditionally called magic mushrooms, thrives on decaying material such as decomposing organic matter or cow dung. Inocybe, commonly known as fiber caps, are symbiotic organisms that form intimate, mutually beneficial relationships with trees. In 1958, Albert Hofmann, the Swiss chemist who discovered LSD, became the first researcher to isolate psilocybin from Psilocybe mushrooms. Some scientists later suspected that a few Inocybe mushrooms also produced the compound. Since then, psilocybin has been identified in around half a dozen Inocybe species. (The other species tend to produce a potent neurotoxin.) © 2025 The New York Times Company

Keyword: Drug Abuse; Evolution
Link ID: 29985 - Posted: 10.25.2025

By Holly Barker At first glance, the mice in Pierre Vanderhaeghen’s lab in Leuven, Belgium, seem unremarkable. But inside their tiny heads, their cerebral cortex contains a mix of mouse and human neurons at two stages of development: Their native synapses are fully mature, but the connections formed from human cells are delayed and comparable to those of a newborn human baby. Vanderhaeghen and his colleagues are studying the chimeric mice to explore this drawn-out process of synaptic development, a feature that distinguishes human brains from those of other mammals. Many aspects of human brain development proceed slowly—neurogenesis, myelination, gliogenesis—but synaptic maturation is particularly protracted. In the prefrontal cortex, for instance, some synapses don’t fully develop until a person reaches their mid-20s. Deviations from this maturation rate could mean that “milestones won’t be reached at the same time” and might underlie some forms of autism or intellectual disability, says Vanderhaeghen, professor of neurosciences and group leader at the VIB-KU Leuven Center for Brain and Disease Research. An evolutionarily conserved protein called SRGAP2 controls this timing in most mammals. Humans, however, have partially duplicated copies—SRGAP2B and SRGAP2C—that inhibit the ancestral protein, two teams reported in 2012. Like other duplicated genes found only in humans, SRGAP2 resides in a repetitive—and therefore unstable—part of the genome, says Evan Eichler, professor of genome sciences at the University of Washington, and an investigator on one of the 2012 studies. “These regions create liability by predisposing us to genomic rearrangement, [but] to persist in the population, they must have an advantage. It’s part of the cost of what it is to be human.” © 2025 Simons Foundation

Keyword: Development of the Brain
Link ID: 29984 - Posted: 10.25.2025

Will Stone Doctors have long known that antidepressants come with side effects for cardiovascular and metabolic health. But a major analysis from a team of researchers in the U.K. has, for the first time, pulled together data from more than 150 clinical trials to compare the physical side effects of dozens of antidepressants. The study, published in the Lancet this week, details how each medication can affect weight, blood pressure, heart rate, cholesterol and other areas of health. The end result is something akin to a "sports league table" for 30 different antidepressants based on their side effect profile, says lead author Dr. Toby Pillinger, a psychiatrist at King's College London. "It's never been done at this scale before and no one's ever put specific numbers to the amount of weight you'll put on, or to the amount that your cholesterol goes up," he says. The findings are based on existing data, mostly from 8-week drug studies, that altogether represent more than 58,000 patients. The most frequently prescribed antidepressants in the U.S. — selective serotonin reuptake inhibitors, or SSRIs, like Zoloft and Prozac — tended to have fewer physical side effects, according to the analysis. Other medications, particularly some of the older drugs, were shown to have more significant impacts. © 2025 npr

Keyword: Depression
Link ID: 29983 - Posted: 10.25.2025

By Meghan Rosen It sounds like something from a horror movie: A disease that eats through bone, dissolving the fused plates of the skull like bubbling acid. But a type of brain cancer called glioblastoma actually does something similar, triggering the erosion of living skull tissue, researchers report October 3 in Nature Neuroscience. The work shows in gory detail that brain cancer can erode bone, a harmful effect that wasn’t previously known, says Jinan Behnan, a brain tumor immunologist at Albert Einstein College of Medicine in Bronx, New York. Behnan’s findings uncover a creepy new facet of glioblastoma, an enigmatic cancer still cloaked in scientific questions. “We really still don’t understand exactly what this disease is,” she says. Glioblastoma is an aggressive form of brain cancer that’s particularly lethal and nearly impossible to cure. In the United States, doctors diagnose more than 12,000 new cases every year. Five years after diagnosis, only about five percent of patients over 40 years old survive. © Society for Science & the Public 2000–2025

Keyword: Miscellaneous
Link ID: 29982 - Posted: 10.25.2025

By Gina Kolata For the first time, researchers restored some vision to people with a common type of eye disease by using a prosthetic retinal implant. If approved for broader use in the future, the treatment could improve the lives of an estimated one million, mostly older, people in the United States who lose their vision to the condition. The patients’ blindness occurs when cells in the center of the retina start to die, what is known as geographic atrophy resulting from age-related macular degeneration. Without these cells, patients see a big black spot in the center of their vision, with a thin border of sight around it. Although their peripheral vision is preserved, people with this form of advanced macular degeneration cannot read, have difficulty recognizing faces or forms and may have trouble navigating their surroundings. In a study published Monday in The New England Journal of Medicine, vision in 27 out of 32 participants improved so much that they could read with their artificial retinas. The vision that is restored is not normal: It’s black and white, blurry, and the field of view is small. But after getting the retinal implant, patients who could barely see gained on average five lines on a standard eye chart. The implant gets signals from glasses and a camera that projects infrared images to the artificial retina. The camera has a zoom feature that can magnify images like letters, allowing people to read, albeit slowly because with the zoom they don’t see many letters at a time. “This is at the forefront of science,” said Dr. Demetrios Vavvas, director of the retina service at Massachusetts Eye and Ear, a specialty hospital in Boston. He was not involved in the study and emphasized that the implant was not a cure for macular degeneration. But he called it the dawn of a new technology that he predicted will significantly advance. The treatment is only for people with a loss of retinal photoreceptors, so it would not work for other forms of blindness. The study participants had an average age of 79 and had been told that once vision was lost, it was gone forever. © 2025 The New York Times Company

Keyword: Vision; Robotics
Link ID: 29981 - Posted: 10.22.2025

Rachel Fieldhouse Slow, sleep-like brain waves persist in part of the brain that has been surgically disconnected from the rest of the organ even though the person is awake. The findings1, published in PLoS Biology, add to researchers’ understanding of what conscious and unconscious brain states look like. Children with severe epilepsy who do not respond to medication can undergo a surgical procedure called a hemispherotomy. During surgery, clinicians disconnect the part of the brain in which seizures originate from the rest of the brain, stopping them from spreading. The disconnected tissue is left in the skull and has an intact blood supply. The team wanted to find out whether the disconnected part has some form of awareness — or was capable of exhibiting consciousness, says co-author Marcello Massimini, a neurophysiology researcher at the University of Milan in Italy. “The question arises because we have no access” to the disconnected region, he says, adding that it was unclear what happens once part of the brain is isolated. Studies investigating consciousness are difficult because there is no consensus on what conscious and unconscious states in the brain look like, says Ariel Zeleznikow-Johnston, a neuroscientist at Monash University in Melbourne, Australia. “There’s no generally accepted definitive signatures of consciousness in terms of electrical readings or brain activity,” he adds. Even defining unconsciousness is challenging, because activities associated with consciousness, such as remembering dreams, can occur during states associated with unconsciousness, such as sleep or anaesthesia, Massimini says. © 2025 Springer Nature Limited

Keyword: Sleep
Link ID: 29980 - Posted: 10.22.2025

By Grigori Guitchounts On a mellow spring night, I gazed at the setting desert sun in Joshua Tree National Park in California. The sun glowed a warm blood-orange and the sky shimmered pink and purple. I had just defended my Ph.D. in neuroscience, and my partner and I had flown west to celebrate and exhale. It was early March 2020, and we were hoping to quiet our minds in the desert. I was also hoping to change mine. I had been curious about psychedelics for years, but it wasn’t until I read How to Change Your Mind by Michael Pollan about the new science of psychedelics, that I felt ready. The book made a compelling case that psychedelics provided a fascinating introspective experience. Still, I was nervous. I’d heard stories about bad trips and flashbacks. I knew enough neuroscience to know these were serious drugs—compounds that could temporarily dismantle how the brain makes sense of reality and potentially change it irreversibly. I also knew I was burned out. My Ph.D. had been hard in the way Ph.D.s often are: thrilling, lonely, disorienting. My advisor had left academia halfway through, and I’d spent years without much supervision, never quite sure whether I was on the right track and if I had a future in academia. But I didn’t take LSD seeking healing or clarity. I just wanted to see what the fuss was about. After years of hunkering down, I was craving a freeing experience. What followed was strange, intense, and beautiful. The wooden floorboards of our cabin turned into a bustling cityscape. The mirror in the bathroom showed my face aged beyond recognition: The natural lines in my skin became deep wrinkles, my eyes sunken, as if time had decided to give me a sneak peak of what would come. Later, absorbed with coloring pencils, I watched the marks I was making dissolve in real time, as if the paper were being erased by invisible rain. © 2025 NautilusNext Inc.,

Keyword: Drug Abuse; Consciousness
Link ID: 29979 - Posted: 10.22.2025

By Susan Dominus Spend enough time speaking to women who are taking testosterone — specifically, in very high doses — and you start to notice that they sound messianic. They’re often talking fast and intensely; they’re amped up; they’re describing what they clearly consider a miracle drug; and they have no intention of lowering their dose, despite the unknown risks or some problems with facial hair. After all, how can they worry about facial hair when they feel so alive? It’s nothing they can’t take care of with a quick waxing, which they now have the energy to do at the end of the day — right after they prepare a high-protein dinner for their family and before they put the finishing touches on their spreadsheets, close their laptops and light a few mood candles for the sex that they know will be great, maybe even better than the sex they had last night, even though they’re a day older. “It’s changed my marriage,” Jessica Medina, a 41-year-old marketing consultant in Orange County, Calif., told me. With four kids in the house, and sex happening six times a week (up from “How about never?” pre-testosterone), she had to put a lock on the bedroom door. She and her husband had attended a “marriage growth” group at church for years, but it took testosterone for their relationship to be, as she put it, “100 times closer.” She was a little less emotional, a little less sentimental than she used to be, but she didn’t have time for that kind of thing, anyway. “It’s more like: Get stuff done, handle business, work out,” she said. “In order to do all that and still have time for our kids and their sports, there’s no time to whine about how hard it is.” Catherine Lin, a single mother who ran a bicoastal fashion media company, went on testosterone in her early 40s to raise her energy. She got the boost she wanted, started lifting heavier weights, decided to pursue a degree in holistic nutrition and enjoyed an unexpected side effect: She started having orgasms for the first time in years. © 2025 The New York Times Company

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 29978 - Posted: 10.22.2025

By Giorgia Guglielmi Male and female human fetuses show distinct patterns of gene activity and DNA regulation in the cerebral cortex, according to a new analysis of thousands of individual brain cells. The study offers one of the most detailed maps to date of how such activity differs between boys and girls’ brains during the second trimester. It also compares sex differences in gene activity in fetuses with spontaneous genetic changes in autistic people, revealing clues as to how these de novo changes affect boys and girls. “As the field evolves, this [work] will be a helpful reference” for exploring sex-related molecular differences in early brain development, says Matthew Oetjens, assistant professor of human genetics at Geisinger Medical Center, who was not involved in the study. Understanding these differences may help explain why certain neurodevelopmental conditions are more common in one sex than the other, he says. Autism, for example, is diagnosed about four times more often in boys than in girls, but scientists are still trying to understand why. Theories include the possibility that boys are more vulnerable, girls are sometimes protected, or a combination of both. “We know that autism … has a very strong genetic component. What is not known is how the genetic risk architecture intersects with any differences at the molecular level that might exist between male and female human brains,” says study investigator Tomasz Nowakowski, associate professor of neurological surgery, anatomy and psychiatry, and behavioral sciences at the University of California, San Francisco. More than 940 genes are expressed differently between the sexes, according to the new analysis of more than 38,000 brain cells from 21 female and 27 male mid-gestation fetuses. Most of these differentially expressed genes are more active in females. © 2025 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 29977 - Posted: 10.22.2025

Jon Hamilton Scientists are reporting the first compelling evidence in people that cognitive training can boost levels of a brain chemical that typically declines with age. A 10-week study of people 65 or older found that doing rigorous mental exercises for 30 minutes a day increased levels of the chemical messenger acetylcholine by 2.3% in a brain area involved in attention and memory. This illustration shows a pink human brain with stick legs and stick arms. The pink stick arms are holding up a black barbell with black disk-shaped weights on each end. The background is light blue. Your Health Even healthy brains decline with age. Here's what you can do The increase "is not huge," says Étienne de Villers-Sidani, a neurologist at McGill University in Montreal. "But it's significant, considering that you get a 2.5% decrease per decade normally just with aging." So, at least in this brain area, cognitive training appeared to turn back the clock by about 10 years. The chemical change observed after intensive brain training is persuasive, says Michael Hasselmo, director of the Center for Systems Neuroscience at Boston University, who was not involved in the study. "It was compelling enough that I thought, 'Maybe I need to be doing this,'" he says. The result backs earlier research in animals showing that environments that stimulate the brain can increase levels of certain neurotransmitters. Studies of people have suggested that cognitive training can improve thinking and memory. Never skip brain day The study, funded by the National Institutes of Health, comes amid a proliferation of online brain-training programs, including Lumosity, Elevate, Peak, CogniFit and BrainHQ. © 2025 npr

Keyword: Alzheimers; Learning & Memory
Link ID: 29976 - Posted: 10.22.2025

Katie Kavanagh Why are we able to remember emotional events so well? According to a study published today in Nature1, a type of cell in the brain called an astrocyte is a key player in stabilizing memories for long-term recall. Astrocytes were thought to simply support neurons in creating the physical traces of memories in the brain, but the study found that they have a much more active role — and can even be directly triggered by repeated emotional experiences. The researchers behind the finding suggest that the cells could be a fresh target for treating memory conditions such as those associated with post-traumatic stress disorder and Alzheimer’s disease. “We provide an answer to the question of how a specific memory is stored for the long term,” says study co-author Jun Nagai, a neuroscientist at RIKEN Center for Brain Science in Wako, Japan. By studying astrocytes, Nagai said, the study identifies how the brain selectively filters important memories at the cellular level. Stable memories Nagai and his colleagues focused on the question of memory stabilization: how a short-term memory becomes more permanent in the brain. Previous research had found physical traces of memories in neuronal networks in brain regions such as the hippocampus and amygdala2. But it was unclear how these ‘engrams’ were stored in the brain as lasting memories after repeated exposure to the same stimulus. To dig deeper, the researchers developed a method for measuring activation patterns in astrocytes across a whole brain of a mouse as it completes a memory task. They measured the upregulation of a gene called Fos — an early marker of cell activity that is associated with the physical traces of memories in the brain3. © 2025 Springer Nature Limited

Keyword: Learning & Memory; Emotions
Link ID: 29975 - Posted: 10.18.2025

By Yasemin Saplakoglu The pillow is cold against your cheek. Your upstairs neighbor creaks across the ceiling. You close your eyes; shadows and light dance across your vision. A cat sniffs at a piece of cheese. Dots fall into a lake. All this feels very normal and fine, even though you don’t own a cat and you’re nowhere near a lake. You’ve started your journey into sleep, the cryptic state that you and most other animals need in some form to survive. Sleep refreshes the brain and body in ways we don’t fully understand: repairing tissues, clearing out toxins and solidifying memories. But as anyone who has experienced insomnia can attest, entering that state isn’t physiologically or psychologically simple. To fall asleep, “everything has to change,” said Adam Horowitz (opens a new tab), a research affiliate in sleep science at the Massachusetts Institute of Technology. The flow of blood to the brain slows down, and the circulation of cerebrospinal fluid speeds up. Neurons release neurotransmitters that shift the brain’s chemistry, and they start to behave differently, firing more in sync with one another. Mental images float in and out. Thoughts begin to warp. “Our brains can really rapidly transform us from being aware of our environments to being unconscious, or even experiencing things that aren’t there,” said Laura Lewis (opens a new tab), a sleep researcher at MIT. “This raises deeply fascinating questions about our human experience.” It’s still largely mysterious how the brain manages to move between these states safely and efficiently. But studies targeting transitions both into and out of sleep are starting to unravel the neurobiological underpinnings of these in-between states, yielding an understanding that could explain how sleep disorders, such as insomnia or sleep paralysis, can result when things go awry. Sleep has been traditionally thought of as an all-or-nothing phenomenon, Lewis said. You’re either awake or asleep. But the new findings are showing that it’s “much more of a spectrum than it is a category.” © 2025 Simons Foundation

Keyword: Sleep
Link ID: 29974 - Posted: 10.18.2025

Jon Hamilton In Alzheimer's, brain cells die too soon. In cancer, dangerous cells don't die soon enough. That's because both diseases alter the way cells decide when to end their lives, a process called programmed cell death. "Cell death sounds morbid, but it's essential for our health," says Douglas Green, who has spent decades studying the process at St. Jude Children's Research Hospital in Memphis, Tennessee. For example, coaxing nerve cells to live longer could help people with Alzheimer's disease, Parkinson's disease or ALS (Lou Gehrig's disease), he says, while getting tumor cells to die sooner could help people with cancer. So researchers have been searching for disease treatments that "modify or modulate the tendency of a cell to die," Green says. One of these researchers is Randal Halfmann at the Stowers Institute for Medical Research in Kansas City, Missouri. He has been studying immune cells that self-destruct when they come into contact with molecules that present a threat to the body. "They have to somehow recognize that [threat] in this vast array of other complex molecules," he says, "and then within minutes, kill themselves." They do this much the way a soldier might dive on a grenade to save others' lives. Halfmann's team has been focusing on special proteins inside cells that can trigger this process. When these proteins recognize molecules associated with a virus or some other pathogen, he says, "they implode." The proteins crumple and begin linking up with other crumpled proteins to form a structure called a "death fold" polymer. That starts a chain reaction of polymerization that ultimately kills the cell. Halfmann's team knew this process takes a burst of energy. But they couldn't locate the source. © 2025 npr

Keyword: Alzheimers; Apoptosis
Link ID: 29973 - Posted: 10.18.2025

By Michele Cohen Marill Like many first-time mothers, Lisette Lopez-Rose thought childbirth would usher in a time of joy. Instead, she had panic attacks as she imagined that something bad was going to happen to her baby, and she felt weighed down by a sadness that wouldn’t lift. The San Francisco Bay Area mother knew her extreme emotions weren’t normal, but she was afraid to tell her obstetrician. What if they took her baby away? At about six months postpartum, she discovered an online network of women with similar experiences and ultimately opened up to her primary care doctor. “About two months after I started medication, I started to feel like I was coming out of a deep hole and seeing light again,” she says. Today, Lopez-Rose works at Postpartum Support International, coordinating volunteers to help new mothers form online connections. About one in eight US women go through a period of postpartum depression, making it among the most common complications of childbirth. It typically occurs in the first few weeks after delivery, when there’s a sudden drop in the reproductive hormones estrogen and progesterone. As scientists unravel chemical and genetic changes caused by those shifting hormones, they are discovering new ways to diagnose and treat postpartum depression, and even ways to identify who is at risk for it. Graph showing a steady rise in levels of estradiol and progesterone after conception and then a very steep drop-off right after birth. The hormones estradiol (the main form of estrogen) and progesterone rise during pregnancy. In some women, their sudden drop after childbirth triggers the onset of postpartum depression. The first-ever drug for postpartum depression, containing a derivative of progesterone, received US Food and Drug Administration approval in 2019. That marked a new approach to the disorder. This winter, in another major advance, a San Diego-based startup company will launch a blood test that predicts a pregnant woman’s risk of postpartum depression with more than 80 percent accuracy. © 2025 Annual Reviews

Keyword: Depression; Hormones & Behavior
Link ID: 29972 - Posted: 10.18.2025

Vladyslav Vyazovskiy After decades of research, there is still no clearly articulated scientific consensus on what sleep is or why it exists. Yet whenever sleep comes up as a topic of discussion, it is quickly reduced to its necessity and importance. Popular media remind us of what can, and will, go wrong if we do not sleep enough, and serve up some handy tips on how to overcome insomnia. Discussed exclusively in utilitarian terms, we are force-fed the idea that sleep exists solely for our immediate benefit. Is this really all we ever want to know about a third of our existence? Sleep is perhaps the biggest blind spot, or the longest blind stretch, if you will, of our life. Naturally, the health and societal implications of sleep are huge: from technogenic disasters caused by tiredness, to sleep deprivation as a form of torture or weapon of war, and to sleep disorders, some of which inflict so much suffering that they compete with chronic pain. However, in my opinion, to say sleep is important is to miss the point entirely. Sleep is the single most bizarre experience that happens to all of us, against our will, every day. The disconnect between old questions about sleep that have remained open for centuries and new, increasingly sophisticated technologies applied to solve them is ever growing. The predominant view is that sleep provides some sort of restoration for the brain or the body: what goes awry – out of balance – in waking is almost magically recalibrated by sleep. At the centre of this narrative is the individual-who-sleeps, a lone castaway, locked in a permanent, inexorable cycle of sleeping and waking, without hope of breaking free (except in death). From the moment of opening one’s eyes, the clock starts ticking, and there is a price to pay for every minute of wakeful time, measured precisely in proportion to the transgression of staying awake. Like a snake eating its own tail, waking and sleep consume each other in an endless cycle, without beginning or end. There is no mercy, and lack of sleep can be paid back only by sleep. The image of burning a candle at both ends endures. Despite vast technological advances in recent years, exponential growth in our understanding of nature and the cosmos, and major breakthroughs in biology and medicine, there is still no unified theory of sleep. I find myself pondering whether it is time to step back and seek a different angle. Medieval manuscript illustration depicting people sleeping in three beds, with two standing figures in dialogue beside them, and an ornate floral border. © Aeon Media Group Ltd. 2012-2025.

Keyword: Sleep
Link ID: 29971 - Posted: 10.15.2025

By Grace Lindsay Neuroscientists have spent decades characterizing the types of information represented in the visual system. In some of the earliest studies, scientists recorded neural activity in anesthetized animals passively viewing stimuli—a setup that led to some of the most famous findings in visual neuroscience, including the discovery of orientation tuning by David Hubel and Torsten Wiesel. But passive viewing, whether while awake or anesthetized, sidesteps one of the more intriguing questions for vision scientists: How does the rest of the brain use this visual information? Arguably, the main reason for painstakingly characterizing the information in the visual system is to understand how that information drives intelligent behavior. Connecting the dots between how visual neurons respond to incoming stimuli and how that information is “read out” by other brain regions has proven nontrivial. It is not clear that we have the necessary experimental and computational tools at present to fully characterize this process. To get a sense for what it might take, I asked 10 neuroscientists what experimental and conceptual methods they think we’re missing. Decoding is a common approach for understanding the information present in the visual system and how it might be used. But decoding on its own—training classifiers to read out prespecified information about a visual stimulus from neural activity patterns—cannot tell us how the brain uses information to perform a task. This is because the decoders we use for data analysis do not necessarily match the downstream processes implemented by neural circuits. Indeed, there are pieces of information that can reliably be read out from the visual system but aren’t accessible to participants during tasks. Primary visual cortex contains information about the ocular origin of a stimulus, for example, but participants are not able to accurately report this information. © 2025 Simons Foundation

Keyword: Vision
Link ID: 29970 - Posted: 10.15.2025

By John Branch Photographs by Sophie Park It starts with a tingle, a tremor, a sense that something is off. Dr. Sue Goldie doesn’t recognize the symptoms at first. Maybe she ignores them, wishes them away. It is 2021. She is 59, in the prime of a long teaching career at Harvard. She has just immersed herself in the sport of triathlon. One coach notes something off with her running cadence. Another wonders why her left arm isn’t fully lifting out of the water. A trainer sees a slight tremor. The first time Sue races, she feels a strange vibration, like an internal tremble. Then Sue sees it herself: Twitching fingers on her left hand. Tests reveal it is Parkinson’s, the incurable neurological disease that robs its victims of their motor skills, and sometimes their minds, one extinguished neuron at a time. Parkinson’s doesn’t always alter life spans, but it always upends lives. The diagnosis elicits a storm of emotions, but also raises questions, both pragmatic and deep, that have consumed Sue since. At what point, if ever, do I have to say something? Who needs to know? What do I reveal and what do I conceal? And, most profoundly: Does a diagnosis have to be an identity? For nearly four years, she keeps her diagnosis from most Harvard administrators, colleagues and students, worried about what it will do to her reputation. She grows more comfortable revealing herself away from work, in the world of triathlon. “I feel very strongly that I should be able to disclose this when I want, how I want, and it’s under my control,” she tells me last year. But Parkinson’s does not wait. Maybe others don’t notice the physical signs, not yet. They don’t see her in the early morning, shuffling off-balance to the bathroom before her medications kick in, a daily reminder that Parkinson’s was not something she dreamed last night. Maybe they don’t see the pill boxes in her purse, the exposed feeling she gets when the dopamine medications wear off, the persistent worry behind her cheerful disposition. Her symptoms are worsening. Disguising them is exhausting. Starting today, she is Sue with Parkinson’s. © 2025 The New York Times Company

Keyword: Parkinsons
Link ID: 29969 - Posted: 10.15.2025

Rachel Fieldhouse During ageing, men experience a greater reduction in volume across more regions of the brain than women do, according to a longitudinal study published today in the Proceedings of the National Academy of Sciences1. The authors suggest this means that age-related brain changes do not explain why women are more frequently diagnosed with Alzheimer’s disease than men are. “It’s really important that we understand what happens in the healthy brain so that we can better understand what happens when people get these neurodegenerative conditions,” says Fiona Kumfor, a clinical neuropsychologist at the University of Sydney, Australia. This study adds to scientists’ understanding of typical brain ageing, she adds. Nearly twice as many women are diagnosed with Alzheimer’s disease as men, and ageing is the biggest risk factor for the disease. This has prompted research into age-related sex differences in the brain. “If women’s brains declined more, that could have helped explain their higher Alzheimer’s prevalence,” says co-author Anne Ravndal, a PhD student at the University of Oslo. Previous research investigating sex differences in brain ageing has shown mixed results, Ravndal adds. Several studies have found that men experience greater loss of total grey matter and hippocampus size compared with women, whereas other work has reported a sharper decline of grey matter in women. Brain scans The latest study included more than 12,500 magnetic resonance imaging (MRI) brain scans from 4,726 people — at least two scans per person, taken an average of three years apart — who did not have Alzheimer’s disease or any cognitive impairments and were control participants in 14 larger data sets. The researchers compared how the individuals’ brain structures changed over time, looking at factors including the thickness of grey matter and the size of areas that are associated with Alzheimer’s disease, such as the hippocampus, which is essential to memory. © 2025 Springer Nature Limited

Keyword: Alzheimers; Sexual Behavior
Link ID: 29968 - Posted: 10.15.2025

By Siddhant Pusdekar Taste and smell are so intimately connected that a whiff of well-loved foods evokes their taste without any conscious effort. Now, brain scans and machine learning have for the first time pinpointed the region responsible for this sensory overlap in humans, a region called the insula, researchers report September 12 in Nature Communications. The findings could explain why people crave certain foods or are turned away from them, says Ivan de Araujo, a neuroscientist at Max Planck Institute for Biological Cybernetics in Tübingen, Germany. Smell and taste become associated from the moment we bite into something, says Putu Agus Khorisantono, a neuroscientist at Karolinska Institutet in Stockholm. Some food chemicals activate sweet, salty, sour, bitter or umami taste receptors on the tongue. Others travel through the roof of the mouth, activating odor receptors in the back of the nose. These “retronasal odors” are what distinguish mangoes from peaches, for example. Both taste mostly sour, Khorisantono says, “but it’s really the aroma that differentiates them.” The brain combines these signals to create our sense of flavor, but scientists have struggled to identify where this happens in the brain. In the new study, Khorisantono and colleagues gave 25 people drops of beverages designed to activate only their taste or retronasal receptors, while scanning brain activity over multiple sessions. Previously, the participants had learned to associate the combination of smells and tastes with particular flavors. © Society for Science & the Public 2000–2025.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29967 - Posted: 10.11.2025

By Jennie Erin Smith The marine whiff of ambergris. The citrusy tang of grapefruit. The must of “corked” wine. The human nose can detect a virtually infinite palette of odors, some at vanishingly low concentrations. But puzzlingly, our bodies only use about 400 receptor proteins to interpret them. Now, fragrance researchers in Switzerland have landed on a new way to study the proteins in the laboratory—and their results, they say, challenge a foundational theory of how smell works. For decades, scientists have struggled to get cells commonly used in laboratory settings to express the genes that encode olfactory receptors (ORs), proteins primarily found on neurons in our nasal cavities. Using a process they describe today in Current Biology, researchers at the Swiss fragrance and flavorings company Givaudan say they have tweaked lab-friendly cells into readily expressing ORs. The result was an in vitro system for identifying specific ORs, including those that strongly respond to molecules in ambergris, grapefruit, and corked wine. The Swiss group’s discovery, other olfaction researchers say, stands to make ORs much easier to study. But more controversially, the group also claims to have observed patterns of receptor activity that call into question combinatorial coding, a long-standing hypothesis of olfaction that helped Linda Buck and Richard Axel win a Nobel Prize in 2004. Combinatorial coding holds that multiple ORs act in concert to pick up different parts of an odorant molecule, creating patterns or codes that are recognized by the brain. Beyond that, says neuroscientist Joel Mainland of the Monell Chemical Senses Center, the model is “pretty vague on the details.” It has been hard to test, because olfactory neurons can’t be cultured in the lab. Determining which OR detects which odorant required extensive tests in rodents, and it’s not ideal “to have to sacrifice an animal each time you want to do an experiment,” says Claire de March, a chemist at CNRS, the French national research agency. As a result, investigators were left with many so-called orphan receptors whose ligands, or binding molecules, are unknown. © 2025 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Development of the Brain
Link ID: 29966 - Posted: 10.11.2025