By Marija Kundakovic The role of sex and gender in the brain is a popular but controversial research topic. Neuroscience has a reputation for being male-centric and focused on studying male brains, although researchers have recently embraced the idea that it is critical to study female brains as well. Generally speaking, human female and male brains are morphologically similar, but that does not suggest they don’t differ in their activity and function, or in their underlying molecular and cellular mechanisms. In fact, sex and gender bias in neuropsychiatric conditions is the rule rather than the exception. Men are three to five times as likely as women to have autism or attention-deficit/hyperactivity disorder, for example, and women are twice as likely as men to have anxiety or depression disorders. Understanding the biological factors and mechanisms that underlie gender- and sex-related bias in brain function and psychiatric conditions is essential to improve our fundamental knowledge of the brain and to open a path to develop novel, sex-informed treatments. But simply including females in research studies is insufficient to resolve the role of sex and gender in neuroscience. “Sex” and “gender” are both complex and evolving concepts, extending beyond a simple binary. In practice, people are assigned female or male at birth based on external genitalia, although up to 2 percent do not belong to either category because of differences in sex development. Though gender has traditionally been co-assigned with sex—females/women and males/men—the binary nature of sex does not suffice to account for today’s expanding gender landscape. Gender exists on a spectrum, including nonbinary, gender-fluid and agender people. In transgender people, gender identity differs from gender or sex assigned at birth. Some researchers would say that this complexity cannot (and perhaps should not) be tackled by science, and that we should stick to scientifically discernible female-male comparisons, particularly in animal research. But science should not exist in a vacuum; when detached from society, it does not serve its purpose. Indeed, in the case of gender, biology can be falsely used to fuel discriminatory laws and practices against gender-diverse and gender-non-conforming people, supposedly based on a scientific understanding of “biological sex.” © 2025 Simons Foundation

Keyword: Sexual Behavior
Link ID: 29651 - Posted: 02.01.2025

By Jackson Ryan Fruit fly larvae can sense the texture of rotting fruit.Credit: Scott Bauer/USDA/SPL For maggots, the experience of eating a succulent meal isn’t just about how their food tastes, but also how it feels. Researchers used genetic tools to reveal that certain neurons in the brain control food choice and can sense both taste and texture1 . The conventional view of taste sensing holds that specific neurons carry single signals to the brain, says study co-author Simon Sprecher, a neurobiologist at the University of Fribourg in Switzerland. For instance, sweet taste neurons carry sweet signals and bitter taste neurons carry bitter signals. But those assumptions have been challenged over the past two decades by studies in fruit flies and mice that suggest neurons might have the capacity to respond to both chemical signals, such as bitter or sweet, as well as mechanical signals, such as texture. In the current study, published in PLoS Biology on 30 January, Sprecher and his colleagues set out to see whether individual neurons in taste organs have this ‘multimodal’ capacity. They fed fruit-fly larvae — maggots — different preparations of agarose, a sugary gel. The maggots showed a propensity for a ‘Goldilocks’ preparation, one that was neither too hard nor too soft. The preferred hardness for larvae is “similar to [that] of decaying fruit”, says Sprecher. The researchers then used genetic engineering tools to disable a subset of taste-sensing neurons in the larval taste-sensing organs. Disabling the neurons prevented the maggots from tasting the sweetness of the agarose, as expected, but it also changed which preparations they ate — the maggots no longer preferred Goldilocks preparations, suggesting that they had also lost their ability to feel their food. By studying individual neurons, the researchers determined that C6 neurons can both taste sugar and sense mechanical simulation. © 2025 Springer Nature Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29650 - Posted: 02.01.2025

Nicola Davis Science correspondent Wiggling your ears might be more of a pub party piece than a survival skill, but humans still try to prick up their ears when listening hard, researchers have found. Ear movement is crucial in many animals, not least in helping them focus their attention on particular noises and work out which direction they are coming from. But while the human ear is far more static, traces of our ancestors’ ear-orienting system remain in what has been called a “neural fossil”. “It is believed that our ancestors lost their ability to move their ears about 25m years ago. Why, exactly, is difficult to say,” said Andreas Schröer, the lead author of the research from Saarland University in Germany. “However, we have been able to demonstrate that the neural circuits still seem to be present in some state, [that is] our brain retained some of the structures to move the ears, even though they apparently are not useful any more.” The team previously found the movement of these muscles in humans is related to the direction of the sounds they are paying attention to. Now, they have found that some of these muscles become activated when humans listen hard to a sound. Writing in the journal Frontiers in Neuroscience, the team reported how they asked 20 adults without hearing problems to listen to an audiobook played through a speaker at the same time as a podcast was played from the same location. The team created three different scenarios: in the “easiest” scenario the podcast was quieter than the audiobook, with a large difference in pitch between the voices. In the “hardest” scenario, two podcasts were played which, taken together, were louder than the audiobook, with one of the podcasts spoken at a similar pitch to the audiobook. © 2025 Guardian News & Media Limited

Keyword: Hearing; Evolution
Link ID: 29649 - Posted: 02.01.2025

By Laura Sanders Scratching an itch can bring a contradictory wave of pleasure and misery. A mouse study on scratching, reported in the Jan. 31 Science, fleshes out this head-scratching paradox and could point out ways to better curb pernicious itch in people. First, the bad news: Scratching itchy ears led to a round of inflammation. Itch-provoking substances, such as the oil in poison ivy, activate mast cells, immune sentries that release itch signals and kick off inflammation. But so does scratching, the new study suggests. “The act of scratching is actually triggering the inflammation by synergizing with mast cells to make them more effective,” says study coauthor Daniel Kaplan, a dermatologist and immunologist at the University of Pittsburgh. Mice that couldn’t scratch their itchy ears, thanks to tiny cones of shame, had less inflammation than mice that scratched. The same was true for mice that didn’t sense the itch, the researchers report. Kaplan relates the results to a mosquito bite. “Most of the time, it’ll go away in five, 10 minutes,” he says. “But if you start scratching it, now, you get a really big, inflamed, itchy lesion on your skin that can stick around for several days. It’s a lot worse. And I think this could be a mechanism that explains why.” Now onto the good news: Scratching lessened the amount of potentially harmful bacteria (Staphylococcus aureus) on mice’s skin, perhaps through the heightened immune reaction it prompts. “That was a clear demonstration that scratching can have a benefit in the context of an acute infection,” Kaplan says. But too much scratching can rip the skin and usher in more bacteria, he cautions. “In that sense, scratching, through a different mechanism, also makes things even worse.” © Society for Science & the Public 2000–2025.

Keyword: Pain & Touch
Link ID: 29648 - Posted: 02.01.2025

By Katie J.M. BakerMegan TwoheyDanielle Ivory and Jeremy Singer-Vine At Stiiizy, the best-selling cannabis brand in America, the goal is explicit: producing powerful and cheap marijuana. Inside its Los Angeles headquarters, crews dust joints with concentrated THC, the intoxicating component of cannabis. They package pocket-size vape cartridges that promise “the highest potency possible.” On its website, the company declares that “it has never been easier (or quicker) to get silly high for an affordable price.” Dispensaries operating under the brand of another leading company, Cookies, have promoted “powerful medical benefits,” including “cancer fighting” qualities. A cannabis-infused chocolate bar was, until recently, described as containing properties “beneficial to those suffering” from glaucoma, bacterial infections and Huntington’s disease, a devastating genetic illness. More than a decade after states began legalizing recreational marijuana, businesses are enticing customers with unproven health claims, while largely escaping rigorous oversight. A New York Times review of 20 of the largest brands found that most were selling products with such claims, potentially violating federal and state regulations. And as companies compete, potency has gone up — with some products advertised as having as much as 99 percent THC — and prices have gone down. “What we’re seeing is really a race to the bottom,” said Matt Zehner, a senior analyst at Brightfield Group, which tracks the legal cannabis industry. Some executives said their companies are trying to navigate complex rules while satisfying their customers. Stiiizy’s co-founder and chief executive, James Kim, said in an interview that many are heavy users in search of a good deal, something he had sought as a broke “pothead” in his early 20s. “This is why I believe we’re very successful,” he said. But in a $32 billion industry that has been volatile — only about a quarter of businesses turned a profit last year, one survey found — companies say they also face pressure to do whatever they can to survive. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29647 - Posted: 01.29.2025

By Katharine Gammon Today more than 55 million people around the world have Alzheimer’s disease and other dementias, which ravage the minds of those who suffer from them and have devastating impacts on their family members. In spite of decades of research, the precise origins of these diseases continue to elude scientists, though numerous factors have been found to be associated with higher risk, including genetics and various lifestyle and environmental factors. Nautilus Members enjoy an ad-free experience. Log in or Join now . The quest has recently taken a turn to a newer model for studying the brain: brain organoids. These three-dimensional clumps of neuronal tissue derived from human stem cells have been used to study everything from epilepsy to the origins of consciousness. And now, researchers in Massachusetts are slamming them with miniature metal pistons to test out whether they can lend credence to a controversial hypothesis: that concussions might reactivate a common virus in the brain, increasing dementia risk. A decade of research suggests traumatic brain injury, whether from accidents or high-contact sports, is a standout risk factor for Alzheimer’s and other forms of neurodegenerative decline. Some estimates suggest that up to 10 percent of cases could be attributed to at least one prior head injury, but why is not fully understood. Separately, a growing body of research proposes that viral infection, including a common virus known as herpes simplex one, can also increase susceptibility to these diseases. But all three things—head trauma, viral infection, and dementia—have not been directly connected in experimental research, until now. One of the challenges in getting to the roots of dementia is that humans lead complex, messy lives. In the soup of risk factors—from high blood pressure to loneliness to genetic inheritance—it can be hard to filter out the most impactful forces that have contributed to the onset of any one dementia case. There are no ethical ways to test these questions on humans, of course, while using lab animals presents its own ethical and cost challenges. Animals are never a perfect match for humans anyway, and dementia-related findings in animals have so far not translated well to human patients. © 2025 NautilusNext Inc.,

Keyword: Alzheimers; Brain Injury/Concussion
Link ID: 29646 - Posted: 01.29.2025

By Katherine Ellison “American Ninja Warrior” contestant Jimmy Choi was 27 when he was diagnosed with young-onset Parkinson’s disease after a routine medical exam. Today, Choi, 50, is an adviser to the Michael J. Fox Foundation for Parkinson’s Research who champions physical fitness and works to inspire others via public speaking and social media posts. More than 1 million Americans have Parkinson’s disease, a neurological illness that can cause tremors, loss of balance, confusion and depression. Choi spent the eight years after his diagnosis in denial as his symptoms grew worse. After a mortifying fall, however, his perspective changed, and he embraced exercise — in a big way. Since 2011, the Chicago-based former tech executive (he retired from full-time work in 2018, though he still works as a consultant) has run 16 marathons and earned three Guinness World records, the most recent in 2023 for consecutive double high five push-ups. He has also competed seven times on “American Ninja Warrior,” the reality-TV show in which contestants make their way past daunting obstacles, crossing unstable bridges, running up walls and leaping through the air, all while trying to avoid falling into a large pool of water. Last year Choi finished his seventh, and, he insists, last “Ninja” appearance. It’s set to air this spring. Q: What led to your diagnosis? A: It was a routine exam for health insurance, in 2003. A nurse noticed the way I was walking and said I should talk to my doctor. I had to see four neurologists before I got diagnosed, and for several years afterward, I lost my motivation. I started isolating from friends, gained a lot of weight and couldn’t walk without a cane.

Keyword: Parkinsons
Link ID: 29645 - Posted: 01.29.2025

By Tina Hesman Saey After nearly 350 years, a depiction of a bee’s brain is getting some buzz. A manuscript created in the mid-1670s contains the oldest known depiction of an insect’s brain, historian of science Andrea Strazzoni of the University of Turin in Italy reports January 29 in Royal Society Notes and Records. Handwritten by Dutch biologist and microscopist Johannes Swammerdam, the manuscript contains a detailed description and drawing of a honeybee drone’s brain. The illustration, based on his own dissections, was just one of Swammerdam’s firsts. In 1658, he was also the first to see and describe red blood cells. Since no one had previously reported dissecting a bee brain, Swammerdam based his descriptions on what was known about the brain anatomy of humans and other mammals. “He knew what to expect from or to imagine in his observations: in particular, the pineal gland and the cerebellum,” Strazzoni writes. Bees have neither of those parts but have brain structures that the 17th century scientist mistook for them. But Swammerdam deserves some slack, Strazzoni suggests. He was working with single-lens microscopes and developing new techniques for dissecting and observing insects’ internal organs. Even with those crude instruments, he was able to identify some nerves and describe how parts of the brain connected. © Society for Science & the Public 2000–2025.

Keyword: Brain imaging; Evolution
Link ID: 29644 - Posted: 01.29.2025

By Ellen Barry A study of more than 30,000 British adults diagnosed with attention deficit hyperactivity disorder, or A.D.H.D., found that, on average, they were dying earlier than their counterparts in the general population — around seven years earlier for men, and around nine for women. The study, which was published Thursday in The British Journal of Psychiatry, is believed to be the first to use all-cause mortality data to estimate life expectancy in people with A.D.H.D. Previous studies have pointed to an array of risks associated with the condition, among them poverty, mental health disorders, smoking and substance abuse. The authors cautioned that A.D.H.D. is substantially underdiagnosed and that the people in their study — most of them diagnosed as young adults — might be among the more severely affected. Still, they described their findings as “extremely concerning,” highlighting unmet needs that “require urgent attention.” “It’s a big number, and it is worrying,” said Joshua Stott, a professor of aging and clinical psychology at University College London and an author of the study. “I see it as likely to be more about health inequality than anything else. But it’s quite a big health inequality.” The study did not identify causes of early death among people with A.D.H.D. but found that they were twice as likely as the general population to smoke or abuse alcohol and that they had far higher rates of autism, self-harming behaviors and personality disorders than the general population. In adulthood, Dr. Stott said, “they find it harder to manage impulses, and have more risky behaviors.” He said health care systems might need to adjust in order to better serve people with A.D.H.D., who may have sensory sensitivity or difficulty managing time or communicating with clinicians during brief appointments. He said he hoped treatments for substance abuse or depression could be adapted for patients with A.D.H.D. © 2025 The New York Times Company

Keyword: ADHD; Drug Abuse
Link ID: 29643 - Posted: 01.25.2025

By Shaena Montanari For evolutionary neuroanatomists who compare diverse animal brains, access to a gold mine of 500,000 histological sections and whole mounts is now only a mouse-click away. The R. Glenn Northcutt Collection of Comparative Vertebrate Neuroanatomy and Embryology at Harvard University—which comprises 33,000 slides of tissue samples from more than 240 vertebrate genera—is one of the world’s largest and most diverse collections of its kind. Northcutt, a prolific comparative vertebrate neuroanatomist and emeritus professor of neurosciences at the University of California, San Diego, amassed the collection over the course of five decades. Since 2021, James Hanken, research professor of biology at Harvard University and curator at the Museum of Comparative Zoology, has led an effort to digitize it. The scanning process is still ongoing and may take another two years to complete, Hanken says, but more than 8,000 slides are already publicly available in two online data repositories: MCZBase and MorphoSource. A comprehensive inventory of the entire collection appears in a paper Hanken and his colleagues published last week in the Bulletin of the Museum of Comparative Zoology. It provides researchers with an in-depth guide for using the collection, Hanken says. Few other resources of this type are available online to researchers interested in evolutionary biology and brain anatomy, says Andrew Iwaniuk, professor of neuroscience at the University of Lethbridge. For example, neither the Welker Comparative Anatomy Collection nor the Starr Collection, both housed at the U.S. National Museum of Health and Medicine in Silver Spring, Maryland, are available online. To access slide collections such as these, scientists have had to travel to see them in person, which can be difficult for those outside the United States, Iwaniuk adds. © 2025 Simons Foundation

Keyword: Brain imaging; Evolution
Link ID: 29642 - Posted: 01.25.2025

By Smriti Mallapaty For the first time, scientists have tracked microplastics moving through the bodies of mice in real time1. The tiny plastic particles are gobbled up by immune cells, travel through the bloodstream and eventually become lodged in blood vessels in the brain. It’s not clear whether such obstructions occur in people, say researchers, but they did seem to affect the mice’s movement. Microplastics are specks of plastic, less than 5 millimetres long, that can be found everywhere, from the deep ocean to Antarctic ice. They are in the air we breathe, the water we drink and the food we eat. They can even enter our bloodstreams directly through plastic medical devices. Studies show that microplastics, and smaller nanoplastics, have made their way into humans’ brains, livers and kidneys, but researchers are just beginning to understand what happens to these plastic intruders and their effect on human health. One study last year, for example, found that people with micro- and nano-plastics in fatty deposits in their main artery were more likely to experience a heart attack, stroke or death2. In the latest study, published in Science Advances today, Haipeng Huang, a biomedical researcher at Peking University in Beijing, and his colleagues wanted to better understand how microplastics affect the brain. They used a fluorescence imaging technique called miniature two-photon microscopy to observe what was happening in mouse brains through a transparent window surgically implanted into the animal’s skull. The imaging technique can trace microplastics as they move through the bloodstream, says Eliane El Hayek, an environmental-health researcher at University of New Mexico in Albuquerque. “It’s very interesting, and very helpful.” © 2025 Springer Nature Limited

Keyword: Neurotoxins; Stroke
Link ID: 29641 - Posted: 01.25.2025

By Meredith Wadman, Jocelyn Kaiser President Donald Trump’s return to the White House is already having a big impact at the $47.4 billion U.S. National Institutes of Health (NIH), with the new administration imposing a wide range of restrictions, including the abrupt cancellation of meetings such as grant review panels. Officials have also ordered a communications pause, a freeze on hiring, and an indefinite ban on travel. The moves have generated extensive confusion and uncertainty at the nation’s largest research agency, which has become a target for Trump’s political allies. “The impact of the collective executive orders and directives appears devastating,” one senior NIH employee says. Today, for example, officials halted midstream a training workshop for junior scientists, called off a workshop on adolescent learning minutes before it was to begin, and canceled meetings of two advisory councils. Panels that were scheduled to review grant proposals also received eleventh-hour word that they wouldn’t be meeting. “This kind of disruption could have long ripple effects,” says Jane Liebschutz, an opioid addiction researcher at the University of Pittsburgh who posted on Bluesky about the canceled study sections. “Even short delays will put the United States behind in research.” She and colleagues are feeling “a lot of uncertainty, fear, and panic,” Liebschutz says. The hiring freeze is governmentwide, whereas a pause on communications and travel appears to be limited to the Department of Health and Human Services (HHS), NIH’s parent agency. Such pauses are not unprecedented when a new administration comes in. But some NIH staff suggested these measures, which include pulling job ads and rescinding offers, are more extreme than any previously. Researchers who planned to present their work at meetings must cancel their trips, as must NIH officials promoting agency programs off site or visiting distant branches of the agency. “Future travel requests for any reason are not authorized and should not be approved,” the memo said.

Keyword: Miscellaneous
Link ID: 29640 - Posted: 01.25.2025

By Yasemin Saplakoglu Imagine you’re on a first date, sipping a martini at a bar. You eat an olive and patiently listen to your date tell you about his job at a bank. Your brain is processing this scene, in part, by breaking it down into concepts. Bar. Date. Martini. Olive. Bank. Deep in your brain, neurons known as concept cells are firing. You might have concept cells that fire for martinis but not for olives. Or ones that fire for bars — perhaps even that specific bar, if you’ve been there before. The idea of a “bank” also has its own set of concept cells, maybe millions of them. And there, in that dimly lit bar, you’re starting to form concept cells for your date, whether you like him or not. Those cells will fire when something reminds you of him. Concept neurons fire for their concept no matter how it is presented: in real life or a photo, in text or speech, on television or in a podcast. “It’s more abstract, really different from what you’re seeing,” said Elizabeth Buffalo (opens a new tab), a neuroscientist at the University of Washington. For decades, neuroscientists mocked the idea that the brain could have such intense selectivity, down to the level of an individual neuron: How could there be one or more neurons for each of the seemingly countless concepts we engage with over a lifetime? “It’s inefficient. It’s not economic,” people broadly agreed, according to the neurobiologist Florian Mormann (opens a new tab) at the University of Bonn. But when researchers identified concept cells in the early 2000s, the laughter started to fade. Over the past 20 years, they have established that concept cells not only exist but are critical to the way the brain abstracts and stores information. New studies, including one recently published in Nature Communications, have suggested that they may be central to how we form and retrieve memory. © 2025 Simons Foundation

Keyword: Learning & Memory; Attention
Link ID: 29639 - Posted: 01.22.2025

By Holly Barker Previously unrecognized genetic changes on the X chromosome of autistic people could explain the higher prevalence of the condition among men and boys than among women and girls, according to two new studies. About 60 variants are more common in people with autism than in those without the condition, an analysis of roughly 15,000 X chromosomes revealed. Several of the variants are in Xp22.11, a region of the X chromosome linked to autism in boys and men. In the second study, the team pinpointed 27 autism-linked variants in DDX53, one of the genes in the vulnerable region that had not been tied to the condition in past research. Those findings could help explain why autism is diagnosed three to four times more often in boys than girls, according to the study investigators, led by Stephen Scherer, chief of research at SickKids Research Institute. Although that disparity is likely influenced by social factors—male-only studies could lead to autism being less recognizable in women and girls, and girls may be conditioned to mask their autism traits—there is also a clear biological component. The X chromosome plays an outsized role in brain development, and many genes on the chromosome are strongly linked to autism, previous studies have found. Still, the sex chromosomes have been mostly ignored in genetic searches of autism variants, says Aaron Besterman, associate clinical professor of psychiatry at the University of California, San Diego, who was not involved in the work. “It’s been a dirty little secret that for a long time the X chromosome has not been well interrogated from a genetics perspective,” he says. Sex chromosomes are often sidelined because of difficulties interpreting data, given that men possess half the number of X-linked genes as women. What’s more, random inactivation of X chromosomes makes it hard to tell how a single variant is expressed in female tissues. And the existence of pseudoautosomal regions—stretches of DNA that behave like regular chromosomes and escape inactivation—complicates matters further. © 2025 Simons Foundation

Keyword: Autism; Sexual Behavior
Link ID: 29638 - Posted: 01.22.2025

Hannah Devlin Science correspondent A groundbreaking NHS trial will attempt to boost patients’ mood using a brain-computer-interface that directly alters brain activity using ultrasound. The device, which is designed to be implanted beneath the skull but outside the brain, maps activity and delivers targeted pulses of ultrasound to “switch on” clusters of neurons. Its safety and tolerability will be tested on about 30 patient in the £6.5m trial, funded by the UK’s Advanced Research and Invention Agency (Aria). In future, doctors hope the technology could revolutionise the treatment of conditions such as depression, addiction, OCD and epilepsy by rebalancing disrupted patterns of brain activity. Jacques Carolan, Aria’s programme director, said: “Neurotechnologies can help a much broader range of people than we thought. Helping with treatment resistant depression, epilepsy, addiction, eating disorders, that is the huge opportunity here. We are at a turning point in both the conditions we hope we can treat and the new types of technologies emerging to do that.” The trial follows rapid advances in brain-computer-interface (BCI) technology, with Elon Musk’s company Neuralink launching a clinical trial in paralysis patients last year and another study restoring communication to stroke patients by translating their thoughts directly into speech. However, the technologies raise significant ethical issues around the ownership and privacy of data, the possibility of enhancement and the risk of neuro-discrimination, whereby brain data might be used to judge a person’s suitability for employment or medical insurance. © 2025 Guardian News & Media Limited

Keyword: Depression; Brain imaging
Link ID: 29637 - Posted: 01.22.2025

By Angie Voyles Askham More than 150 years after the first known description of Huntington’s disease and 32 years after the causative gene, HTT, was identified, new evidence has emerged to explain how variants linked to the disease devastate the brain: The toxicity comes not from the initial variant itself but rather from its dynamic expansion past a set threshold in specific cells, according to a study published today in Cell. The results help explain why most people with Huntington’s disease don’t start to show symptoms—including muscle rigidity, irregular movements and severe psychological issues—until age 30 to 50, with the gradual loss of striatal projection neurons, also called medium spiny neurons, says co-lead researcher Steven McCarroll, professor of biomedical science and genetics at Harvard Medical School. “We hadn’t been thinking about mutations as dynamic things” that become toxic only later in life, he says. The HTT variants associated with Huntington’s disease all have extra repeats of the DNA triplet CAG. Typical people carry about 15 to 30 of these repeats, and those with the disease tend to have 40 or more. The disease-linked expansions, which are known to grow even larger over time, result in a gangly version of the Huntington’s protein that is thought to cause neurons to malfunction and degenerate. But the expansion does not appear to affect a cell’s biology until it exceeds 150 CAG copies, according to the new study. And the repeats accumulate quietly over the course of years, and at different rates for different cells. Striatal projection neurons with more than 150 repeats have severely dysregulated transcriptomes, McCarroll and his colleagues found by analyzing gene expression in postmortem tissue from people with Huntington’s disease. But other cell types in the striatum, including oligodendrocytes and interneurons, do not end up with as many repeats, nor do they undergo similar transcriptomic changes, the work shows. © 2025 Simons Foundation

Keyword: Huntingtons; Genes & Behavior
Link ID: 29636 - Posted: 01.22.2025

Rachael Elward Lauren Ford Severance, which imagines a world where a person’s work and personal lives are surgically separated, will soon return to Apple TV+ for a second season. While the concept of this gripping piece of science fiction is far-fetched, it touches on some interesting neuroscience. Can a person’s mind really be surgically split in two? Remarkably, “split-brain” patients have existed since the 1940s. To control epilepsy symptoms, these patients underwent a surgery to separate the left and right hemispheres. Similar surgeries still happen today. Later research on this type of surgery showed that the separated hemispheres of split-brain patients could process information independently. This raises the uncomfortable possibility that the procedure creates two separate minds living in one brain. In season one of Severance, Helly R (Britt Lower) experienced a conflict between her “innie” (the side of her mind that remembered her work life) and her “outie” (the side outside of work). Similarly, there is evidence of a conflict between the two hemispheres of real split-brain patients. When speaking with split-brain patients, you are usually communicating with the left hemisphere of the brain, which controls speech. However, some patients can communicate from their right hemisphere by writing, for example, or arranging Scrabble letters. A young patient was asked what job he would like in the future. His left hemisphere chose an office job making technical drawings. His right hemisphere, however, arranged letters to spell “automobile racer”. Split brain patients have also reported “alien hand syndrome”, where one of their hands is perceived to be moving of its own volition. These observations suggest that two separate conscious “people” may coexist in one brain and may have conflicting goals. In Severance, however, both the innie and the outie have access to speech. This is one indicator that the fictional “severance procedure” must involve a more complex separation of the brain’s networks. © 2010–2025, The Conversation US, Inc.

Keyword: Learning & Memory; Consciousness
Link ID: 29635 - Posted: 01.18.2025

By Phie Jacobs For more than 30 years, scientists have known the genetic culprit behind Huntington disease, a devastating neurodegenerative disorder that causes cells deep in the brain to sicken and die. But they couldn’t account for why people who inherit the faulty gene variant take so long to develop symptoms, or why disease progression varies so widely from person to person. A study published today in Cell helps explain: In the brain cells that die off in Huntington, a repetitive stretch of a gene’s DNA gets longer and longer over a person’s life, and this accelerating expansion turns deadly to the cell—and ultimately to the person. The findings represent “a really remarkable insight,” says Leslie Thompson, a neuroscientist at the University of California, Irvine who wasn’t involved in the new research. “This study and some others are changing the way that we’re thinking about the disease.” People who develop Huntington inherit a flawed version of the HTT gene, which produces a protein called huntingtin. This gene contains an unusual stretch of DNA, where a sequence of three of its nucleotide bases—cytosine, adenine, and guanine, or CAG in genetic parlance—are repeated multiple times in a row. And although most people inherit versions of HTT with about 15 to 30 consecutive CAG repeats and never develop Huntington, those with 40 or more in the gene almost always have symptoms later in life, including psychological and cognitive problems and uncontrolled, jerking movements known as chorea. The genetic stutter produces an abnormally large, unstable version of the huntingtin protein, which forms clumps inside brain cells. The condition usually leads to early death, often from issues related to difficulty swallowing, injuries from falls, or suicide. The longer a person’s stretch of repeats, the earlier the disorder rears its head. Scientists originally thought the number of CAG repeats only increased as the HTT gene was passed down through generations; a child of a parent with Huntington might themselves develop the condition at an earlier age. But it turns out the length of this genetic “stutter” can change over a person’s life in at least some of their cells. A 2003 study analyzed brain samples donated by people who had died of Huntington and found shockingly large CAG expansions in a part of the brain known as the striatum.

Keyword: Huntingtons; Genes & Behavior
Link ID: 29634 - Posted: 01.18.2025

By Anna Victoria Molofsky Twenty years ago, a remarkable discovery upended our understanding of the range of elements that can shape neuronal function: A team in Europe demonstrated that enzymatic digestion of the extracellular matrix (ECM)—a latticework of proteins that surrounds all brain cells—could restore plasticity to the visual cortex even after the region’s “critical period” had ended. Other studies followed, showing that ECM digestion could also alter learning in the hippocampus and other brain circuits. These observations established that proteins outside neurons can control synaptic plasticity. We now know that up to 20 percent of the brain is extracellular space, filled with hundreds of ECM proteins—a “matrisome” that plays multiple roles, including modulating synaptic function and myelin formation. ECM genes in the human brain are different than those in other species, suggesting that the proteins they encode could be part of what makes our brains unique and keeps them healthy. In a large population study, posted as a preprint on bioRxiv last year, that examined blood protein biomarkers of organ aging, for example, the presence of ECM proteins was most highly correlated with a youthful brain. Matrisome proteins are also dysregulated in astrocytes from people at high risk for Alzheimer’s disease, another study showed. Despite the influence of these proteins and the ongoing work of a few dedicated researchers, however, the ECM field has not caught on. I would challenge a room full of neuroscientists to name one protein in the extracellular matrix. To this day, the only ECM components most neuroscientists have heard of are “perineuronal nets”—structures that play an important role in stabilizing synapses but make up just a tiny fraction of the matrisome. A respectable scientific journal, covering its own paper that identified a critical impact of ECM, called it “brain goop.” © 2025 Simons Foundation

Keyword: Learning & Memory; Glia
Link ID: 29633 - Posted: 01.18.2025

By Aimee Cunningham If cigarettes contained very little of the chemical that keeps people smoking, it could help smokers move away from these deadly products. That’s the rationale behind a new rule proposed on January 15 by the U.S. Food and Drug Administration, which seeks to limit the amount of the addictive chemical nicotine in cigarettes. The reduced-nicotine cigarettes would have less than 5 percent of the amount of nicotine that’s generally found in regular cigarettes. The rule would also cap the nicotine in certain other products in which the tobacco leaves are burned. The FDA rule is just one step toward reduced-nicotine cigarettes and other combusted tobacco products becoming the standard. This process would probably take many years, depending on the priorities of future administrations and whether the tobacco industry challenges the rule in court, as it has the FDA’s rule placing graphic warning labels on their products. The 2009 Family Smoking Prevention and Tobacco Control gave the FDA the authority to require graphic warning labels and to reduce nicotine in tobacco products. The idea for a nicotine limit has been around for decades. And the evidence supporting drastically lowering the amount of nicotine in combusted tobacco products has grown during that time. Randomized controlled trials of reduced-nicotine cigarettes report that people using them end up smoking fewer cigarettes per day. That’s also the case for studies that focused on groups at higher risk for smoking, including people who are socioeconomically disadvantaged and people with mental health conditions. © Society for Science & the Public 2000–2025.

Keyword: Drug Abuse
Link ID: 29632 - Posted: 01.18.2025