By Carl Zimmer and Carolyn Y. Johnson In order to learn more about brain disorders, scientists reported on Wednesday that they had created extraordinary mice whose brains are filled with millions of human neurons. The work marks a startling advance in replicating the complexities of the human brain outside the body. The research, described in the journal Nature, also poses some profound questions. “Will there be some enhancement of function?” asked Dr. Sergiu Pașca, the Stanford University neuroscientist who led the work. “Will they do better than other mice?” Dr. Pașca and his colleagues have consulted regularly with ethicists about the implications of their research. And they’ve kept careful watch on the mice, analyzing their behavior. So far, they behave mostly as if they had ordinary mouse brains. “You wouldn’t be able to tell the difference,” Dr. Pașca said. Other experts not involved in the study agreed. “It may have a large proportion of its brain made up of human cells, but none of its behavior is made up of human behavior,” said Madeline Lancaster, a developmental neurobiologist at the Medical Research Council Laboratory of Molecular Biology in the United Kingdom. Dr. Pașca spent years creating these mice for one reason: It is bogglingly hard to study human brain diseases. Our brains contain about 80 billion neurons, joined by trillions of connections into intricate circuits. Some scientists suspect that when those networks go awry, they give rise to conditions such as schizophrenia and autism. “Neuropsychiatric disorders are largely disorders of circuits,” Dr. Pașca said. © 2026 The New York Times Company

Keyword: Development of the Brain
Link ID: 30416 - Posted: 09.19.2026

Lynne Peeples For decades, many scientists have thought that a single type of starter cell gives rise to the entire brain. But experiments now challenge that fundamental picture, providing evidence that it takes not one but two flavours of progenitor cell to make the complex organ1. The research suggests that one type of precursor cell forms the segment called the hindbrain, which is crucial for basic functions such as heartbeat and breathing. A second type of precursor cell, meanwhile, generates two structures: the forebrain, a central player in higher-order functions such as reasoning and planning, and the midbrain. The work was published today in Nature Neuroscience. “The brain is one organ,” says study co-author Kyle Loh, a development biologist at Stanford University in California. “But it’s built in two different parts that connect and work together.” Not everyone agrees with the study’s conclusion that the brain is descended from two cell populations that don’t mix. But the work does draw broad praise for one aspect: the authors found an efficient way to coax stem cells to grow into hindbrain motor-neuron cells, which help to control movements such as swallowing. That could aid research into diseases that affect these cells, including debilitating neurodegenerative conditions such as motor neuron disease, also known as amyotrophic lateral sclerosis (ALS). Earlier research2 in mouse embryos identified one trademark gene that is broadly expressed in brain-precursor cells. Other work pinpointed a gene expressed in precursor cells destined to form the front of the brain3 and a separate gene expressed in cells destined to form the back4. Yet it remained unclear whether these distinct populations were strictly committed to the brain regions that they were marked for. © 2026 Springer Nature Limited

Keyword: Development of the Brain
Link ID: 30415 - Posted: 09.19.2026

Miryam Naddaf More than 1,000 previously overlooked ‘microproteins’ have been found in samples of human brain tissue, providing researchers with the most comprehensive database yet to study these hidden molecules inside the human brain. Dozens of the tiny proteins showed altered expression in people with Alzheimer’s disease, which could pave the way to unlocking new mechanisms of ageing and neurodegeneration. Microproteins are small proteins with fewer than 150 amino acids and are notoriously difficult to detect with standard gene and protein sequencing techniques. In a study published in Nature Aging on 14 September1, researchers combined several methods to pinpoint the tiny molecules in postmortem samples of the dorsolateral prefrontal cortex — a region of the brain involved in cognitive control — from people with and without Alzheimer’s disease. The team identified more than 4,300 microproteins, creating the largest atlas of microproteins in Alzheimer’s disease made so far. “We might be actually missing a whole layer of biology by overlooking these microproteins,” says Bahareh Ajami, a neuroimunologist at Cedars-Sinai Medical Center in Los Angeles, California. “Alzheimer’s disease is a proteinopathy [wherein] the pathology is in part due to the proteins that have misfolded or accumulated and evoked a toxic response,” says study co-author Brendan Miller, a neuroscientist at the Salk Institute for Biological Studies in San Diego, California. “It should be somewhat urgent to understand the full proteome”, including microproteins, he adds. © 2026 Springer Nature Limited

Keyword: Alzheimers
Link ID: 30412 - Posted: 09.16.2026

By Paul Frankland, Sheena Josselyn, Nick Turk-Browne What is your first memory? A birthday party, a fall in the playground, a family trip? For most people, it dates to around age 3 or 4 at the earliest. Infant and toddler experiences are, seemingly, absent from our autobiography. Sigmund Freud named this phenomenon infantile amnesia and argued that early-life memories are so emotionally charged that they must be actively repressed. In this view, infants are capable of forming memories for important life events, but these memories become inaccessible over time (although he argued that psychotherapy might, in principle, recover them). More contemporary psychological accounts have linked infantile amnesia to the immaturity of the hippocampus, a brain structure critical for forming episodic memories in older children and adults. According to these accounts, hippocampal circuits are not sufficiently developed in infancy to form enduring traces of life events. That is, infantile amnesia reflects a failure to encode experiences. Here, we argue for a different view. Early-life experiences are encoded by the hippocampus and may persist over time. What changes is how easily they can be accessed. Infantile amnesia, therefore, reflects not a failure to encode memories but a failure to naturally retrieve them. Infantile amnesia is not uniquely human. Nearly all mammals that have been studied exhibit accelerated forgetting in infancy. For example, similar to young children, mice and rats can form memories of specific events, but these memories do not endure. This phenomenon has been demonstrated across a range of infant-acquired experiences, including fear conditioning, object recognition and spatial learning. The exception is highly precocial animals, such as guinea pigs and degus, whose brains are much more mature at birth. . © 2026 Simons Foundation

Keyword: Learning & Memory; Development of the Brain
Link ID: 30410 - Posted: 09.16.2026

By Bridget Alex One of the biggest downsides of upright walking in humans is the so-called obstetrical dilemma. Babies born with big brains—and thus big heads—must fit through a relatively narrow pelvis shaped for bipedal locomotion. These clashing demands, it’s been suggested, have made human births especially grueling compared with other mammals. But recent studies have questioned the simplicity of this explanation—and whether the phenomenon is even unique to humans. Reporting this month in The Anatomical Record, researchers add another wrinkle to the obstetrical dilemma: fetal sex. Reviewing birth data for 140 species, the authors argue sons are more difficult to birth than daughters for many mammals, including humans and our ancient ancestors. This added risk may be offset by an evolutionary reward: Bigger male babies grow into bigger male adults, who tend to have more grandbabies, meaning more of that mother’s genes are passed down. “Natural selection doesn’t care if it’s easy. It cares if it works,” says Anna Warrener, an anthropologist at the University of Colorado Denver who was not involved with the study. Still, she says the authors may be overinterpreting their finding. Every day, about 700 people die giving birth around the world. A leading cause is obstructed labor, often due to the baby’s head exceeding the size of the birth canal. Even successful births require fetal acrobatics to navigate the narrow path from womb to world: Babies typically enter the pelvis sideways, twist, and rotate as they emerge. Anthropologists have long assumed such perilous births evolved through a tug-of-war between two demands: large brains and upright walking, which favors a pelvis that’s scrunched front to back. Difficult births are not unique to humans, however. © 2026 American Association for the Advancement of Science.

Keyword: Evolution; Development of the Brain
Link ID: 30403 - Posted: 09.12.2026

Kat Lay, Global health correspondent Babies born to mothers with anaemia have smaller brains, particularly in key regions linked to movement, learning and the regulation of emotion, according to a study. Researchers said the differences, first detected at the age of one, could lead to cognitive problems when children started school. More than a third of pregnant women worldwide have anaemia – a condition typically caused by iron deficiency in which the number of red blood cells in the body is lower than normal. Symptoms include fatigue, shortness of breath and dizziness. Rates are highest in sub-Saharan Africa and south Asia. Researchers from King’s College London in the UK, and the University of Cape Town in South Africa, followed more than 300 mothers and their babies in Cape Town, scanning the brains of the infants several times between the ages of three months and two years. On average, the total brain volume of babies born to anaemic mothers was 4% lower than that of babies born to non-anaemic mothers – despite all the anaemic mothers being diagnosed only with a mild version of the condition. Differences were recorded in three specific regions of the brain: the putamen, caudate nucleus and corpus callosum. “All three of these brain regions are implicated in key neuropsychological functions,” said Jessica Ringshaw, first author and researcher at King’s Institute of Psychiatry, Psychology & Neuroscience (IoPPN) and the University of Cape Town, citing processing speed, emotion regulation and executive function as examples. © 2026 Guardian News & Media Limited

Keyword: Development of the Brain
Link ID: 30402 - Posted: 09.09.2026

By Jennie Erin Smith A few years ago, scientists saw something surprising in the brain tissue of people who died with Alzheimer’s disease: white blood cells that multiply in response to foreign threats and are seldom seen inside healthy brains. Whether these so-called CD8+ killer T cells, which normally target infected cells in the body, were there to harm or help was unclear. An answer began to emerge in 2023, when a team led by neuroscientist David Holtzman showed that in mice bred to overexpress tau—a toxic protein that builds up in the neurons of people with Alzheimer’s and several other neurodegenerative diseases—getting rid of the T cells stemmed tissue loss and preserved the mice’s cognition, even as tau kept building up. Now, the same group has explored what prompts these cells to wreak havoc in the brain. In a mouse study published last week in Nature Neuroscience, Holtzman and immunology researcher Hao Hu, both at Washington University in St. Louis, report that immune cells in the lymph nodes of the neck instruct the T cells to clone themselves before they enter the brain. Without them, the mice had far fewer cloned T cells inside their brains and experienced less neurodegeneration. The study is “beautiful work,” says neuroscientist Kenneth Kosik of the University of California, Santa Barbara, who studies tau but was not involved in the research. It also suggests that existing drugs, developed for other conditions, might work in Alzheimer’s by shielding the brain from the destructive cells. The new study homes in on a type of dendritic cells, immune cells that, in effect, give the killer T cells their orders. After cutting up the invader’s proteins, the dendritic cells present the antigens as bite-size pieces that T cells can recognize. T cells with compatible receptors can then become activated, which causes the cells to start to clone themselves, attack cells bearing the antigen, and cause inflammation. © 2026 American Association for the Advancement of Science.

Keyword: Neuroimmunology; Alzheimers
Link ID: 30401 - Posted: 09.09.2026

By Emily Baumgaertner Nunn Are you naturally anxious? Highly adventurous? More argumentative than you’d like to admit? Those tendencies are often measured through what psychologists call the “Big Five” dimensions of personality: extroversion, agreeableness, conscientiousness, neuroticism and openness to experience. Each trait exists on a continuum and tends to remain fairly stable throughout adult life. But what determines where you land on those spectra? Scientists have long known that personality is influenced by a host of factors — including DNA. The challenge has been deciphering the specific pathways through which a genetic blueprint nudges the direction of a person’s life. To map this sprawling architecture, a group of experts formed a research consortium and analyzed more than one million genomes, searching for variants associated with personality. The researchers also compared the genes of thousands of siblings and parent-child pairs to rule out other factors that could be at play. With data from 46 different study cohorts, they found a symphony of 1,260 genetic markers tied to personality, nearly two-thirds of them identified for the first time. The findings, published on Wednesday in the journal Nature, reaffirmed scientists’ understanding that temperament and disposition are shaped not by a few particular genes, but by thousands of tiny variants that can be expressed in different circumstances. The sheer scale of the project also brought new statistical power to the study of personality genetics, giving researchers a tool kit to investigate the biological mechanisms behind how we think, feel and behave. “I view the 1,260 variants as kind of a testament to the fact that we’ve now got the power to answer all of these other questions that we couldn’t answer before,” said Elliot Tucker-Drob, a professor of psychology at the University of Texas at Austin and a leader of the study. © 2026 The New York Times Company

Keyword: Emotions; Genes & Behavior
Link ID: 30395 - Posted: 09.05.2026

By Carl Zimmer and Azeen Ghorayshi Scientists have uncovered a wealth of clues about how genetic mutations lead to severe forms of autism, offering opportunities for testing drugs that could treat the condition, according to a study published Thursday. The researchers charted how mutations change the way proteins work together in cells, altering the development of the brain. “This is making maps of unknown territories that’s really necessary to move the biology forward,” said Dan Geschwind, a neurogeneticist at the University of California, Los Angeles, who was not involved in the study. Researchers have been studying autism for over 80 years, but it has only been in recent years that they have been able to explore its molecular biology. One reason that progress has been so slow is that autism is not just one condition, but a broad constellation of them. People with autism can have difficulty with language and making social connections, and often display restricted or repetitive behaviors. While many children with an autism diagnosis can grow up to lead independent adult lives, others may be nonspeaking, have intellectual disabilities, and require round-the-clock care. But in around 30 percent of people diagnosed with autism, typically those with the most severe disabilities, scientists have identified single gene mutations that are almost guaranteed to cause the disorder. When those genes started coming to light 20 years ago, scientists eagerly hoped they could find precise treatments for severe autism. In some studies, they engineered mice with the mutations and then tried different drugs to reverse their autism-like symptoms. But those efforts have not led to any effective treatment targeting a specific gene. © 2026 The New York Times Company

Keyword: Autism; Genes & Behavior
Link ID: 30390 - Posted: 08.29.2026

By Claudia López Lloreda The proteins encoded by 100 genes involved in autism form an interconnected network consisting of multiple protein complexes that serve different cellular functions, according to a study published today in Science. Autism-associated variants may cause this network to rewire, the study also found. Even though autism is a genetically heterogeneous condition, “when you look at the proteins encoded by the genes, and also the specific mutations and the interfaces of protein interactions, the biology starts to converge,” says Kasper Lage, managing director of the Novo Nordisk Foundation Center at the Broad Institute, who was not involved in the work. Many of the proteins the study considered converge on complexes already associated with autism and that are involved in processes such as neural progenitor proliferation and differentiation and neuronal migration, the researchers found. The idea behind the work was to go beyond the genetic studies, which have linked about 250 genes to autism, says study investigator Belinda Wang, assistant professor of psychiatry at the University of California, San Francisco. “Genes can tell us where autism risk begins, but proteins do a lot of the work inside the cells, and so by studying autism at the protein level, maybe this can give us a more direct view of the underlying biology.” Previous network analyses did not reach this magnitude, Lage says. “When you get to the scale that they’re doing in this paper, you can start to do really interesting secondary analysis and pathway and discovery.” © 2026 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 30388 - Posted: 08.29.2026

By Claudia López Lloreda For five years, several small batches of cortical organoids grew in an isolated incubator, away from possible contamination and doted upon by a Harvard University research team. The organoids didn’t merely survive, though—they generated diverse neurons and glia and acquired transcriptional and epigenetic features of postnatal brains, all on a human-like schedule, according to a new study published today in Nature. Organoids typically model only pre- and perinatal brains and notoriously lack robust electrical activity, says In-Hyun Park, associate professor of neuroscience and genetics at Yale University, who was not involved with the study. The new work provides an avenue to study postnatal stages of development, he says. However, the long-lived organoids started losing neuronal signals around the one-year mark, which continued as they aged, the team found. “Yes, the organoid was maturing, everything was great, but the neurons were suffering,” says study investigator Paola Arlotta, professor of stem cells and regenerative biology at Harvard. Modifying the culture medium enabled the team to grow a new set of organoids that had more mature excitatory neurons, greater neuronal complexity and enhanced electrical activity. “If you want to move forward with more network activity, mature human neurons, you need to adapt your tissue culture,” says Alysson Muotri, professor of pediatrics and cellular and molecular medicine at the University of California, San Diego, who was not involved with the study. “I think it’s an important message.” © 2026 Simons Foundation

Keyword: Development of the Brain
Link ID: 30382 - Posted: 08.22.2026

By Aimee Cunningham In 2025, the number of children receiving a drug promoted — but unproven — for autism treatment grew, especially toward the end of the year. A new study suggests the late rise was influenced by a Trump administration announcement. At a White House briefing on September 22, 2025, President Trump touted the drug leucovorin as a potential therapeutic for autism. The week before the announcement, roughly 5 children per 100,000 received leucovorin via a prescription in the United States. The week of the announcement, the pharmacy dispensing rate climbed to roughly 7 children per 100,000. By the end of the year, the rate rose to 8 children per 100,000, researchers reported August 12 in the New England Journal of Medicine. “Our study demonstrates the power of the federal government to influence clinical practice,” says Kao-Ping Chua, a pediatrician and health policy researcher at the University of Michigan Medical School in Ann Arbor. If administration communications and decisions are not based on rigorous scientific evidence, it could lead to harms “including giving people false hope and potentially exposing them to the side effects of ineffective medical treatments.” Leucovorin is a form of the essential vitamin folic acid. The drug is prescribed when the body’s method for breaking down folic acid from food is impaired. The U.S. Food and Drug Administration had approved leucovorin for use with certain genetic disorders and to help reduce the side effects of chemotherapy drugs that disrupt that break down. The American Academy of Pediatrics does not recommend leucovorin for autism because of the lack of evidence surrounding dosing, effectiveness and safety. © Society for Science & the Public 2000–2026.

Keyword: Autism
Link ID: 30380 - Posted: 08.22.2026

By Zoe Beketova Efforts to explain rising rates of myopia, or nearsightedness, in children worldwide have made two things clear: More time spent outdoors seems protective, and more time spent indoors increases risk. A new study in tree shrews now suggests a key to preventing myopia may be the indigo portion of sunlight. Adding this part of the light spectrum to the animals’ environment prevented them from developing myopia, researchers report today in Cell Reports Medicine. The findings have not yet been confirmed in humans, but some researchers are cautiously optimistic that increasing children’s exposure to indigo wavelengths could preserve their developing vision as well. “No one knows why outdoor light is good for kids’ eyes,” says Lisa Ostrin, a vision scientist at the State University of New York College of Optometry, who was not involved in the study. “If it turns out to be [the presence of certain wavelengths], it could be so simple to just add in overhead lights and enhance them with additional short wavelengths.” But she stresses that more research is needed to draw that conclusion. Myopia, or nearsightedness, affects almost 3 billion people worldwide, and this number is projected to climb to almost 5 billion by 2050. The condition occurs when the eyeball grows too long in childhood, instead of developing its typical spherical shape. This causes light to focus in front of the retina, the light-sensing layer of tissue along the back of the eye, instead of directly on it, making the resulting image transmitted to the brain unclear. Human genetics do not change fast enough over time to account for the rising rates, which some have blamed on increased reading or computer screen use. Others have said greater exposure to indoor light, with its more limited spectrum of wavelengths compared with outdoor light, could be the problem. © 2026 American Association for the Advancement of Science.

Keyword: Vision; Development of the Brain
Link ID: 30377 - Posted: 08.19.2026

By Siddhant Pusdekar Visual experiences during early life famously shape cortical circuits. Animals deprived of vision in one eye rewire their cortex to favor the other eye, according to Nobel Prize-winning work by Hubel and Wiesel. And animals raised in controlled visual environments—surrounded by vertical stripes or horizontal ones, for example—adjust their cortical neurons’ orientation tuning. This kind of experience-dependent plasticity also occurs in the retina itself, leading to lasting changes in behavior, according to a recent zebrafish study in Neuron. The sensory structure had long been thought to be hardwired. “The field in general doesn’t think that activity has any effect on the retina, and it’s always [acting] downstream,” says Marla Feller, professor of neuroscience at University of California Berkeley, who wasn’t involved in the study. Previous research suggests that waves of spontaneous neuronal activity in the retina that begin prenatally and continue till mice open their eyes help shape visual circuitry. The new work is the first to show that what an animal sees can prompt retinal activity that changes the shape and function of its interneurons, altering downstream processes including behavior, Feller says. Vertebrates share many aspects of wiring in the retina, where layers of interneurons transform the pixel-like input from photoreceptors into distinct information channels encoding features of the visual environment. This commonality includes amacrine cells, which are one of the most diverse kinds of interneurons, says Robert Hindges, professor of developmental neurobiology at King’s College London and an investigator on the new study. © 2026 Simons Foundation

Keyword: Development of the Brain; Vision
Link ID: 30373 - Posted: 08.15.2026

Elie Dolgin The video opens with a man in his 80s slumped in a hospital bed, his face hollow as he scrunches his eyes. A jump cut advances the scene three days: the man is alert now, words gathering as he identifies his son. Six months later, he is pictured sitting upright, engaged in conversation. His gaze is animated. At eight months, the man walks briskly down a hospital corridor. He recites a near-century-old Maoist military anthem from memory. He is practically unrecognizable from the withered figure in the opening frame. The footage records the recovery of a man who, in September 2020, became the first person in the world to undergo a surgery known as deep cervical lymphatic-venous anastomosis (dcLVA) to treat Alzheimer’s disease. The procedure involves connecting tiny lymphatic vessels in the neck — part of the drainage system that carries waste away from the brain — to nearby veins, creating a route that, in theory, allows fluid and waste proteins to flow more easily into the bloodstream. The treatment was first reported1 in 2022 in a Chinese-language journal by microsurgeon Qingping Xie, president of the Qiushi Hospital in Hangzhou, China. At the time, it drew little notice. But that changed the following year, when Wei Chen, a lymphatic microsurgeon at the Cleveland Clinic in Ohio, began showing the footage (with consent from Xie and the man’s family) at surgical meetings around the world. “A lot of jaws dropped,” recalls Chen. “It basically started a frenzy of this surgery being performed left and right.” Almost all of the surgeries took place in China, where hundreds of hospitals were soon offering the experimental procedure. Propelled by viral testimonial videos and aggressive marketing campaigns on social-media platforms such as Douyin and WeChat, it was sought out by thousands — with many people paying more than 200,000 yuan (US$30,000) for a chance of recovery. © 2026 Springer Nature Limited

Keyword: Alzheimers
Link ID: 30370 - Posted: 08.12.2026

By Sara Reardon The protein tau is best known for its potential to clog the brain. In neurodegenerative conditions including Alzheimer’s disease, chains of the molecule twist into tangles inside neurons and choke out the cells. But a new study suggests tau may play an earlier and more fundamental role in neurodegeneration: sneaking into the cell’s power-generating mitochondria—the cell’s power generators—and interfering with aging neurons’ energy production. If this process gets out of control, it creates tangle-prone forms of tau and other toxic byproducts that damage neurons, long before a person’s cognitive symptoms start. The research, published today in Neuron, also showed interrupting this process can prevent brain damage and disease symptoms in mice. “It really is opening up something we’ve needed for a while, which is some really new ideas and fresh directions” for understanding neurodegenerative diseases, says Kenneth Kosik, a neuroscientist at the University of California, Santa Barbara who was not involved in the research. “I think this paper will reinvigorate the idea that [modifying tau] is going to be a possible therapeutic approach.” Researchers and companies developing treatments for Alzheimer’s have long seen tau as a potential drug target. One recent clinical trial, for instance, showed lowering the levels of tau in the brains of people with Alzheimer’s reduced their rate of cognitive decline by as much as 26%. Other approaches have tried to prevent enzymes from adding chemical tags called phosphate groups to tau proteins. These phosphorylated forms of tau (p-tau) are especially prone to misfolding and clumping into tangles. But tau therapies have seen limited success so far, leading researchers to wonder whether the protein actually drives neurodegeneration or is merely a sign of it. So geneticist Bingwei Lu of Stanford University and his colleagues set out to find specific ways in which p-tau affects cells. Previous research has suggested Alzheimer’s and other so-called tauopathies, including frontotemporal dementia and Parkinson’s disease, all involve problems with energy production in the brain’s mitochondria © 2026 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 30365 - Posted: 08.08.2026

By RJ Mackenzie LONDON — A protein marker of Alzheimer’s disease in the brain may also help diagnose cases of the brain condition chronic traumatic encephalopathy, or CTE, early data suggest. The condition, which is linked to repeated head trauma, currently can be identified only in autopsies. But measurements of an Alzheimer’s-associated protein, eMTBR-tau243, might one day bring testing to the living: In confirmed CTE cases, levels of the protein increased the more advanced the disease had been at death, researchers reported July 15 at the Alzheimer’s Association International Conference. The data, which have yet to be peer-reviewed, suggest a path toward a first way of diagnosing CTE in living people, says Chihiro Sato, a neuroscientist at Washington University in St. Louis. While the results would need to be confirmed in a larger dataset, “we think there’s potential.” The ability to diagnose patients while they are still alive would provide clarity to patients about their well-being and be invaluable to getting them involved in future trials of any CTE treatments, says John Arena, a neurosurgeon at the University of Pennsylvania who was not involved in the research. Diagnosing CTE currently requires a careful examination of the brain after death, which has complicated efforts to identify how many people are affected by the condition. A 2018 study found that CTE-like damage affected 1 of 164 donated brains. But CTE is far more common in people repeatedly exposed to head trauma, like athletes in contact sports. In 2023, the Boston University CTE Center reported that CTE pathology was present in more than 90 percent of brains in a sample of 376 former NFL players. © Society for Science & the Public 2000–2026.

Keyword: Brain Injury/Concussion; Alzheimers
Link ID: 30355 - Posted: 08.01.2026

By Ailie McWhinnie On a research trip to Indonesia in 2007, Yosuke Kaifu saw for himself the skull of “Flo”—the skeletal remains first discovered 4 years earlier that heralded the existence of a diminutive human relative called Homo floresiensis. These so-called “Hobbits,” which stood about 1 meter tall, lived on the Indonesian island of Flores until about 50,000 years ago. The University of Tokyo anthropologist was drawn to one anatomical peculiarity: The skull’s right side is slightly smooshed. Some researchers had previously attributed this abnormality to disease, others to distortion after burial. But when Kaifu showed it to a clinician back in Japan, he received a surprising response: It looked like a harmless condition known as deformational plagiocephaly, or flattening of the skull, that occurs today in about one in six babies. Usually, the skull rounds out over time, but in some cases, it can persist into adulthood. The condition arises because the human skull remains soft for the first months of life to allow for the enormous amount of brain growth that occurs after birth. Repeated pressure on one side can cause flattening, and because babies cannot hold up their own heads, they are prone to resting it on one side when put down. Such helplessness is thought to be a concession to babies’ brains being relatively underdeveloped at birth to allow them to fit through the birth canal. Kaifu reasoned that deformational plagiocephaly in the skulls of ancient hominins could be a good indicator that they, too, were helpless as infants. After examining hundreds of skulls, they conclude today in the Proceedings of the Royal Society B that at least two other lineages of humans shared this trait with us, suggesting it has deep evolutionary origins. “I thought it was a very ingenious study,” says Lia Betti, an anthropologist at University College London. © 2026 American Association for the Advancement of Science.

Keyword: Evolution; Development of the Brain
Link ID: 30352 - Posted: 08.01.2026

By Liz Seegert More than one in 10 Americans takes a GLP-1 medication for weight loss. As more people take a GLP-1, or glucagonlike peptide 1, receptor agonist, such as Wegovy, so, too, do more older adults—and those numbers are set to skyrocket. Last week the Trump administration launched the Medicare GLP-1 Bridge program, a new initiative that would set the cost of three weight-loss medications— Wegovy, the KwikPen version of Zepbound (tirzepatide) and Foundayo (orforglipron)—at $50 a month. That may be welcome news for the estimated 38.9 percent of adults aged 60 and up in the U.S. who are living with obesity. But it could also supercharge an ongoing and risky experiment in growing old on weight-loss drugs. For years, clinicians have had few good options to safely treat obesity in older adults. But while GLP-1s, long used to treat diabetes, are now approved for weight loss, the evidence supporting their use in the age-60-and-older population is limited. Someone in their 70s may benefit as much from weight loss as a person in their 30s but may respond very differently to these drugs’ side effects; we simply don’t have enough evidence yet to make informed conclusions, experts advise. “Eligibility doesn’t mean benefit automatically,” says Ruchi Gaba, an associate professor of endocrinology at Baylor College of Medicine. “We have to individualize.” And within the 60-and-older group, there is huge variety: a healthy, active 68-year-old with obesity and sleep apnea is a very different patient than an 88-year-old who’s frail, has poor appetite and is at risk of falls, Gaba says. Older adults are underrepresented in the clinical trials for GLP-1 drugs. Despite the high prevalence of obesity among this age group, only about one in 10 participants in early GLP-1 trials was age 65 or older, says Alissa Chen, a primary care physician and a researcher at the Yale School of Medicine, who specializes in obesity. Older adults are more heterogeneous than people in younger age groups in terms of chronic conditions and multiple medications, Chen says, which can pose challenges with both prescriptions and side effects. © 2026 SCIENTIFIC AMERICAN

Keyword: Obesity; Development of the Brain
Link ID: 30334 - Posted: 07.22.2026

By Elie Dolgin Jeff Carroll was in his mid-twenties, fresh out of the U.S. Army, when a genetic test confirmed his worst fear: He was going to develop Huntington’s disease. He had watched his mother’s illness for years; the tremors first, small enough to explain away, then the involuntary movements that looked almost like dancing. The test revealed that the same mutation that caused her disease lived in him: a stretch of three DNA letters in a gene called HTT, repeated over and over again dozens of times. Carroll himself was not sick yet. He would not get sick for many years. But the countdown had begun. In fact, it had likely been running all his life, deep inside vulnerable neurons in his brain. There, the mutant HTT gene was slowly growing longer, its internal repeats piling up toward a threshold that, once crossed, would tip the cell into disarray. The first outward signs of Huntington’s often begin with mood changes and subtle cognitive effects. The hallmark jerky movements come later. Eventually, and relentlessly, patients lose the ability to speak, swallow or move. Most people die within a decade or two of symptom onset. Huntington’s disease is rare, affecting roughly 1 in 20,000 people worldwide. Yet because each child of an affected parent has a 50 percent chance of inheriting the mutation, the disease can haunt families for generations. It had already claimed Carroll’s grandmother and would take his mother at age 54. Without a therapy capable of altering its course, Carroll — along with three of his five siblings who also inherited the mutation — seemed fated to follow his ancestors into an early grave. Carroll decided the only rational response was to become one of the scientists seeking ways to beat the disease. He was midway through his undergraduate studies when he learned, in 2003, that he carried the mutation. He pressed on, earning a Ph.D. and completing postdoctoral training before establishing his own research group devoted to understanding and slowing the disease stalking him from within. © Society for Science & the Public 2000–2026.

Keyword: Huntingtons
Link ID: 30332 - Posted: 07.18.2026