By Elie Dolgin Two U.S. states and more than a dozen cities and counties have moved in the past year to stop adding fluoride to community drinking water, citing research suggesting the mineral could harm children’s brain development. But a new analysis of cognitive outcomes tracked over decades finds no evidence that water fluoridation is associated with lower adolescent IQ or diminished mental abilities later in life, researchers report April 13 in the Proceedings of the National Academy of Sciences. The results, based on standardized intelligence testing of more than 10,000 people in Wisconsin followed since their senior year of high school in 1957, challenge the idea that typical fluoridation levels in public drinking water pose a neurodevelopmental risk, a central point of contention in ongoing policy debates. “It’s very strong data,” says Steven Levy, a dentist and public health researcher at the University of Iowa in Iowa City who was not involved in the research. “There’s no strong signal at all coming through that should give us concern.” However, given the politically charged nature of water fluoridation and continued differences in how researchers interpret the available evidence, the findings are unlikely to be the last word on the issue. © Society for Science & the Public 2000–2026

Keyword: Intelligence; Neurotoxins
Link ID: 30200 - Posted: 04.15.2026

Alison Abbott The development of the human brain, with its extraordinary range of cognitive abilities, is an awe-inspiring feat of evolution. Each of its tens of billions of cells must be born at precisely the right time, migrate to the correct locations, differentiate into as many as 3,000 distinct cell types, and form exquisitely specific synaptic connections with one another. Most of this happens before birth, but development continues for nearly three more decades. None of this is easy to study. Conventionally, scientists have relied on animal models and scarce human brain tissue. But the advent of tiny laboratory-grown models of human brains called organoids has transformed their options. First created more than a decade ago, these organoids started off as very simple models. But in the past few years, scientists have refined the technology to grow more-intricate systems that represent more brain regions. Research has snowballed as scientists have used organoids to probe brain development, model neurodevelopmental conditions such as autism and schizophrenia and test new treatments for brain diseases. These tiny spheres are helping researchers to get at difficult-to-answer questions such as why the human brain develops so much more slowly than other mammalian brains do. And this year, researchers are hoping to run the first clinical trial of a brain-disorder treatment developed entirely in organoids. “The field is at an inflection point,” says developmental biologist Jürgen Knoblich at the Institute for Molecular Biotechnology in Vienna. But organoids are not without their limitations. It’s hard to sustain them in the lab for more than a few months, for instance. And they lack complexity. © 2026 Springer Nature Limited

Keyword: Development of the Brain
Link ID: 30194 - Posted: 04.08.2026

By Jennie Erin Smith For a person who may be in the early stages of Alzheimer’s disease, getting a clear diagnosis is simpler than ever. Blood tests that detect biological changes linked to the disease are now considered reliable alternatives to brain imaging and invasive spinal fluid tests. And one biomarker, called phosphorylated tau 217 (p-tau217), has risen to the top. More accurate than other blood-based measures, p-tau217 is widely used in research, and the first commercial test was approved in the United States last year. Guidance from the influential Alzheimer’s Association says a positive result in a patient with cognitive symptoms can justify starting therapy with antibody drugs recently approved for the disease. “P-tau217 is the biomarker of the day,” says Alzheimer’s researcher Lon Schneider of the University of Southern California. But its success has sparked worries among some researchers and clinicians about inappropriate use of the test. Some doctors have begun to use it in people without confirmed symptoms, and telehealth companies peddle p-tau217 testing, for as little as a few hundred dollars, to anyone concerned about their memory. A positive result doesn’t mean a person will develop cognitive impairment or dementia, Schneider and other researchers warn. And some fear the tests will be used to push people without symptoms toward pricey infusion drugs that they may not need. At the Alzheimer’s Disease and Parkinson’s Disease (AD/PD) meeting last month in Copenhagen, Denmark, scientists seemed to agree that for better or for worse, p-tau217 is poised to become a widespread screening tool for healthy people. That assumption is driving an ongoing trial called TRAILBLAZER-3, in which people with positive p-tau217 but no symptoms are taking the antiamyloid drug donanemab to see whether it delays the onset of cognitive impairment. “People keep thinking or talking about early treatment,” says neurologist Richard Mayeux of Columbia University, who is not involved with that study. “What you want to do is get to that fine area just before cognitive impairment starts to occur.” © 2026 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 30185 - Posted: 04.01.2026

By Angie Voyles Askham The idea that some neural representations can “drift,” or change over time, even in the seeming absence of learning, is broadly accepted. But characterizing the phenomenon across the brain has proved challenging. “The interesting part is what exactly seems to be stable and what exactly seems to be drifting. That’s not an easy question,” says Tobias Rose, a group leader at the University of Bonn Medical Center, who presented findings on drift in the mouse primary visual cortex earlier this month at the Computational and Systems Neuroscience (COSYNE) annual meeting. Other new research adds nuance to the discussion: Neurons that code for head direction in the mouse post-subiculum show little drift, retaining their tuning for multiple weeks, according to a study published last month in Nature. And they differ from hippocampal place cells, which are also part of the spatial navigation system but have highly variable responses, as reported in previous research. The new findings raise questions about how stable and flexible representations interact in the brain, given that signals from the post-subiculum ultimately feed into the hippocampus, says Rose, who was not involved in the work. “It’s a rather important study,” he says. The relative stability of head direction cell tuning does not invalidate previous reports of drift elsewhere in the brain, says Adrien Peyrache, associate professor at the Montreal Neurological Institute, who led the head direction study. Instead, it may be that these invariant responses act as a “rigid backbone” onto which more flexible sensory and cognitive responses can be mapped, he says. “I find it reassuring.” Still, the low drift reported in the new work may be partially due to the study’s methods, which eliminated cells that lost their response from one day to the next, says Timothy O’Leary, professor of information engineering and neuroscience at the University of Cambridge, who was not involved in the work. © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30181 - Posted: 03.28.2026

Gemma Conroy Scientists have created the first atlas of specific key patterns of brain ‘chatter’ and determined how these patterns change over the entire human lifespan1. The comprehensive guide draws on brain scans from almost 3,600 people, ranging from infants to centenarians. It maps a property called functional connectivity, which describes the level of coordination between separate brain regions. The data suggest that in young adults, particular patterns of this connectivity are linked to cognitive performance. Such a guide could be useful for understanding when developmental issues and neurodegenerative conditions emerge, says Jakob Seidlitz, a neuroscientist at the University of Pennsylvania in Philadelphia, who was not involved in the research. “This is an important contribution to the field,” he adds. The findings were published today in Nature. The brain is a noisy place. Sometimes two brain regions that are far apart are active at the same time, suggesting that they work together to support the same function. Such regions are said to be functionally connected, even though they do not necessarily sit close to each other in the brain. To understand how this functional connectivity is organized, brain areas are plotted along a scale, or axis, on the basis of their connectivity patterns with the rest of the brain, says study co-author Patrick Taylor, a computer scientist at the University of North Carolina at Chapel Hill who focuses on neuroscience. There are three main functional axes. The sensory-to-association axis, for example, allows researchers to describe brain regions that lie along a continuum from those that focus mainly on processing sensory information to those that are engaged in sophisticated processes such as integrating sensory information into complex thought. The brain regions at each point along the axis have similar patterns of connectivity. © 2026 Springer Nature Limited

Keyword: Development of the Brain
Link ID: 30180 - Posted: 03.28.2026

David Adam When neuroscientists gather in the Spanish city of Seville in May for the annual Dopamine Society meeting, one discussion could be unusually lively. Session 31 will feature a debate between researchers who fundamentally disagree about the role dopamine has in the brain. Dopamine is one of the most extensively studied neurotransmitters, chemicals that convey signals from cell to cell. It’s the one with the highest profile outside neuroscience: often known as the ‘pleasure chemical’, it’s depicted as the hit of reward that people get from recreational drugs or scrolling through social media. That’s a gross simplification of what dopamine does; on that, researchers agree. But beyond that, where once there was a simple model that explained how dopamine works in the brain, now there are challenges that seek to amend the theory — or even to overturn it. This could have implications not only for basic neuroscience, but also for clinicians trying to explain and treat conditions such as attention deficit hyperactivity disorder (ADHD) and addiction. If the model is wrong or needs modification, then so might some of the assumptions about what drives these disorders and the best way to treat them. The classic idea, known as the reward prediction error (RPE) hypothesis, is that bursts of dopamine in the brain link stimuli to rewards, helping to reinforce associations that fulfil a need for an animal or a person. The model has dominated and guided research in the field for decades, offering a mathematical framework to interpret data from animal experiments, and it does a good job of explaining behaviour. This was a valuable rarity for researchers struggling to overlay simple theories onto the intense complexity of the brain. “Dopamine was the one field of neuroscience where we had a computational model that explained what the signal was and what it was computing,” says Mark Humphries, a neuroscientist at the University of Nottingham, UK. People in the field knew that some of the assumptions involved in the RPE model were simplistic. But as a working understanding of part of the brain, it was seen as a major step forwards. © 2026 Springer Nature Limited

Keyword: Learning & Memory; Drug Abuse
Link ID: 30166 - Posted: 03.19.2026

By Claudia López Lloreda As cells age and acquire damage, they stop dividing and enter a comatose-like state. This natural process, called senescence, has several classic hallmarks, including the expression of cell cycle arrest genes and enlarged nuclei, and can spread among neighboring cells. But senescence arises and expands differently across human brain cell types and in response to various stressors, two new studies suggest. “We’re living in the new world of the senescence field,” says Joseph Herdy, investigator at the Salk Institute for Biological Studies, who was not involved with the work. Any cell type, it seems, can senesce under the right conditions, he adds, but each responds in its own way, complicating the picture. Human brain cell lines—neurons, astrocytes, microglia, oligodendrocytes and endothelial cells—present cell-type-specific responses to stressors that trigger senescence, according to one of the new studies, published in Nature Communications in December. And like senescent cells elsewhere in the body, some—though not all—brain cells can release molecules that spread the senescent phenotype to other cells, according to the other study, a preprint posted on bioRxiv last month. These cell-type-specific differences may reflect the various ways cells acquire and enter a state of senescence, says Jalees Rehman, professor of biochemistry and molecular genetics at the University of Illinois, who was not involved with either work. “They might all have some shared universal features, such as no more cell cycle, some degree of inflammation, but maybe the path of how you get there might be different between cell types.” Senescent cells are sparse and difficult to find in the brain, says Markus Riessland, assistant professor of neurobiology and behavior at Stony Brook University and an investigator on both new studies. So to study the cell-type specificity, Riessland and his colleagues decided to induce senescence in different cells in culture. “Otherwise, if you only have one cell, there’s no way you could characterize how the cell goes into senescence and what the difference between the senescent cells are,” he says. © 2026 Simons Foundation

Keyword: Development of the Brain; Alzheimers
Link ID: 30164 - Posted: 03.19.2026

By Catherine Offord Scientists have plenty of ideas about why aging impairs memory. Reductions in blood flow in the brain, shrinking brain volume, and malfunctioning neural repair systems have all been blamed. Now, new research in mice points to another possible culprit: microbes in the gut. In a study published today in Nature, scientists show how a bacterium that is particularly common in older animals can drive memory loss. This microbe makes compounds that impair signaling along neurons connecting the gut with the brain, dampening activity in brain regions associated with learning and memory, the team found. “This is a tour de force,” says Haijiang Cai, a neuroscientist at the University of Arizona who studies gut-brain communication and was not involved in the work. “They define the pathway all the way from aging and bacteria … to cognitive function—it’s really impressive.” However, he and others emphasize it remains to be seen whether a similar mechanism exists in humans—and if so, how important it is compared with other drivers of cognitive decline. Research on the so-called gut-brain axis has exploded in recent decades. Multiple studies have identified differences in microbiome composition between healthy people and those with cognitive disorders such as Alzheimer’s disease. This kind of research can’t establish cause and effect, though, and the literature is rife with conflicting results. Some groups have used animal experiments to probe the microbe-memory link. In the new study, Stanford University researchers Christoph Thaiss and Maayan Levy tinkered with the microbiomes of young mice—either by housing them with older animals or feeding them these animals’ poop—and then gave them memory tests. For example, one such test rates animals higher if they spend more time exploring new objects than those they’ve seen before. © 2026 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 30162 - Posted: 03.14.2026

By Catherine Offord Scientists have plenty of ideas about why aging impairs memory. Reductions in blood flow in the brain, shrinking brain volume, and malfunctioning neural repair systems have all been blamed. Now, new research in mice points to another possible culprit: microbes in the gut. In a study published today in Nature, scientists show how a bacterium that is particularly common in older animals can drive memory loss. This microbe makes compounds that impair signaling along neurons connecting the gut with the brain, dampening activity in brain regions associated with learning and memory, the team found. “This is a tour de force,” says Haijiang Cai, a neuroscientist at the University of Arizona who studies gut-brain communication and was not involved in the work. “They define the pathway all the way from aging and bacteria … to cognitive function—it’s really impressive.” However, he and others emphasize it remains to be seen whether a similar mechanism exists in humans—and if so, how important it is compared with other drivers of cognitive decline. Research on the so-called gut-brain axis has exploded in recent decades. Multiple studies have identified differences in microbiome composition between healthy people and those with cognitive disorders such as Alzheimer’s disease. This kind of research can’t establish cause and effect, though, and the literature is rife with conflicting results. Some groups have used animal experiments to probe the microbe-memory link. In the new study, Stanford University researchers Christoph Thaiss and Maayan Levy tinkered with the microbiomes of young mice—either by housing them with older animals or feeding them these animals’ poop—and then gave them memory tests. For example, one such test rates animals higher if they spend more time exploring new objects than those they’ve seen before. © 2026 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 30161 - Posted: 03.14.2026

By Natalia Mesa Experience kindles most of our learning throughout life, without any explicit instruction or reward. Thanks to this process, called statistical learning, people unconsciously recognize patterns in their surroundings, and infants soak up language. The hippocampus, it turns out, may be essential for this capability, according to a new preprint, beginning to resolve a long-standing debate. Numerous functional MRI studies have suggested that the structure is involved in statistical learning, but lesion studies have produced mixed results. “This is a tour-de-force study,” says Anna Schapiro, associate professor of psychology at the University of Pennsylvania, who was not involved in the work. “It makes me feel more confident that, yes, the hippocampus is involved in statistical learning, but it’s also necessary for that learning across species.” In the study, people and mice learned to respond—by pressing a key or licking a waterspout, respectively—to a particular sound. As they performed this “cover” task, they also heard an irrelevant four-note sequence at random times, interspersed with the other sound. After repeating this cover task 100 times, both people and rodents showed strong pupil dilation, a sign of surprise, whenever the sequence of notes changed slightly, with more similar sequences evoking a smaller response—indicating that they had passively learned the original musical motif and abstract rules about its structure. Neuronal populations in the hippocampus encoded not only the original and altered tone sequences but also how frequently each occurred. Pharmacologically or optogenetically shutting down hippocampal neurons in the mice prevented them from passively learning the auditory pattern and making generalizations about how often it played, but it didn’t disrupt their performance on the cover task. © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30154 - Posted: 03.11.2026

Rachel Fieldhouse A group of specialized cells play a crucial part in clearing toxic proteins from inside the brain1. But in people with Alzheimer’s disease, these cells malfunction, leading to the build up of tau proteins — a hallmark of the disease. Tanycytes, specialized cells that line the third ventricle of the brain, are unique because they are in direct contact with both the bloodstream and the cerebrospinal fluid (CSF). This means that they can circumvent the blood–brain barrier to allow molecules into and out of the brain. “Tanycytes are highways for the brain,” says Vincent Prévot, a neuroendocrinologist based in Paris at Inserm, the French National Institute of Health and Medical Research. Although it was known that tanycytes transport molecules into the CSF, Prévot and his colleagues are the first to show that tanycytes also transport molecules out of the CSF. In particular, they move tau proteins from the CSF surrounding the brain into the bloodstream. The findings are fascinating, says Amy Brodtmann, a cognitive neurologist and researcher at Monash University in Melbourne, Australia. “No one has looked at these cells before” in relation to Alzheimer’s disease, she adds. The works shows a potential explanation for how abnormal tau proteins accumulate in the brain, she adds. Tau proteins usually help to support the internal structure of cells and make them stronger, including cells in the brain. But in people with Alzheimer’s disease, the protein stops working properly. Brodtmann says tau then becomes “sticky”, forming clumps in the cells and causing them to die. These tau tangles tend to accumulate in regions of the brain that are involved in memory. © 2026 Springer Nature Limited

Keyword: Alzheimers; Glia
Link ID: 30152 - Posted: 03.07.2026

By Jake Currie Struggling to remember a forgotten memory is an all-too-common frustration—one that unfortunately becomes more common as we age. We realize that there’s something we can’t recall, but we simply can’t raise it from the depths of our brains. So where did it go? New research published in the Journal of Neuroscience suggests these memories are still lurking in our minds, even though we think they’re long gone. Subscribe to skip ads Featured Video Psychologists from the University of Nottingham led by Benjamin Griffiths strapped participants into a magnetoencephalography machine to measure the magnetic fields surrounding the electrical activity in their brains. Participants were asked to vividly associate a short video clip with a word, and when they were later shown that word, they were asked to recall the video clip while psychologists monitored the magnetic activity of their brains. They found that the brain reactivated memories whether they were consciously recalled or not, meaning the memories were there. When memories were successfully recalled, the reactivated memory signal fluctuated rhythmically in the alpha band. Alpha brain waves, research has shown, are associated with the memorization of visual information, but it was the rhythmicity of the waves that proved key to conscious recall. “What we showed is that even when the brain can reactivate the right memory, it doesn’t guarantee you’ll become aware of it,” Griffiths explained. “Instead, what seems to matter is that the memory rhythmically pulses so that it can be detected above and beyond other neural activity.”

Keyword: Learning & Memory; Brain imaging
Link ID: 30151 - Posted: 03.07.2026

Jon Hamilton A human brain consumes less power than a light bulb, while artificial intelligence systems guzzle electricity to do the same tasks. Now, scientists have created a highly efficient AI model that hints at how living brains are able to do so much with so little, a team reports in the journal Nature. Light enters the compound eye of the fly, causing the photoreceptors to send electrical signals through a complex neural network, enabling the fly to detect motion The model, which mimics a part of the brain's visual system, started out using 60 million variables. But the team was able to compress it into a version that performed nearly as well using just 10,000 variables. "That is incredibly small," says Ben Cowley, an author of the study and an assistant professor at Cold Spring Harbor Laboratory. "This is something we could send in a tweet or an email." The compact model also appears to work more like a living brain, which could help scientists study what goes wrong in diseases like Alzheimer's, Cowley says. More broadly, if the AI model really does replicate strategies found in nature, it could help scientists understand the inner workings of human brains, says Mitya Chklovskii, a group leader at the Simons Foundation's Flatiron Institute, who was not involved in the study. Compact, biology-inspired models of the brain could also lead to "more powerful and more humanlike artificial intelligence," says Chklovskii, who is also on the faculty at NYU. © 2026 npr

Keyword: Robotics; Vision
Link ID: 30147 - Posted: 03.04.2026

By Bethany Brookshire When solving a puzzle, the answer could lie in your dreams. In a study of lucid dreamers, playing soundtracks linked with unsolved puzzles helped the sleepers solve the problems the next day, researchers report February 5 in Neuroscience of Consciousness. Stories of brilliant insights after a nap or daydream abound, but scientists have struggled to successfully influence people’s dreams and rigorously test the idea. “This study provides one of the first experimentally grounded demonstrations of such a link,” says Giulio Bernardi, a cognitive neuroscientist at IMT School for Advanced Studies Lucca, in Italy, who was not involved with the work. Whether we remember our dreams or not, we have countless dreams in our sleep, according to Karen Konkoly, a cognitive neuroscientist who performed the study at Northwestern University in Evanston, Ill. “Your dreams are such a big part of your inner life,” she says. And in the right circumstances, manipulating those dreams could help people think of problems in new ways. While some scientists have shown that sleeping on a problem increases the odds of solving it the next day, others have shown no benefit. Of course, it might help only if you actually think about the problem in your sleep. Konkoly and her colleagues were especially interested in helping sleepers think about specific topics using targeted memory reactivation, or TMR. “It’s this research technique where you have a sensory stimuli that’s associated with a memory,” Konkoly says. “It could be a very soft sound or a smell that’s presented to a sleeper, and it functions to remind the sleeping brain of the full memory.” While people dream in every stage of sleep, the effects of TMR have been strongest in deep, slow-wave sleep, she says. Konkoly wanted to look at the effects of TMR at a different sleep stage — rapid eye movement sleep, which could be helpful for creative thinking. © Society for Science & the Public 2000–2026.

Keyword: Sleep; Learning & Memory
Link ID: 30145 - Posted: 03.04.2026

By Dana G. Smith Many people’s brains deteriorate as they age, becoming riddled with malfunctioning proteins that result in cell death and the loss of memory and cognition. But other people’s brains remain almost perfectly intact, their thinking as sharp at 80 as it was in their 50s. A paper published Wednesday in the journal Nature provides a new potential explanation for this discrepancy, and it taps into one of the hottest debates in neuroscience: whether human brains can grow new neurons in adulthood, a phenomenon called neurogenesis. The study found that so-called super-agers — people 80 and up who have the memory ability of someone 30 years younger — had roughly twice as many new neurons as older adults with normal memory for their age, and 2.5 times more than people with Alzheimer’s disease. The research focused on an area of the brain called the hippocampus, which is important for learning and memory and is thought to be the primary birthplace of new neurons. “This paper shows biological proof that the aging brain is plastic,” even into a person’s 80s, said Tamar Gefen, an associate professor of psychiatry and behavioral sciences at the Northwestern University Feinberg School of Medicine, who contributed to the research. To look for neurogenesis in older adults, the scientists first tried to detect signs of it in the autopsied brains of young adults, age 20 to 40, who died with normal cognition. They identified genetic markers for three key types of cells: neural stem cells, neuroblasts and immature neurons. © 2026 The New York Times Company

Keyword: Neurogenesis; Alzheimers
Link ID: 30144 - Posted: 02.28.2026

Mariana Lenharo Adults whose brains still have strong neuron production seem to have better memory and cognitive function than do those in whom the ability wanes, finds a study published today in Nature1. The authors examined brain samples from deceased donors ranging from young adults to ‘super agers’ — people older than 80 with exceptional memory. She lived to 117: what her genes and lifestyle tell us about longevity They found that young and old adults with healthy cognition generated neurons, a process called neurogenesis, at high levels for their age. The team estimated that the new neurons made up only a small fraction — 0.01% — of those in the hippocampus, a brain region that’s essential for memory. By contrast, in people experiencing cognitive decline, including individuals with Alzheimer’s disease, neurogenesis seems to falter: the researchers spotted fewer developing, or immature, neurons in those brain samples. Surprisingly, a group of ‘super agers’ had an even higher number of immature neurons than did other groups, and significantly more than did those with Alzheimer’s. However, the group sizes were small, so the findings were not all statistically significant. Maura Boldrini Dupont, a neuroscientist and psychiatrist at Columbia University in New York City, says that the small size of the groups — each had ten or fewer individuals — is a reason to take the results with a grain of salt. Understanding the tools that the brain uses to generate neurons and maintain cognitive function in old age could help researchers to develop drugs that induce neurogenesis in people with cognitive decline, says co-author Orly Lazarov, a neuroscientist at the University of Illinois Chicago. © 2026 Springer Nature Limited

Keyword: Neurogenesis; Alzheimers
Link ID: 30143 - Posted: 02.28.2026

By Nora Belblidia To the naked eye, Annie Kathuria’s experiments look a bit like tiny tufts of cotton floating in pink Petri dishes. These unassuming orbs are clusters of millions of human brain cells called brain organoids — brainstem organoids in this case — cultured in a lab in East Baltimore. Roughly a month old, the tufts are each around a millimeter wide, smaller than a coarse grain of salt. “We have about maybe 500 to 600 organoids growing,” said Kathuria, an assistant professor of biomedical engineering and neurosurgery at Johns Hopkins University. In addition to the brainstem organoids, her lab is also growing other types that correspond to different parts of the nervous system: cortical organoids, which mimic a brain’s developing cortex, and spinal cord organoids, to model the spinal nerve tissue that connects to the brain. Each of these clumps of neural tissue functions similarly to specific regions of the human brain. That similarity has led to some media coverage referring to them as “mini-brains” or “brains in a dish” — now irksome terms to many researchers in the field, some of whom also prefer the term neural organoids to brain organoids. Annie Kathuria, assistant professor of biomedical engineering and neurosurgery, in her lab at Johns Hopkins University in Baltimore. Visual: Nora Belblidia for Undark “Whatever else they are, they aren’t brains. They aren’t organized like brains. They aren’t big enough,” said Hank Greely, a Stanford University professor and expert in law and biosciences who works with researchers in the field. “But more importantly, they don’t have the right architecture.” By that he means organoids are basic parts of a whole, similar to how a broom closet or stairwell would never be considered a skyscraper.

Keyword: Development of the Brain
Link ID: 30141 - Posted: 02.28.2026

By Justin O’Hare For decades, two complementary but often siloed approaches have guided neuroscience: cellular neuroscience, which seeks to understand how individual neurons work; and systems neuroscience, which aims to uncover how networks of neurons coordinate to produce thoughts, movements and behaviors. One studies the tree; the other studies the forest. Each approach has produced tremendous advances. For instance, cellular neuroscientists have revealed how ion channels shape the electrical language of the brain, how synapses strengthen or weaken with experience and how gene expression governs neuronal function. Meanwhile, systems neuroscientists have mapped entire circuits, recorded the activity of tens of thousands of neurons during behavior and identified patterns of activity that correlate with memory, decision-making and emotion. But for all these advances, a question lingers: Are we actually any closer to understanding how the brain works? The jaw-dropping datasets produced by systems-level studies are seldom reconciled with biology, and the exquisite detail uncovered by cellular-level studies is rarely extrapolated from circuits to behavior. These disconnects don’t reflect failures of either approach. Rather, they reflect the vast intellectual and material resources that each requires. Nevertheless, the brain is a multiscale organ. It is organized across multiple hierarchical levels operating in concert, not in parallel. To unravel the brain’s deepest complexities, we need to bridge cellular and systems neuroscience. Because of recent technological advances in high-density electrical probes, genetically encoded fluorescent sensors, multiphoton imaging and high-performance computing, we are better suited to do this now than ever before. © 2026 Simons Foundation

Keyword: Learning & Memory; Brain imaging
Link ID: 30140 - Posted: 02.28.2026

Rachel Fieldhouse Alzheimer’s disease is about to become a big problem for China. Nearly 30% of all people with the condition or related forms of dementia already live in the country. And with its ageing population and falling birth rate, the burden on health and social welfare is expected to multiply dramatically in the coming decades. The Chinese government has responded with programmes and funding that are aimed at improving screening, diagnosis and treatment of Alzheimer’s disease by 2030. And the research has started to take off. Scientists have been working on new drugs and innovative — if controversial — surgical techniques. The government has also encouraged the development of drugs derived from traditional Chinese medicine. And researchers are accelerating the search for biological markers that precede the onset of Alzheimer’s disease, including genetic contributors, which could explain how the condition develops and reveal the best way to identify it early. Although the investments don’t yet match the level of funding in the United States, the improving quality and quickening pace of clinical and preclinical research has attracted attention from researchers around the world. “Maybe China is the next place that will take the lead,” says John Hardy, a neurogeneticist at the UK Dementia Research Institute in London, who is also affiliated with the Hong Kong Center for Neurodegenerative Diseases. Treating the root of the problem Nearly 17 million people in China had Alzheimer’s disease and related dementias in 2021 — about 9 in 1,000, according to a report published last year1. Projections suggest that this number could reach as high as 66 million by 2050 (see ‘Dementia’s rise’) or even exceed 100 million by then2,3. The problem is compounded by China’s low fertility rate, which means that there will be fewer people of working age to support the growing population of older individuals with debilitating conditions. © 2026 Springer Nature Limited

Keyword: Alzheimers
Link ID: 30139 - Posted: 02.25.2026

Heidi Ledford A simple blood test might one day serve as a molecular ‘clock’ that predicts not only whether someone will develop Alzheimer’s disease — but when. Blood tests are now approved for Alzheimer’s: how accurate are they? The test, published in Nature Medicine on 19 February1, is based on an abnormal form of a protein called tau that circulates in the blood, and begins to accumulate in the brains of people with Alzheimer’s well before symptoms such as memory loss appear. If validated in larger studies, the test could provide a way to intervene in the neurodegenerative disease at an earlier stage, when treatment is more likely to be effective. It could also provide a measurable biological marker, or ‘biomarker’, to make clinical trials of potential Alzheimer’s disease treatments easier and cheaper. “Predicting if and when patients are likely to develop Alzheimer’s symptoms could be useful in designing trials of interventions to prevent or delay symptom onset,” says Howard Fink, a physician at the Minneapolis Veterans Affairs Health Care System in Minnesota. But until further studies are done, people should not take the test themselves, says Suzanne Schindler, a neurologist at Washington University School of Medicine in St. Louis, Missouri, and lead author of the study. (In-home blood tests for the form of tau that the study focuses on are available to consumers.) “At this point, we do not recommend that any cognitively unimpaired individuals have any Alzheimer’s disease biomarker test,” Schindler adds. Abnormal tau proteins can form tangled fibres that disrupt communication among the brain’s nerve cells. Brain-imaging tests that detect tangled tau are sometimes used when diagnosing Alzheimer’s, and preliminary studies suggest that such tests might also be able to predict when a person’s Alzheimer’s symptoms will appear2,3. © 2026 Springer Nature Limited

Keyword: Alzheimers
Link ID: 30130 - Posted: 02.21.2026