Jon Hamilton Scientists who've spent decades learning how the brain works say they're now ready to start fixing it when it breaks. That's the premise of the Brain Health accelerator, a collaborative effort launched by the Allen Institute in Seattle, which has become a major player in brain research. The initiative includes plans to develop new genetic therapies — a term that includes gene editing as well as traditional gene therapy — for diseases including Alzheimer's, Parkinson's, ALS, and Huntington's. "The latest genetic treatments allow scientists to control the activity of particular genes," says Ed Lein, who directs the institute's brain health programs. "That opens up the possibility for very specific precision therapies for brain disorders." The accelerator is an outgrowth of the BRAIN Initiative, an ambitious research program unveiled by President Obama in 2013. The goal of this public-private partnership was to create tools that would allow scientists to see the brain's inner workings, and, eventually, to develop treatments. But the effort has progressed far faster than many scientists expected. "I am shocked at how far we've come in the last 10, 12 years," says John Ngai, a senior investigator at the National Institutes of Health who directs the BRAIN Initiative. "It's just been beyond my wildest imagination — and I've been accused of having a pretty good imagination." © 2026 npr

Keyword: Parkinsons; Alzheimers
Link ID: 30267 - Posted: 06.03.2026

By Sarah Kliff and Margot Sanger-Katz On a sunny Wednesday morning last month, dozens of preschoolers filed into a Compleat Kidz autism clinic in Concord, N.C. One wore light-up sneakers. Another had a Spider-Man lunchbox. They settled into tiny green cubicles, each accompanied by a staff member, and started their work. A decade ago, this Charlotte suburb had no clinics providing therapy to children with autism. Now it has 12. Inside this one, children buzzed with activity as they worked long sessions with therapists. One 6-year-old girl, exhausted after hours of therapy, fell fast asleep in her therapist’s lap. Soon, a supervisor, Stephen Schroeder, intervened. “How long?” Mr. Schroeder asked Courtney Evans, the therapist. “I set the timer for 7. We’re almost done,” Ms. Evans said. A couple of minutes later, she nudged the child awake. The girl cried. At Compleat Kidz, a fast-growing chain of autism clinics based in North Carolina, the policy is firm: Naps cannot be longer than seven minutes before children are awakened to resume therapy. The company says this is necessary to prevent fraud since clinics can be paid only when children are awake and getting services. But it also allows the clinic to bill insurers or Medicaid for more hours. Across the United States, where treatment for autistic children was once fairly rare, thousands of clinics have sprung up, turning a once obscure therapy into a multibillion-dollar industry. The growth has been fueled by rising autism diagnoses, state insurance mandates and a federal requirement that Medicaid cover the therapy. Private equity investors have rushed into the business, buying up chains and opening new clinics.. © 2026 The New York Times Company

Keyword: Autism
Link ID: 30254 - Posted: 05.23.2026

By Jennie Erin Smith About 20 years ago, neuropathologists began to report an inconvenient finding in the autopsied brains of people with dementia: Most have evidence of more than one disease. Studies since have shown the brains of up to half of people diagnosed with Alzheimer’s disease also have a key feature of Parkinson’s disease—deposits of the protein alpha synuclein. At the same time, up to half of Parkinson’s patients who develop dementia have elevated levels of beta amyloid and tau proteins, hallmarks of Alzheimer’s. Researchers studying neurodegenerative diseases are catching on to the importance of this phenomenon, often called copathology. It complicates current disease classifications, which are tightly linked to their signature proteins. But it also offers clues as to why some dementia patients show faster cognitive decline, and some people on antiamyloid drugs for Alzheimer’s seem to fare worse than others. Copathology “helps explain why symptoms don’t match biomarkers, why trajectories vary so much, and why treatment results are not necessarily what we expect them to be,” neuropathologist Lea Grinberg of the Mayo Clinic told researchers at the Alzheimer’s and Parkinson’s Diseases Conference (AD/PD) in March. Why the diseases overlap so often remains a mystery, but it’s not a coincidence. “It seems that they stimulate each other,” Grinberg says. Tests now being developed to pick up multiple biomarkers should give a clearer picture of these mixed pathologies in living patients. And an upcoming clinical trial will be the first to take aim at a common dementia copathology, testing the amyloid-clearing Alzheimer’s drug donanemab in people who have both amyloid in their brains and dementia with Lewy bodies—abnormal clumps of alpha synuclein. © 2026 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 30244 - Posted: 05.16.2026

By Lauren Schenkman More than 3,000 genes are differently expressed in the cerebral cortex of people with XX versus XY sex chromosomes, according to a single-cell transcriptomics study published last month in Science. The differences could help explain why certain neurodegenerative and neurodevelopmental conditions affect one group more than the other, or vice versa. The results present “a pretty dramatic shift in how we’re thinking about sex differences,” says Tomasz Nowakowski, associate professor of neurological surgery, anatomy and psychiatry, and of behavioral sciences, at the University of California, San Francisco. He was not involved in the new work but uncovered gene expression differences in prenatal developing brains last year. Previous research traced sex differences to subcortical structures, where sex hormone receptors are expressed, but “the cortex is not the part of the brain that you typically think of when you think about sex differences,” he says. “I think it’s a landmark.” Of the thousands of genes flagged in the new study, 133 showed consistent sex differences across all brain cell types in six cortical regions sampled from postmortem brains, donated by 15 men (who all had XY sex chromosomes) and 15 women (who all had XX sex chromosomes), aged 26 to 78 years. Two of these regions—the fusiform gyrus and the inferior lateral temporo-occipital cortex—have more gray-matter volume in men, previous MRI studies suggest; two others, the caudal insula and intraparietal sulcus, have more gray matter in women; and the final two regions, the angular gyrus and the retrosplenial cortex, show no sex bias in gray-matter volume. Intriguingly, 119 of the 133 genes are autosomal, meaning men and women should have, at least in theory, an equal dose. That makes them “ground zero for molecular sex differences in the brain,” says study investigator Armin Raznahan, chief of the Section on Developmental Neurogenomics at the U.S. National Institute of Mental Health. © 2026 Simons Foundation

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 30235 - Posted: 05.06.2026

By Meghan Rosen For the first time, doctors have used stem cells to try and repair the spinal cords of human fetuses in the womb. The new technique attempts to heal nerve damage caused by spina bifida, a disabling birth defect. In this condition, the bony tissue of a fetus’s spine doesn’t knit together properly around the spinal cord. That can cause a kaleidoscope of medical issues, including lifelong paralysis and bladder and bowel problems. Traditional fetal surgery to patch up the spine can limit the scope of these problems — but it does not repair nerve damage that has already occurred. Adding living stem cells to the procedure might. At least, that’s the goal of fetal surgeon Diana Farmer’s team. So far, the approach appears to be safe, the researchers reported earlier this year in theLancet. In six fetal patients with severe spina bifida, applying a stem cell–loaded patch to their exposed spinal cords did not cause infection, tumor growth or interfere with healing. That’s important because “no one knew what stem cells would do inside a fetus,” says Farmer, of the University of California, Davis. For now, the vital question — whether the technique mends fetal spinal cords — remains unanswered. That’s because researchers are still performing follow-up assessments of the patients, who are now toddlers. At this stage, it’s too early to say how well the surgery worked, and Farmer is careful not to speculate. “If we could get every kid to not be in a wheelchair,” she says, “that would be fantastic.” But the team won’t know for a few years. Until then, Farmer says, she doesn’t want to give people false hope. In some ways, this study represents “a seismic shift” in the field, says Ramen Chmait, director of Los Angeles Fetal Surgery at the University of Southern California, who was not involved with the work. If the technique pans out, he says, it “could be a huge, important step in modern-day medicine.” © Society for Science & the Public 2000–2026.

Keyword: Development of the Brain; Stem Cells
Link ID: 30230 - Posted: 05.02.2026

By Bethany Brookshire It’s easy to think of the human body as a single, fully integrated unit. After all, stub your toe all the way at one end of your body, and your brain registers it at the other. A suite of muscles works together to hop up-and-down and the lungs fill with air to expel curses from your mouth. In this moment, your body is one organism, one set of cells all pulling together against the world — and whatever it was that hurt your toe. But while our cells all work together to help us walk, eat and argue with each other on the internet, they are not all pulling together toward the same goal all the time. Each one of the body’s 30 trillion to 40 trillion human cells is its own world, with its own set of DNA that accumulates its own changes over time. These mutations can mean nothing, but they can also mean everything. While many mutations are inert, others cause harm. Still others bring hope, and could correct some of the body’s problems, science writer Roxanne Khamsi explains in Beyond Inheritance. The book draws on the latest research across multiple fields of science to show that mutations are with us throughout our lives, shaping our health and our lifespans. Many people might think of mutations as things that arise and take over only in times of trouble such as cancer. Otherwise, mutation is something that matters only if it’s passed down to the next generation — whether it produces a new eye color or a serious genetic disorder. But mutations do far more than determine what we look like when we’re born and the manner in which we die, Khamsi argues. “Our genetic destinies are not necessarily defined by what we inherit from our biological parents,” she writes. © Society for Science & the Public 2000–2026.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 30208 - Posted: 04.22.2026

Miryam Naddaf By analysing more than a million brain cells, researchers have uncovered widespread differences in patterns of gene activity between male and female brains. The work, which defined sex on the basis of a person’s combination of sex chromosomes, could help to explain why the risk of developing some brain conditions — such as schizophrenia and Alzheimer’s disease — differs between males and females. Although the differences were subtle, the team identified more than 100 genes that showed consistent variation in their expression between males and females across several brain regions. The work was published on 16 April in Science1. “Having these gene-expression signatures provides a molecular handle to understanding the biology of how the brains of men and women might be functioning slightly differently in the context of the different hormonal environments that their bodies produce,” says Jessica Tollkuhn, a neuroscientist and molecular biologist at Cold Spring Harbor Laboratory in New York. She adds that “understanding sex differences in disease susceptibility could lead to better treatments to benefit everyone”. Subtle differences Previous studies2,3 have documented sex differences when it comes to a person’s risk of developing various neurological conditions. For example, schizophrenia, attention deficit hyperactivity disorder (ADHD) and Parkinson’s disease are more common in biological males — who typically have XY sex chromosomes. By contrast, Alzheimer’s disease and mood disorders such as depression and anxiety tend to be more common in females, whose sex chromosomes are usually XX. © 2026 Springer Nature Limited

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 30207 - Posted: 04.18.2026

By Pam Belluck Since the approval of new Alzheimer’s drugs in recent years, there has been a lingering question: While data indicated that they could modestly slow cognitive decline for some patients, would that effect be meaningful or too slight to make difference? A new review of research spanning a decade, published on Wednesday, concluded that the clinical benefit of these and similar drugs is negligible. But the way the review was conducted spurred heated criticism from many Alzheimer’s experts, including some who had been skeptical of some of them. The review, published by Cochrane, an international network of health researchers, evaluated studies that were conducted on seven monoclonal antibody drugs developed over the last two decades to target amyloids, proteins that form plaques in the brains of people who have Alzheimer’s disease. Some Alzheimer’s experts said the conclusions were meaningless because the review swept under one umbrella drugs that had shown very dissimilar results and worked differently. The experts noted that data from the two most recent drugs studied — Leqembi and Kisunla — showed they could slow cognitive decline, which led to approval from the Food and Drug Administration and made them the only anti-amyloid drugs available to patients. But a vast majority of the studies analyzed in the review involved four earlier drugs that had failed clinical trials or were never approved and a fifth drug that was pulled from the market. “The problem with the review is the mix of ingredients,” said Dr. Jason Karlawish, a director of the Penn Memory Center at the University of Pennsylvania, who has been skeptical or cautious toward some of the drugs over the years. “They took some of the rotten ingredients and mixed it in with the fresh food, and the result is a stinky stew.” © 2026 The New York Times Company

Keyword: Alzheimers
Link ID: 30206 - Posted: 04.18.2026

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

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

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

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 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

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

Jon Hamilton A little brain training today may help stave off Alzheimer's disease and other forms of dementia for at least 20 years. That's the conclusion of a study of older adults who participated in a cognitive exercise experiment in the 1990s that was designed to increase the brain's processing speed. The federally funded study of 2,802 people found that those who did eight to 10 roughly hourlong sessions of cognitive speed training, as well as at least one booster session, were about 25% less likely to be diagnosed with dementia over the next two decades. "We now have a gold-standard study that tells us that there is something we can do to reduce our risk for dementia," says Marilyn Albert, an author of the study and a professor of neurology at Johns Hopkins University School of Medicine. "It's super-exciting to see that these effects are still holding 20 years out," says Jennifer O'Brien, an associate professor of psychology at the University of South Florida who was not involved in the research. The study appears in the journal Alzheimer's & Dementia: Translational Research & Clinical Interventions. The result is good news for people like George Kovach, 74, who started doing cognitive speed training a decade ago. This illustration shows a pink human brain with stick legs and stick arms. The pink stick arms are holding up a black barbell with black disk-shaped weights on each end. © 2026 npr

Keyword: Alzheimers; Learning & Memory
Link ID: 30127 - Posted: 02.18.2026