Links for Keyword: Development of the Brain

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Brain has five ‘eras’, scientists say – with adult mode not starting until early 30s

Hannah Devlin Science correspondent Scientists have identified five major “epochs” of human brain development in one of the most comprehensive studies to date of how neural wiring changes from infancy to old age. The study, based on the brain scans of nearly 4,000 people aged under one to 90, mapped neural connections and how they evolve during our lives. This revealed five broad phases, split up by four pivotal “turning points” in which brain organisation moves on to a different trajectory, at around the ages of nine, 32, 66 and 83 years. “Looking back, many of us feel our lives have been characterised by different phases. It turns out that brains also go through these eras,” said Prof Duncan Astle, a researcher in neuroinformatics at Cambridge University and senior author of the study. “Understanding that the brain’s structural journey is not a question of steady progression, but rather one of a few major turning points, will help us identify when and how its wiring is vulnerable to disruption.” The childhood period of development was found to occur between birth until the age of nine, when it transitions to the adolescent phase – an era that lasts up to the age of 32, on average. In a person’s early 30s the brain’s neural wiring shifts into adult mode – the longest era, lasting more than three decades. A third turning point around the age of 66 marks the start of an “early ageing” phase of brain architecture. Finally, the “late ageing” brain takes shape at around 83 years old. The scientists quantified brain organisation using 12 different measures, including the efficiency of the wiring, how compartmentalised it is and whether the brain relies heavily on central hubs or has a more diffuse connectivity network. From infancy through childhood, our brains are defined by “network consolidation”, as the wealth of synapses – the connectors between neurons – in a baby’s brain are whittled down, with the more active ones surviving. During this period, the study found, the efficiency of the brain’s wiring decreases. © 2025 Guardian News & Media Limited

Aging as adaptation: Learning the brain’s recipe for resilience

By Dana Rubi Levy, Kevin Mastro, Michael Ryan Any seasoned baker knows the importance of being flexible. If you are missing an ingredient or hosting a guest with dietary restrictions, you might need to swap yogurt for eggs or oil for butter. The final product may differ, but it can still be rich and satisfying. In much the same way, our brain constantly makes substitutions and adjustments in response to the inevitable changes in our internal and external environments. To understand these changes, scientists often compare the brain and behavior of older people, aged 60 and up, with those of younger people, aged 20 to 30. Despite considerable individual variability, older people—on average—have slower processing speeds, rely more on past experience to solve problems, and have less behavioral flexibility. These findings have shaped our theories about how age-related changes in the brain drive behavior. In recent years, however, a conceptual shift has emerged, raising questions about whether some age-related changes are not solely the result of cognitive decline. Instead, some may be adaptive and address age-related constraints, such as changes in metabolism and increased inflammation. Moreover, scientists have begun to question whether young adulthood, characterized by a period of highly flexible decision-making, is the right benchmark to assess cognition across the lifespan. Given the evolving landscape of the aging brain, change is necessary, and not all deviations from the young-adult “benchmark” should be seen as decline. The main challenge for neuroscientists is to determine which of these age-related adaptations are beneficial and which are detrimental. In other words, which substitutions retain the original flavors, and which result in a dish that falls flat? © 2025 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 30012 - Posted: 11.15.2025

What We Can Learn From Brain Organoids

By Carl Zimmer In Paola Arlotta’s lab at Harvard is a long, windowless hallway that is visited every day by one of her scientists. They go there to inspect racks of scientific muffin pans. In every cavity of every pan is a pool of pink liquid, at the bottom of which are dozens of translucent nuggets no bigger than peppercorns. The nuggets are clusters of neurons and other cells, as many as two million, normally found in the human brain. On their daily rounds, the scientists check that the nuggets are healthy and well-fed. “No first-year students walk in that corridor,” Dr. Arlotta said. “You have to be experienced enough to go there, because the risk is very high that you’re going to mess up the work that took years to build.” The oldest nuggets are now seven years old. Back in 2018, Dr. Arlotta and her colleagues created them from skin cells originally donated by volunteers. A chemical cocktail transformed them into the progenitor cells normally found in the fetal human brain. The cells multiplied into neurons and other types of brain cells. They wrapped their branches around each other and pulsed with electrical activity, much like the pulses that race around inside our heads. One such nugget can contain more neurons than the entire brain of a honeybee. But Dr. Arlotta is quick to stress that they are not brains. She and her colleagues call them brain organoids. “It’s so important to call them organoids and not brains, because they’re no such thing,” she said. “They are reductionist replicas that can show us some things that are the same, and many others that are not.” And yet the similarities are often remarkable, as Dr. Arlotta and her colleagues recently demonstrated in a new report on their long-lived organoids. After the organoids started growing in 2018, their neurons began behaving like the those in a fetal human brain, down to way their genes switched on and off. And as the months passed, the neurons matured to resemble the neurons in a baby after birth. © 2025 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 30003 - Posted: 11.08.2025

First-ever atlas of brain development shows how stem cells turn into neurons

Miryam Naddaf Scientists have created the most detailed maps yet of how our brains differentiate from stem cells during embryonic development and early life. In a Nature collection including five papers published yesterday, researchers tracked hundreds of thousands of early brain cells in the cortices of humans and mice, and captured with unprecedented precision the molecular events that give rise to a mixture of neurons and supporting cells. “It’s really the initial first draft of any ‘cell atlases’ for the developing brain,” says Hongkui Zeng, executive vice-president director of the Allen Institute for Brain Science in Seattle, Washington, and a co-author of two papers in the collection. These atlases could offer new ways to study neurological conditions such as autism and schizophrenia. Researchers can now “mine the data, find genes that may be critical for a particular event in a particular cell type and at a particular time point”, says Zeng. “We have a very exciting time coming,” adds Zoltán Molnár, a developmental neuroscientist at the University of Oxford, UK, who was not involved with any of the studies. The work is part of the BRAIN Initiative Cell Atlas Network (BICAN) — a project launched in 2022 by the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative at the US National Institutes of Health with US$500 million in funding to build reference maps of mammalian brains. Patterns of development Two of the papers map parts of the mouse cerebral cortex — the area of the brain involved in cognitive functions and perception. Zeng and her colleagues focused on how the visual cortex develops from 11.5-day-old embryos to 56-day-old mice. They created an atlas of 568,654 individual cells and identified 148 cell clusters and 714 subtypes1. “It’s the first complete high-resolution atlas of the cortical development, including both prenatal and postnatal” phases, says Zeng. © 2025 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 7: Vision: From Eye to Brain
Link ID: 30002 - Posted: 11.08.2025

Constellation of studies charts brain development, offers ‘dramatic revision’

By Holly Barker Multiple mouse and human brain atlases track the emergence of distinct cell types during development and uncover some of the pathways that decide a cell’s fate. The findings were published today in a collection of Nature papers. The papers highlight the timing and location of cell diversification and offer fresh insights into the evolution of those cells. Neuronal subtypes emerge at starkly different times in distinct brain regions, according to multiple mouse studies. And the work upends ideas about cell migration, including the notion that a portion of cortical neurons are made on site, developmental maps of the human brain suggest. “This is a dramatic revision of the fundamental principles that we thought were true in the cerebral cortex,” says Tomasz Nowakowski, associate professor of neurological surgery, anatomy and psychiatry, and of behavioral sciences, at the University of California, San Francisco and an investigator on one of the new studies. The special issue comprises 12 papers—including 6 newly published ones—from groups working as part of the BRAIN Initiative Cell Atlas Network. The work builds on the network’s complete cell census, published in 2023, that cataloged 34 classes and 5,322 unique cell types in the adult mouse brain. “Those cell types don’t appear out of a vacuum at the same time,” says Nowakowski, who co-authored a commentary on the new collection. Pinpointing when those cells emerge and where they originate from was the “obvious next question,” he says. At birth, the mouse brain contains all the initial cell classes that diversify into the multitude of neurons and glia found in older rodents. But precisely when that diversification occurs varies among brain regions: In the visual cortex, new cell types emerge weeks after birth and peak twice—once when the animal first opens its eyes and then again at the onset of the critical period, according to one study. © 2025 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 30001 - Posted: 11.08.2025

Marthe Gautier, 96, Dies; Had Key Role in Down Syndrome Breakthrough

By Denise Grady Dr. Marthe Gautier, a physician and researcher who had a major role in identifying the cause of Down syndrome but whose achievement was undermined when a male colleague took credit for her work, died on April 30, 2022. She was 96. Her death, in a retirement home in Meaux, France, though not widely reported at the time, was confirmed by her great-niece Tatiana Giraud. The New York Times, which had prepared an obituary about Dr. Gautier in advance, in 2018, learned of her death only recently. The disputed research in which Dr. Gautier was involved produced a historic breakthrough: It revealed that people with Down syndrome have an extra chromosome, one of the microscopic strands of DNA and protein that carry a person’s genetic blueprint. Most humans have 46 chromosomes. Down syndrome is also called trisomy 21, meaning that three copies of the 21st chromosome are present instead of two, for a total of 47 chromosomes. The discovery, at the Armand-Trousseau Hospital in Paris in 1958, was the first to link an abnormal number of chromosomes to a disorder that causes intellectual disability. More connections between such conditions and aberrant chromosomes were soon found. Those advances led to the development of tests to diagnose the disorders before birth, making it possible to terminate affected pregnancies in many cases. Dr. Gautier’s story “starts like a fairy tale and ends like villainy,” said Dr. Jean Kachaner, a former student of hers who is a pediatric cardiologist at the Necker Hospital for children in Paris. © 2025 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 29997 - Posted: 11.05.2025

Ramping up cortical activity in early life sparks autism-like behaviors in mice

By Sarah DeWeerdt A temporary increase in neuronal activity in the cortex of newborn mice leads to social deficits in adulthood, according to a new preprint. Those adult rodents also show changes in brain electrical activity, gene expression and connectivity that are reminiscent of autism. The analysis lends support to a prominent hypothesis of autism’s origins, which holds that the condition can arise from an excess of excitatory signaling or insufficient inhibitory signaling in the brain, the study investigators write in their paper. Over the years, support for this signaling imbalance hypothesis has come from other studies in mice and observations that some people with autism have seizures or display excess neuronal activity in electroencephalography (EEG) recordings relative to people without the condition. Postmortem analysis suggests autistic people have more excitatory synapses in the prefrontal cortex than non-autistic people. But determining causality and the role of inhibitory signaling has been difficult. In contrast with most earlier work, the new study “really underscore[s] a different way of looking at excitation-inhibition imbalance, which is looking at it during development as a cause of subsequent changes in brain function that could be associated with autism,” says Vikaas Sohal, professor of psychiatry and behavioral science at the University of California, San Francisco, who was not involved in the work. The study was posted on bioRxiv last month. © 2025 Simons Foundation

Protein tug-of-war controls pace of synaptic development, sets human brains apart

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

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 29984 - Posted: 10.25.2025

Neurons can communicate via hidden network of nanotubes

By Catherine Offord Neuroscientists have been studying synapses, the fundamental junctions that allow rapid communication between neurons, for well over a century. But now, a research team has identified a different set of neuronal connections in the brain—one that might bypass synapses altogether, the group reports today in Science. Using high-resolution images of mouse and human brains, the researchers documented a network of tubes, each about 3 micrometers long and just a few hundred nanometers thick, connecting neurons to one another. In mouse cells, the team found evidence of neuron-to-neuron transfer of electrical signals via these nanotubes, and even the passage of proteins linked to Alzheimer’s disease. “We’ve been looking at the brain forever now, and every once in a while, a surprise comes along,” says Lary Walker, a neuroscientist and professor emeritus at Emory University who was not involved in the work. Although there’s still a lot to pin down about these nanotubes’ basic biology, he suggests the discovery could have wide implications for scientists’ understanding of neuronal communication and disease. Researchers already knew some cells form nanotubes. In a 2004 Science paper, a team in Germany described tiny channels that emerged spontaneously between rat kidney cells in a dish and allowed the transfer of organelles. Studies since then have documented these so-called tunneling nanotubes (TNT) in a variety of cell and tissue types, and have linked their presence to processes including organ development, tissue repair, and the spread of viruses within the body. Recent research has identified TNTs forming between neurons and microglia, the brain’s immune cells, and hinted that they have important functions in brain health and disease. But scientists have struggled to find such conduits connecting neurons to one another in the mammalian brain. The search is particularly tricky because neurons’ branching ends, or dendrites, form a tangled mass with one another, and because researchers lack molecular markers distinguishing nanotubes from other cell structures. © 2025 American Association for the Advancement of Science.

Study links greater inequality to structural changes in children’s brains

Tobi Thomas Health and inequalities correspondent Scientists have linked the impact of living in an unequal society to structural changes in the brains of children – regardless of individual wealth – for the first time. A study of more than 10,000 young people in the US discovered altered brain development in children from wealthy and lower-income families in areas with higher rates of inequality, which were also associated with poorer mental health. The data was gathered from the Adolescent Brain Cognitive Development study and published in the journal Nature Mental Health. Researchers at King’s College London, Harvard University, and the University of York then measured inequality within a particular US state by scoring how evenly income is measured. States with higher levels of inequality included New York, Connecticut, California and Florida, while Utah, Wisconsin, Minnesota and Vermont were more equal. MRI scans were analysed to study the surface area and thickness of regions in the cortex, including those involved in higher cognitive functions including memory, emotion, attention and language. Connections between different regions of the brain were also analysed by the scans, where changes in blood flow indicate brain activity. The research found that children living in areas with higher levels of societal inequality, including socioeconomic imbalances and deprivation for example, were linked to having a reduced surface area of the brain’s cortex, and altered connections between multiple regions of the brain. The findings, the first to reveal the impact societal inequality has on the structures of the brain, also provided evidence that the impacted neurodevelopment might relate to future mental health and cognitive function. Notably, these brain changes in children were seen regardless of their economic background. © 2025 Guardian News & Media Limited

Swapping old immune cells in the brain with fresh ones could treat disease

Heidi Ledford After a mouse received treatment to eliminate immune cells called microglia, it was injected with human progenitor cells that developed into human immune cells (green, pink and blue) in the animal’s brain.Credit: M. M.-D. Madler et al./Nature A fresh supply of the immune cells that keep the brain tidy might one day help to treat a host of conditions, from ultra-rare genetic disorders to more familiar scourges, such as Alzheimer’s disease. In the past few months, a spate of new studies have highlighted the potential of a technique called microglia replacement and explored ways to make it safer and more effective. “This approach is very promising,” says Pasqualina Colella, who studies gene and cell therapy at Stanford University School of Medicine in California. “But the caveat is the toxicity of the procedure.” Microglia are immune cells that patrol the brain, gobbling up foreign invaders, damaged cells and harmful substances. They can help to protect neurons — cells that transmit and receive messages to and from other tissues — during seizures and strokes, and they prune unneeded connections between neurons during normal brain development. “Microglia do a lot of important things,” says Chris Bennett, a psychiatrist who studies microglia at the Children’s Hospital of Philadelphia in Pennsylvania. “So, it’s not surprising that they are involved in the pathogenesis of many diseases.” Those diseases include a suite of rare disorders caused by genetic mutations that directly affect microglia. Malfunctioning microglia have also been implicated in more familiar conditions with complex causes, such as Alzheimer’s disease and Parkinson’s disease, as well as ageing, says Bo Peng, a neuroscientist at Fudan University in Shanghai, China. © 2025 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 29944 - Posted: 09.27.2025

Child’s Death Shows How Measles in the Brain Can Kill Years after an Infection

By Andrea Thompson A school-aged child in Los Angeles County has died from a rare but always fatal complication from a measles infection they acquired when they were an infant who was too young to be vaccinated. The first dose of the vaccine is typically not administered until one year of age. Experts say the death underscores the need for high levels of vaccination in a population to protect the most vulnerable against the disease, as well as from side effects that can occur long after the initial illness has passed. “This case is a painful reminder of how dangerous measles can be, especially for our most vulnerable community members,” said Los Angeles County Health Officer Muntu Davis in a recent statement. The child who died suffered from subacute sclerosing panencephalitis (SSPE), a progressive brain disorder that usually develops two to 10 years after a measles infection. The measles virus appears to mutate into a form that avoids detection by the immune system, allowing it to hide in the brain and eventually destroy neurons. “It’s just a virus that goes unchecked and destroys brain tissue, and we have no therapy for it,” said Walter Orenstein, an epidemiologist and professor emeritus at Emory University, to Scientific American earlier this year. People with SSPE experience a gradual, worsening loss of neurological function and usually die within one to three years after diagnosis, according to the Los Angeles County Health Department. The disorder affects only about one in every 10,000 people who contract measles. But the risk may be as high as about one in 600 for those who are infected as infants. “There is no treatment for this. Children who suffer from this will always die,” said Paul Offit, director of the Vaccine Education Center and an attending physician in the Division of Infectious Diseases at Children’s Hospital of Philadelphia, in a previous interview with Scientific American. © 2025 SCIENTIFIC AMERICAN,

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 1: Introduction: Scope and Outlook
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 29927 - Posted: 09.13.2025

Even healthy brains decline with age. Here's what you can do

Jon Hamilton After about age 40, our brains begin to lose a step or two. Each year, our reaction time slows by a few thousandths of a second. We're also less able to recall items on a shopping list. Those changes can be signs of a disease, like Alzheimer's. But usually, they're not. "Both of those things, memory and processing speed, change with age in a normal group of people," says Matt Huentelman, a professor at TGen, the Translational Genomics Research Institute, in Phoenix. Huentelman should know. He helps run MindCrowd, a free online cognitive test that has been taken by more than 700,000 adults. About a thousand of those people had test scores indicating that their brain was "exceptional," meaning they performed like a person 30 years younger on tests of memory and processing speed. Genetics played a role, of course. But Huentelman and a team of researchers have been focusing on other differences. A key protein called Reelin may help stave off Alzheimer's disease, according to a growing body of research. A protein called Reelin keeps popping up in brains that resist aging and Alzheimer's "We want to study these exceptional performers because we think they can tell us what the rest of us should be doing," he says. Early results suggest that sleep and maintaining cardiovascular health are a good start. Other measures include avoiding smoking, limiting alcohol and getting plenty of exercise. Huentelman was one of several dozen researchers who met in Miami this summer to discuss healthy brain aging. The event was hosted by the McKnight Brain Research Foundation, which funds studies on age-related cognitive decline and memory loss. To preserve cognitive function in later life, "we're going to have to understand [brain] aging at a mechanistic level," says Alice Luo Clayton, a neuroscientist who is the group's chief executive officer. © 2025 npr

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 29863 - Posted: 07.19.2025

Protein signatures may one day tell brain diseases apart before symptoms

By Tina Hesman Saey A large-scale study of proteins in blood and cerebrospinal fluid could pave the way for improved blood tests to diagnose multiple brain diseases — and potential early warning signs of disease risk — researchers report July 15 in several papers in Nature Medicine and Nature Aging. Proteins do much of the work to keep cells and bodies working. Trouble with these building blocks can spell disease; protein misfolding, for instance, links many brain diseases. The results, drawn from samples from 18,645 people, reveal biochemical fingerprints of neurodegenerative disorders such as Alzheimer’s, Parkinson’s, frontotemporal dementia and amyotrophic lateral sclerosis, or ALS. These tests could also help identify disease subtypes and track progression before symptoms emerge. Such well-validated and robust results are “more likely to ultimately translate into something that’s medically actionable,” says Andrew Saykin, director of the Indiana Alzheimer’s Disease Research Center in Indianapolis, which contributed samples to the effort. In one key finding, researchers discovered that individuals carrying a form of the APOE gene called APOE4 — the biggest genetic risk factor for developing Alzheimer’s — share a blood signature regardless of diagnosis. That signature appeared not only in people with Alzheimer’s but also in those with other brain diseases or no neurodegeneration at all, neuroscientist Caitlin Finney and colleagues report in Nature Medicine. The APOE4 protein signature involves proteins that respond to infection and inflammation, hinting at how the variant predisposes carriers to brain diseases. It also suggests that the APOE4 protein may be involved in the early stages of multiple diseases. © Society for Science & the Public 2000–2025.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 29860 - Posted: 07.16.2025

Organ age, not just your birthday, may determine your health risks

By Celina Zhao You could be 45 on paper but 60 in your kidneys. Turns out, your organs have birthdays of their own — and how well they’re faring may set the pace for your health, researchers report July 9 in Nature Medicine. Using data from nearly 45,000 people, scientists developed a blood-based test to estimate the biological age of 11 organs, providing a measure of how healthy or worn down each organ is. When a person has an organ substantially “older” than their actual age, disease risks tied to that organ surge. Conversely, extremely youthful brains and immune systems are linked to living longer, the results suggest. “The fact that [the researchers] can create an organ age using proteins — and use it to predict diseases that you would expect to be predicted from that organ — is quite amazing,” says Sarah Harris, a molecular biologist at the University of Edinburgh who was not involved in the study. Aging is far from a uniform process; each organ follows its own clock of decline. One way to track this hidden timeline, previously discovered by Stanford neurology researchers Hamilton Oh and Tony Wyss-Coray, is through the thousands of proteins coursing through our blood. Some unmistakably originate in the liver, while others can be traced to the lungs. Analyzing these proteins can reveal clues about how each organ is holding up. In the new study, the team zeroed in on thousands of patients from the UK Biobank, a long-term database tracking the health of individuals ages 40 to 70 for up to 17 years. By assessing proteins in the blood, the team determined the average protein signature for, say, a 40-year-old liver or 70-year-old arteries. © Society for Science & the Public 2000–2025.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 29859 - Posted: 07.16.2025

How fast are you ageing? Ordinary brain scans reveal the pace

Heidi Ledford Telltale features in standard brain images can reveal how quickly a person is ageing, a study of more than 50,000 brain scans has shown1. Pivotal features include the thickness of the cerebral cortex — a region that controls language and thinking — and the volume of grey matter that it contains. These and other characteristics can predict how quickly a person’s ability to think and remember will decline with age, as well as their risk of frailty, disease and death. Although it’s too soon to use the new results in the clinic, the test provides advantages over previously reported ‘clocks’ — typically based on blood tests — that purport to measure the pace of ageing, says Mahdi Moqri, a computational biologist who studies ageing at Harvard Medical School in Boston, Massachusetts. “Imaging offers unique, direct insights into the brain’s structural ageing, providing information that blood-based or molecular biomarkers alone can’t capture,” says Moqri, who was not involved in the study. The results were published today in Nature Aging. Genetics, environment and disease all affect the speed of biological ageing. As a result, chronological age does not always reflect the pace at which time takes its toll on the body. Researchers have been racing to develop measures to fill that gap. Ageing clocks could be used early in life to assess an individual’s risk of age-related illness, when it might still be possible to intervene. They could also aid testing of treatments aimed at slowing ageing, by providing a marker to track the effects of the intervention in real time. © 2025 Springer Nature Limited

Common Assumption About Aging May Be Wrong, Study Suggests

By Mohana Ravindranath A new analysis of data gathered from a small Indigenous population in the Bolivian Amazon suggests some of our basic assumptions about the biological process of aging might be wrong. Inflammation is a natural immune response that protects the body from injury or infection. Scientists have long believed that long-term, low-grade inflammation — also known as “inflammaging” — is a universal hallmark of getting older. But this new data raises the question of whether inflammation is directly linked to aging at all, or if it’s linked to a person’s lifestyle or environment instead. The study, which was published today, found that people in two nonindustrialized areas experienced a different kind of inflammation throughout their lives than more urban people — likely tied to infections from bacteria, viruses and parasites rather than the precursors of chronic disease. Their inflammation also didn’t appear to increase with age. Scientists compared inflammation signals in existing data sets from four distinct populations in Italy, Singapore, Bolivia and Malaysia; because they didn’t collect the blood samples directly, they couldn’t make exact apples-to-apples comparisons. But if validated in larger studies, the findings could suggest that diet, lifestyle and environment influence inflammation more than aging itself, said Alan Cohen, an author of the paper and an associate professor of environmental health sciences at Columbia University. “Inflammaging may not be a direct product of aging, but rather a response to industrialized conditions,” he said, adding that this was a warning to experts like him that they might be overestimating its pervasiveness globally. “How we understand inflammation and aging health is based almost entirely on research in high-income countries like the U.S.,” said Thomas McDade, a biological anthropologist at Northwestern University. But a broader look shows that there’s much more global variation in aging than scientists previously thought, he added. © 2025 The New York Times Company

How developing neurons simplify their search for a synaptic mate

By Calli McMurray The hunt for a soulmate can be hard work—particularly for naive neurons. During development, the cells’ axons snake through burgeoning brain areas in search of the perfect dendrite to form a synapse with. Cell surface proteins serve as molecular identification tags to help axons distinguish “Mr. Wrong” dendrite from “Mr. Right,” according to the chemoaffinity hypothesis. But there are too many cells and too few cell surface proteins for this to be the only strategy, says Claude Desplan, professor of biology and neural science at New York University. “There is no way you can find your partner in a big mess of many different thousands of types of neurons. So you do need to reduce the issue.” In this brain region, 50 types of olfactory receptor neurons link up with 50 types of neurons that project to a sensory integration hub called the mushroom body; each synapse type bunches together inside the lobe to form its own distinct glomerulus. The axons of olfactory receptor neurons do not search the entire structure for their postsynaptic partner. Instead, the projection neurons inside the lobe send their dendrites to meet axons traveling along the surface. Once the two join up, they descend to their proper place in the lobe, imaging experiments show. “Axons don’t need to delve deep. They only need to survey the surface in order to find their target,” says the study’s principal investigator, Liqun Luo, professor of biology at Stanford University. To make matters even simpler, the axons stick to a narrow, genetically determined trajectory, Luo says. Cortical regions may achieve a similar simplification through columns and layers: Axons travel to a certain brain region and then plunge to a particular depth, Luo suggests. Genetically altering these trajectories precludes the olfactory receptor neurons from finding their proper mate, additional experiments show. Dendrites from the postsynaptic cell still wait for their partner at the surface, but “they will be sitting there waiting forever,” Luo says. Some cells “are still sticking their dendrites out” in adulthood, and in at least one case the team observed, a cell eventually matched with another partner. © 2025 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 29823 - Posted: 06.07.2025

Mice grow bigger brains when given this stretch of human DNA

Gemma Conroy Researchers have identified a genetic dial in the human brain that, when inserted in mice, boosts their brain size by about 6.5%.Credit: Sergey Bezgodov/Shutterstock Taking a snippet of genetic code that is unique to humans and inserting it into mice helps the animals to grow bigger brains than usual, according to a report out in Nature today1. The slice of code — a stretch of DNA that acts like a dial to turn up the expression of certain genes — expanded the outer layer of the mouse brain by increasing the production of cells that become neurons. The finding could partially explain how humans evolved such large brains compared with their primate relatives. This study goes deeper than previous work that attempted to unpick the genetic mechanisms behind human brain development, says Katherine Pollard, a bioinformatics researcher at the Gladstone Institute of Data Science and Biotechnology in San Francisco, California. “The story is much more complete and convincing,” she says. How the human brain grew to be so big and complex remains a mystery, says Gabriel Santpere Baró, a neuroscientist who studies genomics at the Hospital del Mar Medical Research Institute in Barcelona, Spain. “We still do not have a definitive answer to how the human brain has tripled in size since our split from chimpanzees” during evolution, he says. Previous studies2,3 have hinted that human accelerated regions (HARs) — short snippets of the genome that are conserved across mammals, but which underwent rapid change in humans after they evolutionarily diverged from chimpanzees — could be key contributors to brain development and size. But the exact mechanisms that underlie the brain-building effects of HARs are yet to be uncovered, says study co-author Debra Silver, a developmental neurobiologist at Duke University in Durham, North Carolina. © 2025 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 29791 - Posted: 05.17.2025

Recruitment issues jeopardize ambitious plan for human brain atlas

By Calli McMurray At least six new brain donors who can do a functional MRI scan—that’s what it will take to complete the most comprehensive human brain atlas yet, project investigators say. The Human and Mammalian Brain Atlas (HMBA) aims to capture information about the identity and location of cells across the entire brain and tie it, for the first time, to the functional organization of the cortex. The atlas, one of several projects in the BRAIN Initiative Cell Atlas Network funded by the U.S. National Institutes of Health, stands to be “a quantum jump in the quality of the data and the resolution that we can analyze it,” says David Van Essen, professor of neuroscience at Washington University in St. Louis and an HMBA investigator. The first atlas, published by the Allen Institute in 2011, contains gene expression information across the brain projected onto an MRI reference space. “By today’s standards, that’s really low-resolution information,” but it’s still “used like crazy,” says Ed Lein, co-creator of the first atlas and one of the lead investigators of the HMBA project at the Allen Institute for Brain Science. Subsequent iterations mapped more of the human brain’s cellular and molecular landscape and at higher resolution. A “first draft” cell atlas, Lein says, published in a trove of papers in 2023, employed single-cell sequencing techniques to catalog thousands of cell types in the human brain. But as “exceptional” as these resources are, their utility is limited by a lack of functional information about the brain regions, says Avram Holmes, associate professor of psychiatry at Rutgers University, who is not involved with the project. © 2025 Simons Foundation

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