By Giorgia Guglielmi Neuroscience textbooks have long cast mitochondria as pure neuronal powerhouses: These bean-shaped organelles just crank out a cell’s energy. That picture, however, is starting to look incomplete. Mitochondria do far more than fuel neurons, a growing body of research suggests. They also appear to help synapses communicate, regulate neurotransmitter release and shape social behavior. Mitochondrial function has also been tied to autism and related neurodevelopmental conditions, though that link remains debated. Even memory formation may lean on these tiny, double-membraned structures, according to a study published in Nature Metabolism in February. Increasing mitochondrial metabolism boosted long-term memory in both fruit flies and mice. Mitochondria are “not just permissive but also instructive,” says Ezgi Hacisuleyman, assistant professor of molecular medicine at the Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, who was not involved in the February study. Her unpublished results show that mitochondrial proteins are translated near active synapses, for example. Over the past decade, work from Hacisuleyman and others has fast expanded the repertoire of mitochondria in the brain. Taken together, she adds, the findings put mitochondria “more in the center of how we think about brain function and memory.” Mitochondria may be central to brain function, but they are not central inside neurons. Many synapses sit hundreds of micrometers away from a cell’s soma, so small, mobile mitochondria must travel there to deliver fuel in the form of ATP. In dendrites, mitochondria often linger near spines, and activity recruits them to presynaptic boutons, where they help stabilize neurotransmitter release. © 2026 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 30310 - Posted: 07.04.2026

By Michael Howerton Healthy brains may be built through a process of controlled damage and rapid repair. The most dangerous type of DNA damage is a regular feature of healthy early brain development, experiments in mice show. As newborn neurons squeeze through the cramped, narrow spaces of developing brain tissue, they break both strands of their DNA, researchers report June 17 in Nature. The breaks are repaired once neurons reach their destination, usually within a day. It’s a paradox of vulnerability and resilience. Newborn neurons routinely sustain a kind of damage that kills most cells, yet they repair it and emerge intact, the researchers found. The speed of the repair surprised the team. “Somehow neurons can repair [the damage] very quickly without any sign of mutations or bad effect,” says neurobiologist Mineko Kengaku of Kyoto University in Japan. “It seems to be a normal developmental event.” The breaks appear in areas of the genome that aren’t crucial, the team found, which in most cases allows neurons to survive and grow without lasting damage. “It is surprising that, during evolution, the mammalian brain acquires such a clever strategy,” Kengaku says. More research is needed to understand the implications beyond mice, but Kengaku says the effect might even be more pronounced in humans. “During development, neurons have to migrate, and if the brain size is larger, then neurons have to migrate longer distances,” she says. “It is quite likely that neurons in human brains probably generate more DNA damage during development” than neurons in mice brains do. But a flawless break-and-repair cycle is not always guaranteed, Kengaku says. When it fails or is incomplete, the damage could persist. These instances, she says, could help explain some neurological conditions later in life. © Society for Science & the Public 2000–2026.

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: 30302 - Posted: 06.27.2026

Zoe Beketova When Adam Douglass began to study the tiny, transparent fish in the Danionella genus about 10 years ago, he had to get his animals from an out-of-state fish shop, where they were sold as an exotic pet breed. “The only information at all about trying to grow them in captivity came from online,” says Douglass, a neurobiologist at the University of Utah. Compared with zebrafish, which by that point had been a model species for biology research for decades, Danionella was little known to scientists. How things have changed. Last week, the Janelia Research Campus, the in-house research arm of the behemoth Howard Hughes Medical Institute (HHMI), announced a 10-year, roughly $1 billion research effort focused on using Danionella as a model for how brain cells and circuits drive complex behaviors in vertebrates. The effort will also draw on cutting-edge artificial intelligence (AI) tools to make sense of all the new data on the fish. “I think this is one of the most exciting opportunities that we’ve faced in the entire history of Janelia,” says neuroscientist Nelson Spruston, Janelia’s vice president and executive director. “There are a lot of structures in the brain and the rest of the body of fish that are identifiably similar to those of humans,” he adds, and there’s a long history of simple model organisms “leading to important insights that eventually result in cures and treatments for devastating diseases.” Danionella’s growing popularity comes from one (literally) clear advantage: Unlike zebrafish, which are transparent only for the first few weeks of their 3- to 4-year lives, Danionella remain so, meaning their brain is still visible—and easier to image—when they reach adulthood and engage in behaviors such as schooling, navigation, and courtship. The fish, only about the size of a grain of rice, never grow scales, develop pigmentation, or form a complete, bony skull. “All of these features that stand in the way of being able to get photons into and out of your skull [for imaging] are not there,” says Douglass, who has watched Danionella become a focus of dozens of labs worldwide

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: 30294 - Posted: 06.24.2026

Jon Hamilton The most powerful factors affecting a child's brain development involve socioeconomic opportunities, according to a study in the journal Science. The analysis of more than 2,300 9- and 10-year-olds found that environmental factors ranging from household income to education to neighborhood quality are associated with brain differences that can clearly be seen in MRI scans. The researchers also found that preteens who'd grown up in neighborhoods with lower incomes and limited social support had brain differences associated with less sleep and more stress. "Something is going on in these neighborhoods," says Scott Marek, the study's first author and an assistant professor of radiology at WashU School of Medicine. "We need to find out how socioeconomics is becoming biologically embedded." The research "highlights the fact that the environment in which we grow up and live has powerful impacts on our brain," says Russell Poldrack, a psychology professor at Stanford University who was not involved in the study. It also challenges earlier research that focused on links between brain development and factors like IQ and mental health. Those factors do appear to have a small influence on brain development, says Dr. Nico Dosenbach, an author of the new study and a professor at WashU Medicine in St. Louis. "But socioeconomics was, by a wide margin, absolutely the dominant variable," Dosenbach says. © 2026 npr

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: 30280 - Posted: 06.13.2026

By Natalia Mesa IQ is one of the most-studied traits in brain imaging studies. And yet it has a weaker relationship with brain structure and function in children than socioeconomic status does, according to a study published today in Science. The apparent link between IQ and brain differences largely disappears once socioeconomic status is controlled for, the findings suggest. The results point to the importance of factoring in socioeconomic status in analyses of brain imaging datasets, the researchers say. “If you’re not properly taking into account [socioeconomic status]” in brain imaging experiments, “you’re going to fool yourself,” says study investigator Nico Dosenbach, professor of neurology at Washington University in St. Louis. Dosenbach and his colleagues analyzed MRI scans and behavioral data from roughly 12,000 children aged 9 to 10 in the Adolescent Brain Cognitive Development (ABCD) Study, looking for correlations between measures of brain structure and function and 649 psychological, health, social and environmental factors. Socioeconomic variables—such as household income and where the child lives—were the most strongly associated with functional connectivity and cortical thickness. Differences in socioeconomics account for 16 percent of the variance in functional connectivity across the participants, the study found, which is among “the largest effects that are seen in these kinds of studies,” says Russ Poldrack, professor of psychology at Stanford University, who was not involved in the study. Socioeconomic status accounted for roughly 13 percent of the variance in cortical thickness. Sleep and screen time are also strongly linked to these brain features, although not as strongly as socioeconomics. © 2026 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 30279 - Posted: 06.13.2026

By Jake Buehler Zebra finches sing their young into biological preparedness for hot weather, all before they even leave the egg. As the heat punishes sun-crisped Australian woodlands, the adult birds make a rapid, peeping “heat call”. That signal kicks off genetic changes in unhatched baby zebra finches’ brains, researchers report June 11 in the Journal of Experimental Biology. The tune appears to give developing finches a physiology-bending forecast, giving them a leg up once they emerge into the broiling conditions on the other side of the eggshell. A decade ago, behavioral ecologist Mylene Mariette and her colleagues discovered that exposure to these heat calls in the egg shortly before hatching changed how the chicks dealt with high temperatures. They grew more slowly, preferred warmer places to nest and seemed better equipped to handle hot conditions. But it was unknown how hearing a simple song could trigger these kinds of physical and behavioral changes in the young. Mariette, of Deakin University in Waurn Ponds, Australia and Julia George, a neuroscientist at Clemson University in South Carolina wanted to know if the songs might initiate changes in the hypothalamus, a small region of the brain heavily involved in regulating metabolism and responses to heat. Hear the finch’s heat-induced call This high-pitched, rapid peeping is the “heat call” of the Australian zebra finch. The effect the call has on the developing brain’s vasculature may make the chicks more resilient against heat stroke. But the impact lasts the birds’ entire life. © Society for Science & the Public 2000–2026.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 15: Language and Lateralization
Link ID: 30278 - Posted: 06.13.2026

By Helena Kudiabor Microglia, known for scavenging debris and attacking pathogens, may also help regulate the hypothalamic-pituitary-gonadal axis, a new study shows. The findings, published in March in Science, suggest that microglia interact with and influence the function of hypothalamic neurons that release gonadotropin-releasing hormone (GnRH), which stimulates the pituitary to produce the hormones that spark ovulation and spermatogenesis. “One of the biggest surprises was the role of microglia in controlling the GnRH neurons, because this is a link that hadn’t been seen before,” says study investigator Alejandro Collado-Solé, a postdoctoral researcher in Eva González-Suárez’s group at the Spanish National Cancer Research Center. Microglia express a protein called RANK that is crucial to their effects on the hypothalamic-pituitary-gonadal axis. Knocking out RANK in mice reduces microglia’s interactions with GnRH neurons, lowers sex hormone levels and renders some of the animals infertile, the new study found. “The fact that these specific interactions in such a small region of the brain can have such profound effects on fertility—a very fundamental aspect of the survival of a species—was quite unexpected,” says Annie Ciernia, assistant professor of biochemistry and molecular biology at the University of British Columbia, who was not involved in the research. Microglia have been widely studied for their role in brain development, but the new study is the first to explore how these cells support the reproductive system. © 2026 Simons Foundation

Related chapters from BN: Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 8: Hormones and Sex
Link ID: 30239 - Posted: 05.09.2026

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.

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: 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.

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: 30208 - Posted: 04.22.2026

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

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: 30194 - Posted: 04.08.2026

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

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: 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

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: 30164 - Posted: 03.19.2026

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.

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: 30141 - Posted: 02.28.2026

By Holly Barker Synaptic proteins degrade more slowly in aged mice than in younger mice, a new study finds. Microglia appear to unburden the neurons of the excess proteins, but that accumulation may turn toxic, the findings suggest. To function properly, cells need to clear out old and damaged proteins periodically, but that process stalls with age: Protein turnover is about 20 percent slower in the brains of older rodents than in youthful ones, according to an analysis of whole-brain samples. The new study is the first to probe protein clearance specifically in neurons in living animals. “Neurons face unique challenges to protein turnover,” says study investigator Ian Guldner, a postdoctoral fellow in Tony Wyss-Coray’s lab at Stanford University. For instance, their longevity prevents them from distributing old proteins among daughter cells. And unlike other proteins on the path to degradation, neuronal components must first navigate the axon—sometimes traveling as far as 1 meter, Guldner says. In the new study, Guldner and his colleagues engineered mice to express a modified version of aminoacyl-tRNA synthetase—a component of the protein synthesis machinery—in excitatory neurons. Every day for one week, mice of different ages received injections of chemically altered amino acids compatible only with that mutant enzyme. Neurons used the labeled amino acids to replenish proteins, enabling the group to track how quickly those proteins degraded over the subsequent two weeks. “The achievement lies in the technical advance, namely by being able to look at protein degradation and aggregation specifically in neuronal cells,” says F. Ulrich Hartl, director of the Max Planck Institute of Biochemistry, who was not involved in the study. © 2026 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 10: Biological Rhythms and Sleep
Link ID: 30114 - Posted: 02.11.2026

By Sujata Gupta Chimps ages 2 to 5 are more likely than older chimps to free-fall from tree limbs in the forest canopies or leap wildly from branch to branch, researchers report January 7 in iScience. Past age 5, those dangerous canopy behaviors decrease by roughly 3 percent each year. Among humans, teens are the real daredevils. They are, for instance, more likely than other children to break bones and die from injuries. But human toddlers might behave as recklessly as chimp toddlers were it not for parents and caregivers putting the kibosh on all the fun — and broken bones, says biologist Lauren Sarringhaus of James Madison University in Harrisonburg, Va. “If humans scaled back their oversight, our kids would be way more daredevilish.” Humans and chimpanzees show markedly different caregiving patterns, say Sarringhaus and others. Chimp moms largely parent alone. Dads don’t help. Nor, typically, do grandmothers, older siblings or other group members. Chimpanzees cling to their moms for the first five years of life, but by age 2 or so, they begin to explore more independently. Moms can’t readily help kids swinging high up in the air. By comparison, the presence of alloparents, or caregivers beyond the parents, are a defining feature of human groups, Sarringhaus says. In modern times, alloparents have come to include teachers and coaches for a plethora of supervised after-school activities. Nowadays, many developmental experts in the Western world have been decrying the rise of intensive or helicopter parenting in which kids spend less time unsupervised and playing outside than those in generations past. “It’s a really exciting avenue of research of how caregiving influences risk-taking behavior. There’s not a lot of research out there addressing this point,” says Lou Haux, a psychologist and primatologist at the Max Planck Institute for Human Development in Berlin, who was not involved with the study. © Society for Science & the Public 2000–2026

Related chapters from BN: Chapter 6: Evolution of the Brain and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 30078 - Posted: 01.14.2026

Jon Hamilton Research on conditions like autism, schizophrenia and even brain cancer increasingly relies on clusters of human cells called brain organoids. These pea-size bits of neural tissue model aspects of human brain development as they grow for months and even years in a lab. They also make many people uneasy, in part because the brain is so closely tied to our sense of self. A group of scientists, ethicists, patient advocates and journalists met for two days in Northern California this fall to discuss how scientists, and society, should proceed. Among the questions: Is it okay to place human organoids in an animal's brain? Can organoids feel pain? Can they become conscious? Who, if anyone, should regulate this research? "We are talking about an organ that is at the seat of human consciousness. It's the seat of personality and who we are," says Insoo Hyun, a bioethicist at the Museum of Science, Boston, who attended the meeting. "So it's reasonable to be especially careful with the kind of experiments we're doing," he says. Societal issues by the sea The event was hosted by Dr. Sergiu Pașca, a prominent organoid researcher whose lab at Stanford University used the technology to develop a potential treatment for a rare cause of autism and epilepsy. © 2026 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: 30065 - Posted: 01.03.2026

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

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 30027 - Posted: 11.26.2025

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

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

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