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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

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: 29847 - Posted: 07.02.2025

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

Early experiences shape the brain’s ‘communication superhighways’ to affect cognition

By Rodrigo Pérez Ortega It’s clear a child’s early experiences can leave a lasting imprint on how their brain forms and functions. Now, a new study reveals how various environmental factors, including financial struggles and neighborhood safety, affect the quality of the brain’s white matter—the wiring that connects different brain regions—and in turn, a child’s cognitive abilities. The work, published today in the Proceedings of the National Academy of Sciences, also points to social factors that can boost resilience in a young brain. “It’s a really impressive, compelling paper about the long-term consequences of growing up in undersupported environments,” says John Gabrieli, a neuroscientist at the Massachusetts Institute of Technology who was not involved in the study. White matter consists of nerve fibers facilitating communication between brain regions. They are sheathed in an insulating material called myelin that gives white matter its color. Much of the research to date on how the brain supports cognition has focused on gray matter, tissue mostly made of the cell bodies of neurons that process information, which shows up as gray on brain scans. But complex cognitive tasks are “a symphony of a network” formed by multiple brain areas, Gabrieli says. “And the white matter is what mediates that communication.” Previous studies have linked poverty and childhood trauma—among other adverse environments—with a lower quality of white matter in children and lower scores on cognitive tests. However, these studies included a small number or participants and only looked at one or a few environmental variables at a time. For a more complete picture, developmental neuroscientist Sofia Carozza at Brigham and Women’s Hospital and colleagues analyzed data from more than 9000 participants in the Adolescent Brain Cognitive Development (ABCD) Study. Funded by the National Institutes of Health and established in 2015, ABCD is the largest longitudinal study of brain development in a representative group of U.S. children. Surveys of participants and their parents provide data on their home environment, including household income and parents’ level of education. At age 9 or 10, ABCD participants got a form of magnetic resonance imaging that measures the movement of water in the brain. From the strength of this directional signal, researchers can infer how robust and organized the bundles of white matter fibers are, and whether they have signs of deterioration or damage. © 2025 American Association for the Advancement of Science.

Related chapters from BN: Chapter 17: Learning and Memory; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 29736 - Posted: 04.09.2025

Organoids and assembloids offer a new window into human brain

By Sergiu P. Pasca The unbearable inaccessibility of the human brain has been a major barrier to understanding both how the human nervous system assembles itself and how psychiatric and neurological disorders emerge. But thanks to new advances, it is becoming possible to access functional aspects of human brain development and function that were previously out of reach. This progress has been driven primarily by advances in stem cell technologies, which make it possible to recapitulate developmental processes outside the human body. The journey began decades ago with the ability to grow stem cells in a dish, followed by the use of developmental signals to guide them into becoming neural cells. The field was truly catalyzed by the discovery of cell reprogramming and the democratization of stem cell technologies it enabled. Starting more than 15 years ago, my team and others began creating neurons from patients—initially rather inefficiently, but then with increasing ease as culture systems became more sophisticated. For example, cortical neurons derived from people with Timothy syndrome—a genetic form of autism and epilepsy caused by a mutation in a calcium channel present in excitable cells—revealed calcium deficits following depolarization. Some of these defects became more apparent when moving beyond traditional 2D preparations, such as when looking at the morphology of human neurons. For more than a decade, we and others have developed methods for growing these cells into more complex 3D structures, known as organoids, that mimic some of the structure and function of regions of the nervous system, offering a new window into human neurobiology and disease. Giving cells this third dimension of freedom unleashes self-organization: Mirroring in-vivo development, organoids generate diverse neural and glial cell types, starting from radial glia to intermediate progenitors, deep and superficial layer neurons and then astrocytes. These organoids can be maintained in vitro for years. Fascinatingly, developmental timing in organoids is largely preserved. For example, neurons maintained in culture for about nine months can transition to a postnatal state simply by surviving long enough in the dish. This observation in organoids offers a fundamental insight into development: Brain cells have an intrinsic, species-specific developmental “timer.” © 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: 29724 - Posted: 04.02.2025

Targeting NMDA receptor subunit reverses fragile X traits in mice

By Angie Voyles Askham Synaptic plasticity in the hippocampus involves both strengthening relevant connections and weakening irrelevant ones. That sapping of synaptic links, called long-term depression (LTD), can occur through two distinct routes: the activity of either NMDA receptors or metabotropic glutamate receptors (mGluRs). The mGluR-dependent form of LTD, required for immediate translation of mRNAs at the synapse, appears to go awry in fragile X syndrome, a genetic condition that stems from loss of the protein FMRP and is characterized by intellectual disability and often autism. Possibly as a result, mice that model fragile X exhibit altered protein synthesis regulation in the hippocampus, an increase in dendritic spines and overactive neurons. Treatments for fragile X that focus on dialing down the mGluR pathway and tamping down protein synthesis at the synapse have shown success in quelling those traits in mice, but they have repeatedly failed in human clinical trials. But the alternative pathway—via the NMDA receptor—may provide better results, according to a new study. Signaling through the NMDA receptor subunit GluN2B can also decrease spine density and alleviate fragile-X-linked traits in mice, the work shows. “You don’t have to modulate the protein synthesis directly,” says Lynn Raymond, professor of psychiatry and chair in neuroscience at the University of British Columbia, who was not involved in the work. Instead, activation of part of the GluN2B subunit can indirectly shift the balance of mRNAs that are translated at the synapse. “It’s just another piece of the puzzle, but I think it’s a very important piece,” she says. Whether this insight will advance fragile X treatments remains to be seen, says Wayne Sossin, professor of neurology and neurosurgery at Montreal Neurological Institute-Hospital, who was not involved in the study. Multiple groups have cured fragile-X-like traits in mice by altering what happens at the synapse, he says. “Altering translation in a number of ways seems to change the balance that is off when you lose FMRP. And it’s not really clear how specific that is for FMRP.” © 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: 29700 - Posted: 03.12.2025

Assembloids illuminate circuit-level changes linked to autism, neurodevelopment

By Sarah DeWeerdt A few months ago, Sergiu Paşca, professor of psychiatry and behavioral sciences at Stanford University, shared his lab’s new work at the Gordon Research Conference on Thalamocortical Interactions. His talk concerned assembloids, lab-grown combinations of spherical organoids that mimic different parts of the nervous system. Paşca showed a video depicting waves of calcium signals traveling along a line of organoids modeling sensory neurons; the dorsal root ganglia of the spinal cord; a subcortical structure called the thalamus; and, finally, the cerebral cortex. In the audience, Audrey Brumback, assistant professor of neurology and pediatrics at the University of Texas at Austin, felt something move through her own subcortical structures as she watched the video: a visceral feeling of awe. “I just thought, ‘Holy crap, this is amazing,’” she recalls. “‘The future is now.’” The work, described in a preprint posted on bioRxiv in March, is part of a series of recent studies from Paşca’s lab that highlight the potential of assembloids to help researchers understand brain development at the circuit level, and how these circuits go awry in autism and other neurodevelopmental conditions. Autism, after all, involves differences in how various parts of the brain connect with each other, Brumback points out. “So to be able to model that in vitro is exactly what we need to be doing to be able to understand these network dysfunction disorders,” she says. For example, a lack of synchrony between the cortex and the thalamus is known to be associated with autism and schizophrenia, whereas too much synchrony between the two regions is implicated in absence seizures in epilepsy. Using a two-part assembloid representing this pair of brain structures, Paşca and his team probed the roots of these alterations in a study published 16 October in Neuron. © 2024 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: 29610 - Posted: 12.28.2024

How fast is your brain ageing? Proteins in blood offer clues

By Miryam Naddaf Researchers have identified 13 proteins in the blood that predict how quickly or slowly a person’s brain ages compared with the rest of their body. Their study1, published in Nature Aging on 9 December, used a machine-learning model to estimate ‘brain ages’ from scans of more than 10,000 people. The authors then analysed thousands of scans alongside blood samples and found eight proteins that were associated with fast brain ageing, and five linked to slower brain ageing. “Previous studies mainly focused on the association between the proteins and the chronological age, that means the real age of the individual,” says study co-author Wei-Shi Liu, a neurologist at Fudan University in Shanghai, China. However, studying biomarkers linked to a person’s brain age could help scientists to identify molecules to target in future treatments for age-related brain diseases. “These proteins are all promising therapeutic targets for brain disorders, but it may take a long time to validate them,” says Liu. Using machine learning to analyse brain-imaging data from 10,949 people, Liu and his colleagues created a model to calculate a person’s brain age, on the basis of features such as the brain’s volume, surface area and distribution of white matter. They wanted to identify proteins that are associated with a large brain age gap — the difference between brain age and chronological age. To do this, the researchers analysed levels of 2,922 proteins in blood samples from 4,696 people, more than half of whom were female, and compared them with the same people’s brain ages derived from the scans. They identified 13 proteins that seemed to be connected with large brain age gaps, some of which are known to be involved in movement, cognition and mental health.

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: 29597 - Posted: 12.11.2024

How human brains got so big: our cells learned to handle the stress that comes with size

By Miryam Naddaf Humans have evolved disproportionately large brains compared with our primate relatives — but this neurological upgrade came at a cost. Scientists exploring the trade-off have discovered unique genetic features that show how human brain cells handle the stress of keeping a big brain working. The work could inspire new lines of research to understand conditions such as Parkinson’s disease and schizophrenia. The study, which was posted to the bioRxiv preprint server on 15 November1, focuses on neurons that produce the neurotransmitter dopamine, which is crucial for movement, learning and emotional processing. By comparing thousands of laboratory-grown dopamine neurons from humans, chimpanzees, macaques and orangutans, researchers found that human dopamine neurons express more genes that boost the activity of damage-reducing antioxidants than do those of the other primates. The findings, which are yet to be peer-reviewed, are a step towards “understanding human brain evolution and all the potentially negative and positive things that come with it”, says Andre Sousa, a neuroscientist at the University of Wisconsin–Madison. “It's interesting and important to really try to understand what's specific about the human brain, with the potential of developing new therapies or even avoiding disease altogether in the future.” Just as walking upright has led to knee and back problems, and changes in jaw structure and diet resulted in dental issues, the rapid expansion of the human brain over evolutionary time has created challenges for its cells, says study co-author Alex Pollen, a neuroscientist at the University of California, San Francisco. “We hypothesized that the same process may be occurring, and these dopamine neurons may represent vulnerable joints.” © 2024 Springer Nature Limited

The Power of Small Brain Networks

By Elena Renken Small may be mightier than we think when it comes to brains. This is what neuroscientist Marcella Noorman is learning from her neuroscientific research into tiny animals like fruit flies, whose brains hold around 140,000 neurons each, compared to the roughly 86 billion in the human brain. Nautilus Members enjoy an ad-free experience. Log in or Join now . In work published earlier this month in Nature Neuroscience, Noorman and colleagues showed that a small network of cells in the fruit fly brain was capable of completing a highly complex task with impressive accuracy: maintaining a consistent sense of direction. Smaller networks were thought to be capable of only discrete internal mental representations, not continuous ones. These networks can “perform more complex computations than we previously thought,” says Noorman, an associate at the Howard Hughes Medical Institute. The scientists monitored the brains of fruit flies as they walked on tiny rotating foam balls in the dark, and recorded the activity of a network of cells responsible for keeping track of head direction. This kind of brain network is called a ring attractor network, and it is present in both insects and in humans. Ring attractor networks maintain variables like orientation or angular velocity—the rate at which an object rotates—over time as we navigate, integrating new information from the senses and making sure we don’t lose track of the original signal, even when there are no updates. You know which way you’re facing even if you close your eyes and stand still, for example. After finding that this small circuit in fruit fly brains—which contains only about 50 neurons in the core of the network—could accurately represent head direction, Noorman and her colleagues built models to identify the minimum size of a network that could still theoretically perform this task. Smaller networks, they found, required more precise signaling between neurons. But hundreds or thousands of cells weren’t necessary for this basic task. As few as four cells could form a ring attractor, they found. © 2024 NautilusNext Inc.,

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: 29560 - Posted: 11.16.2024

Cat brains age like ours — and could help scientists to understand cognitive decline

By Heidi Ledford To unlock the secrets of human ageing, researchers might do better to look to the pet napping on their couch than to a laboratory mouse. As cats age, their brains show signs of atrophy and cognitive decline that more closely resemble the deterioration seen in ageing humans than do the changes in the brains of ageing mice, according to findings presented last month at the Lake Conference on Comparative and Evolutionary Neurobiology near Seattle, Washington. The results are part of a large project, called Translating Time, that compares brain development across more than 150 mammal species, and is now expanding to include data on aging. The hope is that the data will aid researchers trying to crack the causes of age-related diseases, particularly conditions that affect the brain, such as Alzheimer’s disease. “To address challenges in human medicine, we need to draw from a wide range of model systems,” says Christine Charvet, a comparative neuroscientist at Auburn University College of Veterinary Medicine in Alabama, who presented the work. “Cats, lemurs, mice are all useful. We shouldn’t focus all our efforts on one.” The Translating Time project started in the 1990s as a tool for developmental biologists1. Project scientists compiled data on how long it takes for the brain to reach a range of developmental milestones in a variety of mammals and used these data to graph the relative development of two species over time. This can help researchers to link observations of animal development to the corresponding human age. Over the years, however, as Charvet presented these data at conferences, researchers kept asking her to extend the database to include not only early development, but also how the brain changes as animals age. © 2024 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: 29545 - Posted: 11.06.2024

Your cells are dying. All the time.

By Amber Dance Billions of cells die in your body every day. Some go out with a bang, others with a whimper. They can die by accident if they’re injured or infected. Alternatively, should they outlive their natural lifespan or start to fail, they can carefully arrange for a desirable demise, with their remains neatly tidied away. Originally, scientists thought those were the only two ways an animal cell could die, by accident or by that neat-and-tidy version. But over the past couple of decades, researchers have racked up many more novel cellular death scenarios, some specific to certain cell types or situations. Understanding this panoply of death modes could help scientists save good cells and kill bad ones, leading to treatments for infections, autoimmune diseases and cancer. “There’s lots and lots of different flavors here,” says Michael Overholtzer, a cell biologist at Memorial Sloan Kettering Cancer Center in New York. He estimates that there are now more than 20 different names to describe cell death varieties. The identification of new forms of cell death has sped up in recent years. Lots of bad things can happen to cells: They get injured or burned, poisoned or starved of oxygen, infected by microbes or otherwise diseased. When a cell dies by accident, it’s called necrosis. There are several necrosis types, none of them pretty: In the case of gangrene, when cells are starved for blood, cells rot away. In other instances, dying cells liquefy, sometimes turning into yellow goop. Lung cells damaged by tuberculosis turn smushy and white — the technical name for this type, “caseous” necrosis, literally means “cheese-like.” Any form of death other than necrosis is considered “programmed,” meaning it’s carried out intentionally by the cell because it’s damaged or has outlived its usefulness.

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: 29495 - Posted: 09.28.2024

Fragile X held him back. An experimental drug is helping him break free

Jon Hamilton For 22 years, Jason Mazzola’s life was defined by Fragile X, a genetic condition that often causes autism and intellectual disability. Jason, who is 24 now, needed constant supervision. He had disabling anxiety, and struggled to answer even simple questions. All that began to change when he started taking an experimental drug called zatolmilast in May of 2023. “It helps me focus a lot, helps me get more confident, more educated,” Jason says. His mother, Lizzie Mazzola, credits zatolmilast with transforming her son. “I have a different child in my house,” she says. “He gets himself to work, he walks downtown, gets his haircut, gets lunch. He wouldn't have done any of that before.” Other parents of children with Fragile X are also reporting big changes with zatolmilast. Those anecdotes are supported by data. A 2021 study of 30 adult male participants with Fragile X found that taking zatolmilast for 12 weeks improved performance on a range of memory and language measures. Now, two larger studies are underway that will determine whether zatolmilast becomes the first drug approved by the Food and Drug Administration to treat Fragile X. Mazzola realized early on that Jason was falling behind. “He could hardly talk by three,” she says. “At four he started to put some words together, but really wasn’t talking in sentences.” Genetic tests revealed the cause: Fragile X. The inherited condition affects the X chromosome, making one segment appear fragile or broken. This anomaly blocks production of a protein that’s important to brain development. © 2024 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: 29492 - Posted: 09.25.2024

The brain aged more slowly in monkeys given a cheap diabetes drug

By Max Kozlov A low-cost diabetes drug slows ageing in male monkeys and is particularly effective at delaying the effects of ageing on the brain, finds a small study that tracked the animals for more than three years1. The results raise the possibility that the widely used medication, metformin, could one day be used to postpone ageing in humans. Monkeys that received metformin daily showed slower age-associated brain decline than did those not given the drug. Furthermore, their neuronal activity resembled that of monkeys about six years younger (equivalent to around 18 human years) and the animals had enhanced cognition and preserved liver function. This study, published in Cell on 12 September, helps to suggest that, although dying is inevitable, “ageing, the way we know it, is not”, says Nir Barzilai, a geroscientist at the Albert Einstein College of Medicine in New York City, who was not involved in the study. Metformin has been used for more than 60 years to lower blood-sugar levels in people with type 2 diabetes — and is the second most-prescribed medication in the United States. The drug has long been known to have effects beyond treating diabetes, leading researchers to study it against conditions such as cancer, cardiovascular disease and ageing. Data from worms, rodents, flies and people who have taken the drug for diabetes suggest the drug might have anti-ageing effects. But its effectiveness against ageing had not been tested directly in primates, and it is unclear whether its potential anti-ageing effects are achieved by lowering blood sugar or through a separate mechanism. This led Guanghui Liu, a biologist who studies ageing at the Chinese Academy of Sciences in Beijing, and his colleagues to test the drug on 12 elderly male cynomolgus macaques (Macaca fasciucularis); another 16 elderly monkeys and 18 young or middle-aged animals served as a control group. Every day, treated monkeys received the standard dose of metformin that is used to control diabetes in humans. The animals took the drug for 40 months, which is equivalent to about 13 years for humans. © 2024 Springer Nature Limited

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: 29481 - Posted: 09.14.2024

Our Bigger Brains Came With a Downside: Faster Aging

By Carl Zimmer The human brain, more than any other attribute, sets our species apart. Over the past seven million years or so, it has grown in size and complexity, enabling us to use language, make plans for the future and coordinate with one another at a scale never seen before in the history of life. But our brains came with a downside, according to a study published on Wednesday. The regions that expanded the most in human evolution became exquisitely vulnerable to the ravages of old age. “There’s no free lunch,” said Sam Vickery, a neuroscientist at the Jülich Research Center in Germany and an author of the study. The 86 billion neurons in the human brain cluster into hundreds of distinct regions. For centuries, researchers could recognize a few regions, like the brainstem, by hallmarks such as the clustering of neurons. But these big regions turned out to be divided into smaller ones, many of which were revealed only with the help of powerful scanners. As the structure of the human brain came into focus, evolutionary biologists became curious about how the regions evolved from our primate ancestors. (Chimpanzees are not our direct ancestors, but both species descended from a common ancestor about seven million years ago.) The human brain is three times as large as that of chimpanzees. But that doesn’t mean all of our brain regions expanded at the same pace, like a map drawn on an inflating balloon. Some regions expanded only a little, while others grew a lot. Dr. Vickery and his colleagues developed a computer program to analyze brain scans from 189 chimpanzees and 480 humans. Their program mapped each brain by recognizing clusters of neurons that formed distinct regions. Both species had 17 brain regions, the researchers found. © 2024 The New York Times Company

What accelerates brain ageing? This AI ‘brain clock’ points to answers

By Julian Nowogrodzki A newly devised ‘brain clock’ can determine whether a person’s brain is ageing faster than their chronological age would suggest1. Brains age faster in women, countries with more inequality and Latin American countries, the clock indicates. “The way your brain ages, it’s not just about years. It’s about where you live, what you do, your socio-economic level, the level of pollution you have in your environment,” says Agustín Ibáñez, the study’s lead author and a neuroscientist at Adolfo Ibáñez University in Santiago. “Any country that wants to invest in the brain health of the people, they need to address structural inequalities.” The work is “truly impressive”, says neuroscientist Vladimir Hachinski at Western University in London, Canada, who was not involved in the study. It was published on 26 August in Nature Medicine. Only connect The researchers looked at brain ageing by assessing a complex form of functional connectivity, a measure of the extent to which brain regions are interacting with one another. Functional connectivity generally declines with age. The authors drew on data from 15 countries: 7 (Mexico, Cuba, Colombia, Peru, Brazil, Chile and Argentina) that are in Latin America or the Caribbean and 8 (China, Japan, the United States, Italy, Greece, Turkey, the United Kingdom and Ireland) that are not. Of the 5,306 participants, some were healthy, some had Alzheimer’s disease or another form of dementia and some had mild cognitive impairment, a precursor to dementia. The researchers measured participants’ resting brain activity — that when they were doing nothing in particular — using either functional magnetic resonance imaging (fMRI) or electroencephalography (EEG). The first technique measures blood flow in the brain, and the second measures brain-wave activity. © 2024 Springer Nature Limited

Five ways the brain can age: 50,000 scans reveal possible patterns of damage

By Michael Eisenstein An analysis of almost 50,000 brain scans1 has revealed five distinct patterns of brain atrophy associated with ageing and neurodegenerative disease. The analysis has also linked the patterns to lifestyle factors such as smoking and alcohol consumption, as well as to genetic and blood-based markers associated with health status and disease risk. The work is a “methodological tour de force” that could greatly advance researchers’ understanding of ageing, says Andrei Irimia, a gerontologist at the University of Southern California in Los Angeles, who was not involved in the work. “Prior to this study, we knew that brain anatomy changes with ageing and disease. But our ability to grasp this complex interaction was far more modest.” The study was published on 15 August in Nature Medicine. Ageing can induce not only grey hair, but also changes in brain anatomy that are visible on magnetic resonance imaging (MRI) scans, with some areas shrivelling or undergoing structural alterations over time. But these transformations are subtle. “The human eye is not able to perceive patterns of systematic brain changes” associated with this decline, says Christos Davatzikos, a biomedical-imaging specialist at the University of Pennsylvania in Philadelphia and an author of the paper. Previous studies have shown that machine-learning methods can extract the subtle fingerprints of ageing from MRI data. But these studies were often limited in scope and most included data from a relatively small number of people. © 2024 Springer Nature Limited

Can we change how our brains age? These scientists think it’s possible

By Lara Lewington, It's long been known that our lifestyles can help to keep us healthier for longer. Now scientists are asking whether new technology can also help slow down the ageing process of our brains by keeping track of what happens to them as we get older. One sunny morning, 76-year-old Dutch-born Marijke and her husband Tom welcomed me in for breakfast at their home in Loma Linda, an hour east of Los Angeles. Oatmeal, chai seeds, berries, but no processed sugary cereal or coffee were served - a breakfast as pure as Loma Linda’s mission. Loma Linda has been identified as one of the world’s so-called Blue Zones, places where people have lengthier-than-average lifespans. In this case, it is the city’s Seventh-Day Adventist Church community who are living longer. They generally don’t drink alcohol or caffeine, stick to a vegetarian or even vegan diet and consider it a duty of their religion to look after their bodies as best they can. This is their “health message”, as they call it, and it has put them on the map - the city has been the subject of decades of research into why its residents live better for longer. Dr Gary Fraser from the University of Loma Linda told me members of the Seventh-Day Adventist community there can expect not only a longer lifespan, but an increased “healthspan” - that is, time spent in good health - of four to five years extra for women and seven years extra for men. Marijke and Tom had moved to the city later in life, but both were now firmly embedded in the community. Copyright 2024 BBC.

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