By Laurie McGinley When Dennis Carr learned he had early Alzheimer’s disease, he immediately thought of his older brother who had died of the illness in 2023. “There was not much anyone could do,” Carr said of his brother’s long decline. “You could see him diminishing.” Today, Carr is trying a new treatment called Leqembi that has been shown to modestly slow the disease for people in the initial stages of Alzheimer’s. Carr knows it is not a cure but he wants to buy time — to be with his family, to work and to give scientists a chance to find more solutions. “I’m hoping this is the first steppingstone to something better,” said Carr, 74, an electrical contractor in Montgomery County, Pa. Carr’s experience offers a glimpse of the shifting landscape of Alzheimer’s, a memory-robbing disease that affects more than 6 million Americans and is the seventh leading cause of death in the United States. Two new treatments, including Carr’s, target toxic clumps of a protein called amyloid beta in the brain and are the first to slow progression of the illness. Blood tests could revolutionize the way the illness is diagnosed. Lifestyle factors such as diet and exercise are showing promise in helping reduce the risk of cognitive decline. “Progress against Alzheimer’s has been unprecedented,” said Howard Fillit, co-founder and chief science officer of the Alzheimer’s Drug Discovery Foundation, a nonprofit that funds the development of drugs and diagnostics. “But we have a long way to go.” The new FDA-approved Alzheimer’s treatment Leqembi is prepared at Abington Neurological Associates in Abington, Pa., on Nov. 7. (Hannah Yoon for The Washington Post) Doctors used to refer to Alzheimer’s as “diagnose and adios” because they had little to offer patients, said Adam Boxer, a neurologist at the University of California at San Francisco. “But now we see light at the end of the tunnel,” he said. “We might be able to have a big impact.”

Keyword: Alzheimers
Link ID: 29510 - Posted: 10.09.2024

By Sara Reardon Researchers have mapped nearly 140,000 neurons in the fruit-fly brain. This version shows the 50 largest. Credit: Tyler Sloan and Amy Sterling for FlyWire, Princeton University (ref. 1) A fruit fly might not be the smartest organism, but scientists can still learn a lot from its brain. Researchers are hoping to do that now that they have a new map — the most complete for any organism so far — of the brain of a single fruit fly (Drosophila melanogaster). The wiring diagram, or ‘connectome’, includes nearly 140,000 neurons and captures more than 54.5 million synapses, which are the connections between nerve cells. “This is a huge deal,” says Clay Reid, a neurobiologist at the Allen Institute for Brain Science in Seattle, Washington, who was not involved in the project but has worked with one of the team members who was. “It’s something that the world has been anxiously waiting for, for a long time.” The map1 is described in a package of nine papers about the data published in Nature today. Its creators are part of a consortium known as FlyWire, co-led by neuroscientists Mala Murthy and Sebastian Seung at Princeton University in New Jersey. Seung and Murthy say that they’ve been developing the FlyWire map for more than four years, using electron microscopy images of slices of the fly’s brain. The researchers and their colleagues stitched the data together to form a full map of the brain with the help of artificial-intelligence (AI) tools. But these tools aren’t perfect, and the wiring diagram needed to be checked for errors. The scientists spent a great deal of time manually proofreading the data — so much time that they invited volunteers to help. In all, the consortium members and the volunteers made more than three million manual edits, according to co-author Gregory Jefferis, a neuroscientist at the University of Cambridge, UK. (He notes that much of this work took place in 2020, when fly researchers were at loose ends and working from home during the COVID-19 pandemic.) © 2024 Springer Nature Limited

Keyword: Brain imaging; Development of the Brain
Link ID: 29508 - Posted: 10.05.2024

By Calli McMurray Daniel Heinz clicked through each folder in the file drive, searching for the answers that had evaded him and his lab mates for years. Heinz, a graduate student in Brenda Bloodgood’s lab at the University of California, San Diego (UCSD), was working on a Ph.D. project, part of which built on the work of a postdoctoral researcher who had left the lab and started his own a few years prior. The former postdoc studied how various types of electrical activity in the mouse hippocampus induce a gene called NPAS4 in different ways. One of his discoveries was that, in some situations, NPAS4 was induced in the far-reaching dendrites of neurons. The postdoc’s work resulted in a paper in Cell, landed him more than $1.4 million in grants and an assistant professor position at the University of Utah, and spawned several follow-up projects in the lab. In other words, it was a slam dunk. But no one else in the lab—including Heinz—could replicate the NPAS4 data. Other lab members always had a technical explanation for why the replication experiments failed, so for years the problem was passed from one trainee to another. Which explains why, on this day in early April 2023, Heinz was poking around the postdoc’s raw data. What he eventually found would lead to a retraction, a resignation and a reckoning, but in the moment, Heinz says, he was not thinking about any of those possibilities. In fact, he had told no one he was doing this. He just wanted to figure out why his experiments weren’t working. To visualize the location of NPAS4, the lab used immunohistochemistry, which tags a gene product with a tailored fluorescent antibody. Any part of the cell that expresses the gene should glow. In his replication attempts, Heinz says he struggled to see any expression, and when he saw indications of it, the signal was faint and noisy. So he wanted to compare his own images to the postdoc’s raw results rather than the processed images included in the 2019 Cell paper. © 2024 Simons Foundation

Keyword: Learning & Memory
Link ID: 29504 - Posted: 10.05.2024

By Miryam Naddaf Neurons in the hippocampus help to pick out patterns in the flood of information pouring through the brain.Credit: Arthur Chien/Science Photo Library The human brain is constantly picking up patterns in everyday experiences — and can do so without conscious thought, finds a study1 of neuronal activity in people who had electrodes implanted in their brain tissue for medical reasons. The study shows that neurons in key brain regions combine information on what occurs and when, allowing the brain to pick out the patterns in events as they unfold over time. That helps the brain to predict coming events, the authors say. The work was published today in Nature. “The brain does a lot of things that we are not consciously aware of,” says Edvard Moser, a neuroscientist at the Norwegian University of Science and Technology in Trondheim. “This is no exception.” To make sense of the world around us, the brain must process an onslaught of information on what happens, where it happens and when it happens. The study’s authors wanted to explore how the brain organizes this information over time — a crucial step in learning and memory. The team studied 17 people who had epilepsy and had electrodes implanted in their brains in preparation for surgical treatment. These electrodes allowed the authors to directly capture the activity of individual neurons in multiple brain regions. Among those regions were the hippocampus and entorhinal cortex, which are involved in memory and navigation. These areas contain time and place cells that act as the body’s internal clock and GPS system, encoding time and locations. “All the external world coming into our brain has to be filtered through that system,” says study co-author Itzhak Fried, a neurosurgeon and neuroscientist at the University of California, Los Angeles. © 2024 Springer Nature Limited

Keyword: Attention; Learning & Memory
Link ID: 29497 - Posted: 09.28.2024

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.

Keyword: Development of the Brain; Apoptosis
Link ID: 29495 - Posted: 09.28.2024

Ian Sample Science editor Where does our personal politics come from? Does it trace back to our childhood, the views that surround us, the circumstances we are raised in? Is it all about nurture – or does nature have a say through the subtle levers of DNA? And where, in all of this, is the brain? Scientists have delved seriously into the roots of political belief for the past 50 years, prompted by the rise of sociobiology, the study of the biological basis of behaviour, and enabled by modern tools such as brain scanners and genome sequencers. The field is making headway, but teasing out the biology of behaviour is never straightforward. Take a study published last week. Researchers in Greece and the Netherlands examined MRI scans from nearly 1,000 Dutch people who had answered questionnaires on their personal politics. The work was a replication study, designed to see whether the results from a small 2011 study, bizarrely commissioned by the actor Colin Firth, stood up. Firth’s study, conducted at UCL, reported structural differences between conservative and liberal brains. Conservatives, on average, had a larger amygdala, a region linked to threat perception. Liberals, on average, had a larger anterior cingulate cortex, a region involved in decision-making. In the latest study of Dutch people, the researchers found no sign of a larger anterior cingulate cortex in liberals. They did, however, find evidence for a very slightly larger amygdala in conservatives. The MailOnline declared evidence that conservatives were more “compassionate”, but later changed their headline noting that the study said nothing about compassion. © 2024 Guardian News & Media Limited

Keyword: Emotions; Attention
Link ID: 29493 - Posted: 09.25.2024

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

Keyword: Development of the Brain; Genes & Behavior
Link ID: 29492 - Posted: 09.25.2024

Natasha May Young people with severe depression experience disruptions in the way regions of their brain communicate with each other which are distinct from those observed in adults, a study has found. The research published on Tuesday in Nature Mental Health could be used to identify potential targets for brain stimulation therapies, extending their existing application from adults to youth. The study analysed the brain scans of 810 young people aged 12-25, of which 440 had major depressive disorder (MDD) and 370 were healthy comparison individuals. The study led by the University of Melbourne found that in those with MDD, some densely connected regions of the brain (known as hubs) showed stronger connectivity and others showed weaker connectivity compared with youth without depression. Young woman running at sunset on Australian beach Nutrition and exercise as good as therapy for mild and moderate depression, study says Prof Andrew Zalesky, the supervising researcher, said they found the connectivity was particularly strong in the part of the brain associated with someone’s internalised thoughts and rumination. “We see that in youth with depression, the default mode is more strongly connected, it’s more activated, which suggests that there is a greater focus on self-thought and self-reflection,” Zalesky said. The study, whose first author was third-year PhD student at the University of Melbourne, Nga (Connie) Yan Tse, also found the extent of these differences could reliably predict how severe a person’s depressive symptoms were. © 2024 Guardian News & Media Limited

Keyword: Depression; Brain imaging
Link ID: 29491 - Posted: 09.25.2024

Jon Hamilton Scientists have created a virtual brain network that can predict the behavior of individual neurons in a living brain. The model is based on a fruit fly’s visual system, and it offers scientists a way to quickly test ideas on a computer before investing weeks or months in experiments involving actual flies or other lab animals. “Now we can start with a guess for how the fly brain might work before anyone has to make an experimental measurement,” says Srini Turaga, a group leader at the Janelia Research Campus, a part of the Howard Hughes Medical Institute (HHMI). The approach, described in the journal Nature, also suggests that power-hungry artificial intelligence systems like ChatGPT might consume much less energy if they used some of the computational strategies found in a living brain. A fruit fly brain is “small and energy efficient,” says Jakob Macke, a professor at the University of Tübingen and an author of the study. “It’s able to do so many computations. It’s able to fly, it’s able to walk, it’s able to detect predators, it’s able to mate, it’s able to survive—using just 100,000 neurons.” In contrast, AI systems typically require computers with tens of billions of transistors. Worldwide, these systems consume as much power as a small country. “When we think about AI right now, the leading charge is to make these systems more power efficient,” says Ben Crowley, a computational neuroscientist at Cold Spring Harbor Laboratory who was not involved in the study. Borrowing strategies from the fruit fly brain might be one way to make that happen, he says. © 2024 npr

Keyword: Brain imaging; Evolution
Link ID: 29484 - Posted: 09.18.2024

By Julian Nowogrodzki Millions of adults around the world take potent drugs such as Wegovy to shed pounds. Should kids do the same? That question is growing more urgent in the face of mounting evidence that children and adolescents, as well as adults, slim down if they take the latest generation of obesity drugs. Clinical trials1,2 have shown that many adolescents with obesity lose substantial amounts of weight on these drugs, which work by mimicking a natural hormone called glucagon-like peptide 1 (GLP-1). The GLP-1 mimics semaglutide, commonly sold as Ozempic and Wegovy, and liraglutide, marketed as Saxenda and Victoza, are approved in the United States and Europe to treat obesity in children as young as 12. Now a trial has produced some of the first data on anti-obesity drugs in even younger children: those aged 6 to 11. The study3 reports that children who were treated with liraglutide showed a decrease in their body mass index (BMI), a measure of obesity. The results were published on 10 September in The New England Journal of Medicine. Nature asked specialists in obesity about the costs and benefits of giving the GLP-1 mimics to youngsters who are still growing and developing. Why test powerful weight-loss drugs on kids? Most kids with obesity become teens with obesity and then adults with obesity. Many young children with severe obesity have “already developed significant health issues”, says physician Sarah Ro, who directs the University of North Carolina Physicians Network Weight Management Program and has served as a consultant to Novo Nordisk, the manufacturer of semaglutide. Her clinic in Hillsborough treats children with severe obesity who have health issues such as high blood pressure, type 2 diabetes or an advanced form of liver disease linked to excess weight. © 2024 Springer Nature Limited

Keyword: Obesity; Development of the Brain
Link ID: 29482 - Posted: 09.18.2024

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

Keyword: Development of the Brain; Obesity
Link ID: 29481 - Posted: 09.14.2024

By Ellen Barry A study of adolescent brain development that tested children before and after coronavirus pandemic lockdowns in the United States found that girls’ brains aged far faster than expected, something the researchers attributed to social isolation. The study from the University of Washington, published on Monday in the Proceedings of the National Academy of Sciences, measured cortical thinning, a process that starts in either late childhood or early adolescence, as the brain begins to prune redundant synapses and shrink its outer layer. Thinning of the cortex is not necessarily bad; some scientists frame the process as the brain rewiring itself as it matures, increasing its efficiency. But the process is known to accelerate in stressful conditions, and accelerated thinning is correlated with depression and anxiety. Scans taken in 2021, after shutdowns started to lift, showed that both boys and girls had experienced rapid cortical thinning during that period. But the effect was far more notable in girls, whose thinning had accelerated, on average, by 4.2 years ahead of what was expected; the thinning in boys’ brains had accelerated 1.4 years ahead of what was expected. “That is a stunning difference,” said Patricia K. Kuhl, a director of the Institute for Learning and Brain Sciences at the University of Washington and one of the study’s authors. The results, she added, suggested that “a girl who came in at 11, and then returned to the lab at age 14, now has a brain that looks like an 18-year-old’s.” Dr. Kuhl attributed the change to “social deprivation caused by the pandemic,” which she suggested had hit adolescent girls harder because they are more dependent on social interaction — in particular, talking through problems with friends — as a way to release stress. The difference between the genders “is just as clear as night and day,” Dr. Kuhl said. “In the girls, the effects were all over the brain — all the lobes, both hemispheres.” © 2024 The New York Times Company

Keyword: Stress; Development of the Brain
Link ID: 29477 - Posted: 09.11.2024

Alzheimer’s disease impairs a patient by destroying neurons, which otherwise live for decades, and by disrupting communication among the remaining brain cells. As neurons die, the areas of the brain they constitute begin to atrophy. A detailed picture of the progression is still under investigation, and the disease follows different tracks in different patients, but researchers have found brains afflicted with Alzheimer’s typically atrophy along the same basic pattern. A better understanding of that pattern may provide the foundation for methods to diagnose the disease earlier, which in turn would give medication and lifestyle changes the best chance of slowing dementia. In broad strokes, here’s how Alzheimer’s tends to change a brain. © 2024 SCIENTIFIC AMERICAN,

Keyword: Alzheimers
Link ID: 29476 - Posted: 09.11.2024

Jon Hamilton Aging and Alzheimer's leave the brain starved of energy. Now scientists think they've found a way to aid the brain's metabolism — in mice. PM Images/Getty Images The brain needs a lot of energy — far more than any other organ in the body — to work properly. And aging and Alzheimer’s disease both seem to leave the brain underpowered. But an experimental cancer drug appeared to re-energize the brains of mice that had a form of Alzheimer’s — and even restore their ability to learn and remember. The finding, published in the journal Science, suggests that it may eventually be possible to reverse some symptoms of Alzheimer’s in people, using drugs that boost brain metabolism. The results also offer an approach to treatment that’s unlike anything on the market today. Current drugs for treating Alzheimer’s, such as lecanemab and donanemab, target the sticky amyloid plaques that build up in a patient’s brain. These drugs can remove plaques and slow the disease process, but do not improve memory or thinking. The result should help “change how we think about targeting this disease,” says Shannon Macauley, an associate professor at the University of Kentucky who was not involved in the study. The new research was prompted by a lab experiment that didn’t go as planned. A team at Stanford was studying an enzyme called IDO1 that plays a key role in keeping a cell’s metabolism running properly. They suspected that in Alzheimer’s disease, IDO1 was malfunctioning in a way that limited the brain’s ability to turn nutrients into energy. © 2024 npr

Keyword: Alzheimers; Learning & Memory
Link ID: 29462 - Posted: 09.04.2024

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

Keyword: Development of the Brain; Evolution
Link ID: 29459 - Posted: 08.31.2024

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

Keyword: Development of the Brain; Stress
Link ID: 29458 - Posted: 08.31.2024

By Rebecca Dzombak Birds can be picky building their nests. They experiment with materials, waffle over which twig to use, take them apart and start again. It’s a complex, fiddly process that can seem to reflect careful thought. “It’s so fascinating,” Maria Tello-Ramos, a behavioral ecologist at the University of St. Andrews in Scotland, said. “But it hasn’t been studied much at all.” New research led by Dr. Tello-Ramos, published on Thursday in the journal Science, provides the first evidence that groups of birds that build their homes together learn to follow consistent architectural styles, distinct from groups just a few dozen feet away. The finding upends longstanding assumptions that nest building is an innate behavior based on the birds’ environment and adds to a growing list of behaviors that make up bird culture. As important for survival as nest building is, scientists know relatively little about it. Most of what is known about bird nests has come from studying their role in reproductive success, focusing on their usefulness in protecting birds and eggs from cold, wind and predators. “The focus has been on the structure, not the behavior that built it,” Dr. Tello-Ramos said. She said she found that surprising because nest building is one of the rare behaviors that has a tangible product, something that can be measured and provide insight into why birds behave the way they do. Part of the reason nest-building behaviors haven’t been researched much, Dr. Tello-Ramos said, boils down to one cliché: bird brain. Nest building is such a complex behavior that, for decades, scientists thought “the little brains of birds couldn’t possibly deal with such a large amount of information, so it must be innate,” she said. Recent work has shown birds repeating others’ nest building, but those studies were often limited to individuals or small groups in labs. © 2024 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 29457 - Posted: 08.31.2024

By Shaena Montanari Mammalian brains famously come with a built-in GPS system: “place cells” in the hippocampus that selectively activate when an animal enters a specific location and power spatial cognition. A comparable navigation system had not been described in fish—until now. As it turns out, zebrafish larvae, too, possess place cells that integrate multiple sources of information and generate new cognitive maps when the animal’s environment changes, according to a study out today in Nature. The search for these cells in fish became “kind of like a myth, almost,” says the study’s co-lead investigator Jennifer Li, research group leader at the Max Planck Institute for Biological Cybernetics. She and her team were hesitant to look for place cells in fish at first, Li says, “because we figured if nobody’s seeing them after all this time,” they might not exist. But Li and her colleagues had already custom-built a microscope that tracks calcium signaling in the brains of zebrafish larvae as they swim freely. The device helped them pinpoint the place cells in the larvae’s telencephalon region. “I think this work is definitely extremely interesting, because it demonstrates that, at least in some fish, you can find place cells,” says Ronen Segev, professor of life sciences at Ben-Gurion University of the Negev, who was not involved in the study. The finding also suggests that spatial cognition has origins deep in the vertebrate evolutionary tree, Li says. There is an idea that the “hippocampus and cortex are these structures that evolved at some point to enable flexible behavior,” but evolutionarily, “it was never clear when that happened.” © 2024 Simons Foundation

Keyword: Learning & Memory; Evolution
Link ID: 29456 - Posted: 08.31.2024

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

Keyword: Development of the Brain; Brain imaging
Link ID: 29446 - Posted: 08.21.2024

Juliana Ki In the United States, it's estimated that about 7 million people are living with Alzheimer's disease and related dementias. But the number of people with a formal diagnosis is far less than that. Now, a new study suggests the likelihood of getting a formal diagnosis may depend on where a person lives. Researchers at the University of Michigan and Dartmouth College found that diagnosis rates vastly differ across the country and those different rates could not simply be explained by dementia risk factors, like if an area has more cases of hypertension, obesity and diabetes. The reasons behind the disparity aren't clear, but researchers speculate that stigma as well as access to primary care or behavioral neurological specialists may impact the odds of getting a formal diagnosis. Sponsor Message "We tell anecdotes about how hard it is to get a diagnosis and maybe it is harder in some places. It's not just your imagination. It actually is different from place to place," said Julie Bynum, the study's lead author and a geriatrician at the University of Michigan Medical School. Those differences may have potential consequences. That's because a formal diagnosis of Alzheimer's opens up access to treatments that may slow down the brain changes associated with the disease. Without that formal diagnosis, patients also would not be eligible for clinical trials or insurance coverage for certain medications. Even in cases of dementia where treatment is not an option, a diagnosis can also help in the planning for a patient's care. The findings, published last week in the journal Alzheimer's & Dementia, emerged from two main questions: What percent of older adults are being diagnosed with dementia across communities in the U.S.? And is the percent we see different from what we would expect? © 2024 npr

Keyword: Alzheimers
Link ID: 29444 - Posted: 08.21.2024