By Charles Q. Choi Tangles of tau protein track with cognitive impairments in Alzheimer’s disease. But even though tau is expressed throughout the brain, it clumps mainly in specific regions, such as the cortex and hippocampus. Other areas, such as the cerebellum and brainstem, are largely spared. Why tau aggregates this way has remained a mystery, but the answer may have to do with a previously overlooked, oversized and naturally occurring variant of the protein called “big tau,” according to a preprint posted 31 July on bioRxiv. Most tau isoforms range from 352 to 441 amino acids in size, but big tau comprises 758 amino acids. This supersized version is significantly more abundant in the cerebellum and brainstem than in the cortex and hippocampus of mice—and it is much less likely to form abnormal clumps than its smaller counterparts, the preprint shows. “Big tau can resist several key pathological changes related to [Alzheimer’s disease],” wrote study investigator Dah-eun Chloe Chung, a postdoctoral researcher in Huda Zoghbi’s lab at Baylor College of Medicine, in a post on X about the work. (Zoghbi declined to comment for this article because she says the study is currently under review for potential publication, and Chung did not respond to email requests for comment.) Scientists identified big tau in the peripheral nervous system in the 1990s, and it is the predominant tau isoform there. But most research on tau since then “ignores the existence of big tau,” according to a 2020 review. “No one has bothered to study this protein in the context of neurodegeneration,” says Veera Rajagopal, a research scientist at Regeneron, who did not take part in the new work. “All tau-related research has been focused on the shorter isoforms that play a key role in the tauopathies like Alzheimer’s disease, frontotemporal dementia and so on. Now many will go after this big guy.” © 2024 Simons Foundation

Keyword: Alzheimers
Link ID: 29440 - Posted: 08.19.2024

By Greg Donahue In late 2018, after an otherwise-normal Christmas holiday, Laurie Beatty started acting strange. An 81-year-old retired contractor, he grew unnaturally quiet and began poring over old accounting logs from a construction business he sold decades earlier, convinced that he had been bilked in the deal. Listen to this article, read by Robert Petkoff Over the course of several days, Beatty slipped further into unreality. He told his wife the year was 1992 and wondered aloud why his hair had turned white. Then he started having seizures. His arms began to move in uncontrollable jerks and twitches. By the end of May, he was dead. Doctors at the Georges-L.-Dumont University Hospital Center in Moncton, the largest city in the province of New Brunswick, Canada, zeroed in on an exceedingly rare condition — Creutzfeldt-Jakob disease, caused by prions, misfolding proteins in the brain — as the most likely culprit. The doctors explained this to Beatty’s children, Tim and Jill, and said they would run additional tests to confirm the post-mortem diagnosis. Three months later, when the siblings returned to the office of their father’s neurologist, Dr. Alier Marrero, that’s what they were expecting to hear. Instead, Marrero told them that Laurie’s Creutzfeldt-Jakob test had come back negative. “We were all looking at one another,” Tim says, “because we were all very confused.” If Creutzfeldt-Jakob hadn’t killed their father, then what had? What Marrero said next was even more unsettling. “There’s something going on,” they recall him saying. “And I don’t know what it is.” It turned out that Laurie Beatty was just one of many local residents who had gone to Marrero’s office exhibiting similar, inexplicable symptoms of neurological decline — more than 20 in the previous four years. The first signs were often behavioral. One patient fell asleep for nearly 20 hours straight before a friend took her to the hospital; another found himself afraid to disturb the stranger who had sat down in his living room, only to realize hours later that the stranger was his wife. © 2024 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 29434 - Posted: 08.15.2024

Andrew Gregory Health editor Almost half of dementia cases worldwide could be prevented or delayed, a study has found, as experts named 14 risk factors. The number of people living with dementia globally is forecast to nearly triple to 153 million by 2050, and researchers warn this presents a rapidly growing threat to health and social care systems. Global health and social costs linked to dementia exceed $1tn (£780bn) a year, the research shows. However, in a seismic report published by the Lancet, 27 of the world’s leading dementia experts concluded that far more cases could be avoided or delayed than previously thought. Addressing 14 modifiable risk factors, starting in childhood and continuing throughout life, could prevent or delay 45% of dementia cases, even as people live longer, the Lancet commission on dementia said. The findings were presented at the Alzheimer’s Association international conference in the US. In an interview with the Guardian, the lead author of the research, Prof Gill Livingston, said it was increasingly clear that there was much more that millions of people could and should do to reduce the risk of dementia. Speaking from the conference in Philadelphia, Livingston said: “Many people around the world believe dementia is inevitable but it’s not. Our report concludes that you can hugely increase the chances of not developing dementia or pushing back its onset. “It’s also important to stress that while we now have stronger evidence that longer exposure to risk has a greater effect … it’s never too early or too late to take action.” © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Learning & Memory
Link ID: 29420 - Posted: 08.03.2024

By Laura Sanders Alzheimer’s disease is hard to diagnose. But proteins in the blood might provide clarity. A series of recent findings, presented at the annual Alzheimer’s Association International Conference in Philadelphia and in research papers, raise the possibility of a simple blood draw to help doctors figure out if a person’s cognitive problems are caused by Alzheimer’s — or something else. Decades ago, the only definitive way to get a diagnosis was an autopsy. Since then, scientists have figured out how to see the disease in living people. Spinal taps reveal levels of key proteins associated with the disease. And brain scans can illuminate the characteristic plaques and tangles that mar the brain in a person with Alzheimer’s disease. But spinal taps and brain scans are expensive and uncomfortable. A blood draw would lower barriers to diagnosis even further. That matters, because while Alzheimer’s has no cure, an easier, faster way to spot the disease could give people more time to discuss therapy options, including the newly available drugs that lower levels of amyloid, the sticky protein that accumulates in the brain in Alzheimer’s (SN: 7/17/23). Those drugs moderately slow the progression of the disease, but they come with serious side effects (SN: 6/7/21). “It’s an exciting moment,” says neuropathologist Eliezer Masliah of the National Institute on Aging in Bethesda, Md. “It’s an explosive moment,” one that has the potential to help reshape the diagnosis and treatment of the nearly 7 million people with Alzheimer’s in the United States, and millions more worldwide, he says. © Society for Science & the Public 2000–2024.

Keyword: Alzheimers
Link ID: 29419 - Posted: 08.03.2024

By Liam Drew In November 2008, neuroscientist Susana Carmona — then a postdoc studying attention deficit hyperactivity disorder — was driving two colleagues to a party when one of them revealed that she was thinking about having a child. The trio became so engulfed in conversation about how pregnancy might change her brain that they diverted from the party and headed to their laboratory to search the literature. They found numerous studies in rodents, but in humans, “there was basically nothing at all”, says Carmona. Shocked by this gap in research, Carmona and her colleagues convinced their mentor at the Autonomous University of Barcelona, Spain, Oscar Vilarroya, to let them run a study using magnetic resonance imaging (MRI) to measure the neuroanatomy of women before they became pregnant, and then again after they gave birth. Squeezed in alongside their main projects, the investigation took eight years and included dozens of participants. The results, published in 2016, were revelatory1. Two to three months after giving birth, multiple regions of the cerebral cortex were, on average, 2% smaller than before conception. And most of them remained smaller two years later. Although shrinkage might evoke the idea of a deficit, the team showed that the degree of cortical reduction predicted the strength of a mother’s attachment to her infant, and proposed that pregnancy prepares the brain for parenthood. Today, Carmona, now at the Gregorio Marañón Health Research Institute in Madrid, is one of several scientists uncovering how pregnancy and parenthood transform the brain. Elseline Hoekzema, one of Carmona’s passengers that evening in 2008, is another. In 2022, Hoekzema, who is now at the Amsterdam University Medical Centre in the Netherlands, confirmed that the cortical regions that shrink during pregnancy also function differently for at least a year after giving birth2. These studies and others, say researchers, highlight a transformational life event that has long been neglected by neuroscience — one that around 140 million women experience annually.

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 29418 - Posted: 08.02.2024

By Laura Hercher It is impossible, of course, to identify the precise moment we first suspected the changes in my mother were something other than normal aging. In my own imperfect memory, what rises up is the first morning of a weeklong trip to Rome, when my mother woke up at 2 A.M., got dressed and went down for breakfast. A hotel employee found her wandering from room to room, looking for toast and coffee. She was jet-lagged, my brother and I assured each other uneasily. It could happen to anyone. But weren’t there cues? Didn’t she notice the darkened lobby, the stillness, the clock? If we had known then, would it have helped? To date, no Food and Drug Administration–approved therapy exists for asymptomatic people at risk of Alzheimer’s disease (AD). My mother was not a smoker, drank in moderation, read books, took classes, and spent the week soaking up everything the tour guide had to tell her about Caravaggio and Bernini like she was prepping for the quiz. It was five years before my mother received a diagnosis of dementia. Today, a simple blood test can detect changes in the brain that predict AD up to 15 years before the first symptoms emerge. For researchers, tools for early detection give a peek at the full spectrum of AD, pinpointing early seeds of pathology deep inside the brain. Cognitive decline—what we typically think of as the disease itself—is merely an end-stage denouement. “Dementia is a result. Dementia is a symptom,” explains Clifford R. Jack, Jr., a neuroradiologist at the Mayo Clinic in Rochester, Minn., and chair of the Alzheimer’s Association (AA) working group responsible for new and controversial guidelines for the diagnosis of AD based on the underlying biology, not clinical presentation. Biomarkers for AD—signs of the physical changes in the brain that contribute to disease progression—have been available for more than two decades. In 2007 an international working group (IWG) of dementia experts described biomarkers as supporting evidence for a diagnosis of the disease, defined at that point largely as it was by neuropathologist Alois Alzheimer back in 1906: progressive memory loss, confusion and personality changes caused by distinctive plaques and tangles in the brain. For almost a century, those brain changes could only be confirmed on autopsy. While the affected person was alive, the label was merely presumptive. In fact, postmortem studies have found that up to 30 percent of people who received a clinical diagnosis of AD did not have the characteristic plaques and tangles.

Keyword: Alzheimers
Link ID: 29416 - Posted: 08.02.2024

Jon Hamilton A key protein that helps assemble the brain early in life also appears to protect the organ from Alzheimer’s and other diseases of aging. A trio of studies published in the past year all suggest that the protein Reelin helps maintain thinking and memory in ailing brains, though precisely how it does this remains uncertain. The studies also show that when Reelin levels fall, neurons become more vulnerable. There’s growing evidence that Reelin acts as a “protective factor” in the brain, says Li-Huei Tsai, a professor at MIT and director of the Picower Institute for Learning and Memory. “I think we’re on to something important for Alzheimer’s,” Tsai says. Various pieces of colorful trash, such as plastic bottle caps and plastics forks, are arranged in the shape of a human brain, on a light blue background. The research has inspired efforts to develop a drug that boosts Reelin or helps it function better, as a way to stave off cognitive decline. “You don't have to be a genius to be like, ‘More Reelin, that’s the solution,’” says Dr. Joseph Arboleda-Velasquez of Harvard Medical School and Massachusetts Eye and Ear. “And now we have the tools to do that.” From Colombia, a very special brain Reelin became something of a scientific celebrity in 2023, thanks to a study of a Colombian man who should have developed Alzheimer’s in middle age but didn’t. The man, who worked as a mechanic, was part of a large family that carries a very rare gene variant known as Paisa, a reference to the area around Medellin where it was discovered. Family members who inherit this variant are all but certain to develop Alzheimer’s in middle age. © 2024 npr

Keyword: Alzheimers; Development of the Brain
Link ID: 29413 - Posted: 07.31.2024

By Katie Moisse Monkeys can memorize a sequence of images and then toggle between them in their minds, a new study has found. Each mental move is associated with a tiny burst of brain activity that could be the neural representation of a thought, the study authors say. The study is the first to find evidence that an animal creates cognitive maps based on experience and later uses them exclusively, without any sensory input, to navigate a new task. It also marks one of the first times researchers have registered brain activity tied to an ongoing, complex thought process. “It’s a very fluid process—the process of thinking. And we have no way in animals to know what they’re thinking and therefore map what we record in the brain to what’s happening in the mind,” says study investigator Mehrdad Jazayeri, professor and director of education, brain and cognitive sciences at MIT’s McGovern Institute and a Howard Hughes Medical Institute investigator. In the new study, however, Jazayeri and his team designed a task that requires the animal to imagine a specific scenario at a specific time. “Imagination: There’s no magic to it; it’s a pattern of activity in the brain,” he says. Previous studies suggest rodents use cognitive maps to recreate the past and predict future possibilities. The new study, published last month in Nature, suggests monkeys also engage in such mental simulation and do so in the present—imagining states of the world that they just can’t see. “It’s a little bit like an animal navigating in the dark, where they’re using an internal map of where they are and where they’re going to update their sense of how close they are to their goal,” says Loren Frank, professor of physiology at the University of California, San Francisco, School of Medicine and a Howard Hughes Medical Institute investigator, who was not involved in the work. “Our brains do this all the time. But this study gives us a sense of how they do it and shows there’s an identifiable underlying process. It’s a really nice step forward.” Research image of the activity of a single neuron in a monkey brain. © 2024 Simons Foundation

Keyword: Learning & Memory; Evolution
Link ID: 29412 - Posted: 07.31.2024

By Pam Belluck Scientists have made another major stride toward the long-sought goal of diagnosing Alzheimer’s disease with a simple blood test. On Sunday, a team of researchers reported that a blood test was significantly more accurate than doctors’ interpretation of cognitive tests and CT scans in signaling the condition. The study, published Sunday in the journal JAMA, found that about 90 percent of the time the blood test correctly identified whether patients with memory problems had Alzheimer’s. Dementia specialists using standard methods that did not include expensive PET scans or invasive spinal taps were accurate 73 percent of the time, while primary care doctors using those methods got it right only 61 percent of the time. “Not too long ago measuring pathology in the brain of a living human was considered just impossible,” said Dr. Jason Karlawish, a co-director of the Penn Memory Center at the University of Pennsylvania who was not involved in the research. “This study adds to the revolution that has occurred in our ability to measure what’s going on in the brain of living humans.” The results, presented Sunday at the Alzheimer’s Association International Conference in Philadelphia, are the latest milestone in the search for affordable and accessible ways to diagnose Alzheimer’s, a disease that afflicts nearly seven million Americans and over 32 million people worldwide. Medical experts say the findings bring the field closer to a day when people might receive routine blood tests for cognitive impairment as part of primary care checkups, similar to the way they receive cholesterol tests. “Now, we screen people with mammograms and PSA or prostate exams and other things to look for very early signs of cancer,” said Dr. Adam Boxer, a neurologist at the University of California, San Francisco, who was not involved in the study. “And I think we’re going to be doing the same thing for Alzheimer’s disease and hopefully other forms of neurodegeneration.” © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29410 - Posted: 07.31.2024

By Vivian La Great Basin was burning the midnight oil on a chilly fall evening in 2016 when he made his move. Slinking out of the shadows in Laramie, Wyoming, the raccoon approached what looked like a metal filing cabinet lying on its side. He could smell a mix of dog kibble and sardines within, but 12 latched narrow doors blocked his entry. Making matters worse, a fellow raccoon had beaten him there. So Great Basin jumped on top of the cabinet and began to fiddle with the latches upside down. He quickly opened one of the doors, securing the treats and filling his belly. Humans have long regarded raccoons—renowned for their ability to jimmy their way into locked garbage cans and enter seemingly impassable attics—with a mixture of awe and scorn. But outside of the lab, researchers have little scientific sense of how clever these “trash pandas” really are. A study published today in the Proceedings of the Royal Society B: Biological Sciences may change that. The work was led by Lauren Stanton, a cognitive ecologist at the University of California, Berkeley who has studied raccoons for 10 years. She says she’s drawn by their quirky personalities and quick ability to adapt to environments such as urban areas. “I think it’s fascinating to think about how raccoons perceive the world.” Despite their reputation for cleverness, Stanton says raccoons generally are understudied because they can be “a menace in the lab,” gnawing on cages and biting scientists. Research on wild raccoons is even more scarce. © 2024 American Association for the Advancement of Science.

Keyword: Learning & Memory; Evolution
Link ID: 29406 - Posted: 07.27.2024

By Bianca Nogrady The ability to remember and recognize a musical theme does not seem to be affected by age, unlike many other forms of memory. “You’ll hear anecdotes all the time of how people with severe Alzheimer’s can’t speak, can’t recognize people, but will sing the songs of their childhood or play the piano,” says Sarah Sauvé, a feminist music scientist now at the University of Lincoln in the United Kingdom. Past research has shown that many aspects of memory are affected by ageing, such as recall tasks that require real-time processing, whereas recognition tasks that rely on well-known information and automatic processes are not. The effect of age on the ability to recall music has also been investigated, but Sauvé was interested in exploring this effect in a real-world setting such as a concert. In her study1, published today in PLoS ONE, she tested how well a group of roughly 90 healthy adults, ranging in age from 18 to 86 years, were able to recognize familiar and unfamiliar musical themes at a live concert. Participants were recruited at a performance of the Newfoundland Symphony Orchestra in St John’s, Canada. Another 31 people watched a recording of the concert in a laboratory. The study focused on three pieces of music played at the concert: Eine kleine Nachtmusik by Mozart, which the researchers assumed most participants were familiar with, and two specially commissioned experimental pieces. One of these was tonal and easy to listen to; the other was more atonal and didn’t conform to the typical melodic norms of Western classical music. A short melodic phrase from each of the three pieces was played three times at the beginning of that piece, and participants then logged whenever they recognized that theme in the piece. © 2024 Springer Nature Limited

Keyword: Learning & Memory; Alzheimers
Link ID: 29405 - Posted: 07.27.2024

By Christina Caron The 6-year-old boy sitting across from Douglas Tynan, a child and adolescent clinical psychologist based in Delaware, clearly did not have attention deficit hyperactivity disorder. Dr. Tynan was sure of that. But the boy’s first-grade teacher disagreed. He could be inattentive in class, but at home his behavior wasn’t out of the ordinary for a child his age. A voracious reader, he told Dr. Tynan that he liked to bring his own books to school because the ones in class were too easy. What his teacher had not considered was that the child was most likely academically gifted, as his mother had been as a child, Dr. Tynan said. (Studies have shown that Black children, like the boy in his office, are less likely to be identified for gifted programs.) Further testing revealed that Dr. Tynan was correct. The child wasn’t inattentive in school because of A.D.H.D. It was because he was bored. A.D.H.D. is a neurodevelopmental disorder that begins in childhood and typically involves inattention, disorganization, hyperactivity and impulsivity that cause trouble in two or more settings, like at home and at school. But those symptoms — for children and adults alike — can overlap with a multitude of other traits and disorders. In fact, difficulty concentrating is one of the most common symptoms listed in the American Psychiatric Association’s diagnostic manual, and it’s associated with 17 diagnoses, according to a study published in April. Patients need a careful evaluation to avoid either being misdiagnosed with A.D.H.D. or having a missed A.D.H.D. diagnosis. Here’s a look at some common problems that can mimic A.D.H.D. Mental health conditions like anxiety, depression or oppositional defiant disorder can show up as A.D.H.D.-like symptoms. © 2024 The New York Times Company

Keyword: ADHD; Development of the Brain
Link ID: 29404 - Posted: 07.27.2024

By Dana G. Smith Getting too little sleep later in life is associated with an increased risk for Alzheimer’s disease. But paradoxically, so is getting too much sleep. While scientists are confident that a connection between sleep and dementia exists, the nature of that connection is complicated. It could be that poor sleep triggers changes in the brain that cause dementia. Or people’s sleep might be disrupted because of an underlying health issue that also affects brain health. And changes in sleep patterns can be an early sign of dementia itself. Here’s how experts think about these various connections and how to gauge your risk based on your own sleep habits. Too Little Sleep Sleep acts like a nightly shower for the brain, washing away the cellular waste that accumulates during the day. During this process, the fluid that surrounds brain cells flushes out molecular garbage and transfers it into the bloodstream, where it’s then filtered by the liver and kidneys and expelled from the body. That trash includes the protein amyloid, which is thought to play a key role in Alzheimer’s disease. Everyone’s brain produces amyloid during the day, but problems can arise when the protein accumulates into sticky clumps, called plaques. The longer someone is awake, the more amyloid builds up and the less time the brain has to remove it. Scientists don’t know whether regularly getting too little sleep — typically considered six hours or less a night — is enough to trigger the accumulation of amyloid on its own. But research has found that among adults aged 65 to 85 who already have plaques in their brains, the less sleep they got, the more amyloid was present and the worse their cognition. “Is lack of sleep sufficient to cause dementia? Probably not by itself alone,” said Dr. Sudha Seshadri, the founding director of the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at the University of Texas Health Science Center at San Antonio. “But it seems to definitely be a risk factor for increasing the risk of dementia, and perhaps also the speed of decline.” © 2024 The New York Times Company

Keyword: Sleep; Alzheimers
Link ID: 29400 - Posted: 07.23.2024

By Elissa Welle One question long plagued memory researcher André Fenton: How can memories last for years when a protein essential to maintaining them, called memory protein kinase Mzeta (PKMzeta), lasts for just days? The answer, Fenton now says, may lie in PKMzeta’s interaction with another protein, called postsynaptic kidney and brain expressed adaptor protein (KIBRA). Complexes of the two molecules maintain memories in mice for at least one month, according to a new study co-led by Fenton, professor of neural science at New York University. The bond between the two proteins “protects each of them,” Fenton says, from normal degradation in the cell. KIBRA preferentially gloms onto potentiated synapses, the study shows. And it may help PKMzeta stick there, too, where the kinase acts as a “molecular switch” to help memories persist, Fenton says. “As Theseus’ Ship was sustained for generations by continually replacing worn planks with new timbers, long-term memory can be maintained by continual exchange of potentiating molecules at activated synapses,” Fenton and his colleagues write in their paper, which was published last month in Science Advances. Before this study, the PKMzeta mystery had two “missing puzzle pieces,” says Justin O’Hare, assistant professor of pharmacology at the University of Colorado Denver, who was not involved in the study. One was how PKMzeta identifies potentiated synapses, part of the cellular mechanism underlying memory formation. The second was how memories persist despite the short lifetime of each PKMzeta molecule. This study “essentially proposes KIBRA as a solution to both of those—and the experiments themselves are pretty convincing and thorough. They do everything multiple ways.” PKMzeta has been widely studied, but its role in memory has been shrouded in controversy for more than a decade, Fenton says. Although early work suggested that PKMzeta is necessary for memory formation, later studies found that they still form in mice missing the gene for PKMzeta. © 2024 Simons Foundation

Keyword: Learning & Memory
Link ID: 29396 - Posted: 07.18.2024

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.

Keyword: Development of the Brain; Learning & Memory
Link ID: 29391 - Posted: 07.13.2024

Anna Bawden The idea that night owls who don’t go to bed until the early hours struggle to get anything done during the day may have to be revised. It turns out that staying up late could be good for our brain power as research suggests that people who identify as night owls could be sharper than those who go to bed early. Researchers led by academics at Imperial College London studied data from the UK Biobank study on more than 26,000 people who had completed intelligence, reasoning, reaction time and memory tests. They then examined how participants’ sleep duration, quality, and chronotype (which determines what time of day we feel most alert and productive) affected brain performance. They found that those who stay up late and those classed as “intermediate” had “superior cognitive function”, while morning larks had the lowest scores. Going to bed late is strongly associated with creative types. Artists, authors and musicians known to be night owls include Henri de Toulouse-Lautrec, James Joyce, Kanye West and Lady Gaga. But while politicians such as Margaret Thatcher, Winston Churchill and Barack Obama famously seemed to thrive on little sleep, the study found that sleep duration is important for brain function, with those getting between seven and nine hours of shut-eye each night performing best in cognitive tests. © 2024 Guardian News & Media Limited

Keyword: Biological Rhythms; Learning & Memory
Link ID: 29389 - Posted: 07.11.2024

By Teddy Rosenbluth The process for diagnosing a child with autism heavily relies on a parent's description of their child’s behavior and a professional’s observations. It leaves plenty of room for human error. Parents’ concerns may skew how they answer questionnaires. Providers may hold biases, leading them to underdiagnose certain groups. Children may show widely varying symptoms, depending on factors like culture and gender. A study published Monday in Nature Microbiology bolsters a growing body of research that suggests an unlikely path to more objective autism diagnoses: the gut microbiome. After analyzing more than 1,600 stool samples from children ages 1 to 13, researchers found several distinct biological “markers” in the samples of autistic children. Unique traces of gut bacteria, fungi, viruses and more could one day be the basis of a diagnostic tool, said Qi Su, a researcher at the Chinese University of Hong Kong and a lead author of the study. A tool based on biomarkers could help professionals diagnose autism sooner, giving children access to treatments that are more effective at a younger age, he said. “Too much is left to questionnaires,” said Sarkis Mazmanian, a microbiome researcher at the California Institute of Technology. “If we can get to something we can measure — whatever it is — that’s a huge improvement.” For decades, researchers have scoured the human genome, medical histories and brain scans for a reliable indicator of A.S.D., with limited success. The Food and Drug Administration has approved two diagnostic tests based on eye-tracking software, which Dr. Su said required significant involvement from a psychiatrist. © 2024 The New York Times Company

Keyword: Autism
Link ID: 29386 - Posted: 07.09.2024

By Tyler Sloan If I ask you to picture a group of “neurons firing,” what comes to mind? For most people, it’s a few isolated neurons flashing in synchrony. This type of minimalist representation of neurons is common within neuroscience, inspired in part by Santiago Ramón y Cajal’s elegant depictions of the nervous system. His work left a deep mark on our intuitions, but the method he used—Golgi staining—highlights just 1 to 5 percent of neurons. More than a century later, researchers have mapped out brain connectivity in such detail that it easily becomes overwhelming; I vividly recall an undergraduate neurophysiology lecture in which the professor showed a wiring diagram of the primary visual cortex to make the point that it was too complex to understand. We’ve reached a point where simple wiring diagrams no longer suffice to represent what we’re learning about the brain. Advances in experimental and computational neuroscience techniques have made it possible to map brains in more detail than ever before. The wiring diagram for the whole fly brain, for example, mapped at single-synapse resolution, comprises 2.7 million cell-to-cell connections and roughly 150 million synapses. Building an intuitive understanding of this type of complexity will require new tools for representing neural connectivity in a way that is both meaningful and compact. To do this, we will have to embrace the elaborate and move beyond the single neuron to a more “maximalist” approach to visualizing the nervous system. I spent my Ph.D. studying the spinal cord, where commissural growth cones are depicted as pioneers on a railhead extending through uncharted territory. The watershed moment for me was seeing a scanning electron micrograph of the developing spinal cord for the first time and suddenly understanding the growth cone’s dense environment—its path was more like squeezing through a crowded concert than wandering across an empty field. I realized how poor my own intuitions were, which nudged me toward learning the art of 3D visualization. © 2024 Simons Foundation

Keyword: Brain imaging; Development of the Brain
Link ID: 29385 - Posted: 07.09.2024

By Charles Q. Choi Chimeroids—brain organoids grown from the cells of multiple people—offer scientists a novel way to compare individual differences in response to drugs, infections or pathogenic variants, according to a new study in Nature. “The possibilities are endless,” says lead investigator Paola Arlotta, professor and chair of stem cell and regenerative biology at Harvard University. The approach overcomes a longstanding issue that has plagued any comparison of organoids derived from different people: Disparities between the organoids might reflect genetic dissimilarities between individual people but could also result just from inadvertent variations in how each organoid was grown, says Aparna Bhaduri, assistant professor of biological chemistry at the University of California, Los Angeles, who did not contribute to the new study. Mixing cells from multiple donors into a single organoid makes it possible to grow all the cells under the same conditions and makes it more likely that any differences seen between the cells are rooted in genetic variations between the people, Bhaduri says. Initially, Arlotta’s team tried to produce chimeroids by mixing pluripotent stem cells from multiple donors. But one person’s cells usually outgrew the others to make up most of each organoid. Even small differences in the stem cells’ extremely high growth rates easily led one person’s cells to overshadow the others, the team noted. So instead, the researchers grew the stem cells independently in organoids until they began to proliferate more slowly as neural stem cells or neural progenitor cells. They then broke these organoids apart and mixed them together, producing the chimeroids that developed with balanced numbers of up to five donors’ cells. Each cell line in the chimeroids could produce all the cell types normally found in the cerebral cortex, Arlotta and her colleagues discovered using DNA and RNA sequencing techniques. © 2024 Simons Foundation

Keyword: Development of the Brain; Genes & Behavior
Link ID: 29381 - Posted: 07.06.2024

By Paula Span About a month ago, Judith Hansen popped awake in the predawn hours, thinking about her father’s brain. Her father, Morrie Markoff, was an unusual man. At 110, he was thought to be the oldest in the United States. His brain was unusual, too, even after he recovered from a stroke at 99. Although he left school after the eighth grade to work, Mr. Markoff became a successful businessman. Later in life, his curiosity and creativity led him to the arts, including photography and sculpture fashioned from scrap metal. He was a healthy centenarian when he exhibited his work at a gallery in Los Angeles, where he lived. At 103, he published a memoir called “Keep Breathing.” He blogged regularly, pored over The Los Angeles Times daily, discussed articles in Scientific American and followed the national news on CNN and “60 Minutes.” Now he was nearing death, enrolled in home hospice care. “In the middle of the night, I thought, ‘Dad’s brain is so great,’” said Ms. Hansen, 82, a retired librarian in Seattle. “I went online and looked up ‘brain donation.’” Her search led to a National Institutes of Health web page explaining that its NeuroBioBank, established in 2013, collected post-mortem human brain tissue to advance neurological research. Through the site, Ms. Hansen contacted the nonprofit Brain Donor Project. It promotes and simplifies donations through a network of university brain banks, which distribute preserved tissue to research teams. Tish Hevel, the founder of the project, responded quickly, putting Ms. Hansen and her brother in touch with the brain bank at the University of California, Los Angeles. Brain donors may have neurological and other diseases, or they may possess healthy brains, like Mr. Markoff’s. “We’re going to learn so much from him,” Ms. Hevel said. “What is it about these superagers that allows them to function at such a high level for so long?” © 2024 The New York Times Company

Keyword: Development of the Brain; Brain imaging
Link ID: 29379 - Posted: 07.06.2024