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

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