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 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 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

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

By Abdullahi Tsanni Time takes its toll on the eyes. Now a funky, Hitchcockian video of 64 eyeballs, all rolling and blinking in different directions, is providing a novel visual of one way in which eyes age. A video display of 64 eyeballs, captured using eye trackers, helped researchers compare the size of younger and older study participants’ pupils under differing light conditions, confirming aging affects our eyes. Lab studies have previously shown that the eye’s pupil size shrinks as people get older, making the pupil less responsive to light. A new study that rigged volunteers up with eye-trackers and GoPro videos and sent them traipsing around a university campus has confirmed what happens in the lab happens in real life, too. While pupils remain sensitive to changing light conditions, pupil size can decrease up to about 0.4 millimeters per decade, researchers report June 19 in Royal Society Open Science. “We see a big age effect,” says Manuel Spitschan, a neuroscientist at Max Planck Institute for Biological Cybernetics in Tubingen, Germany. The change helps explain why it can be increasingly harder for people to see in dim light as they age. Light travels through the dark pupil in the center of the eye to the retina, a layer of cells in the back of the eyes that converts the light into images. The pupil’s size can vary from 2 to 8 millimeters in diameter depending on light conditions, getting smaller in bright light and larger in dim light. “With a small pupil, less light enters the eye,” Spitschan says. © Society for Science & the Public 2000–2024.

Keyword: Vision; Development of the Brain
Link ID: 29375 - Posted: 07.03.2024

Richard Luscombe Federal health authorities on Tuesday gave approval to an experimental new drug that has shown to delay the onset of Alzheimer’s disease in trials. Donanemab, manufactured by Eli Lilly, is the second medication that has won the blessing of the Food and Drug Administration (FDA) to treat patients showing early symptoms of the disease, most prominently cognitive impairment. Last year, authorities cleared the drug lecanemab, marketed under the brand name Leqembi, after it demonstrated a similar decline in the progression of Alzheimer’s in a control group. The treatments are not a cure, but the first to physically alter the course of the disease rather than just addressing its symptoms, the FDA said. The video player is currently playing an ad. Indianapolis-based Eli Lilly reported the success of its trial a year ago, and subsequently applied for the FDA authorization that was announced today. Experts at the time said it “could be the beginning of the end of Alzheimer’s disease”, which affects almost 7 million people, mostly older Americans, according to the Alzheimer’s Association. “Kisunla demonstrated very meaningful results for people with early symptomatic Alzheimer’s disease, who urgently need effective treatment options,” Anne White, executive vice-president of Eli Lilly said on Tuesday, referring to donanemab by the brand name it will be sold under. © 2024 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29374 - Posted: 07.03.2024

By Charles Q. Choi The largest-yet single-cell genomics analysis reveals new details of the molecular pathways and cell types that are altered in the cortex in people with autism. The work, published last month in Science, also hints at how genes linked to the condition contribute to these brain differences. The findings are part of a package of 14 new papers from PsychENCODE, a multi-institution consortium launched in 2015 to study the molecular basis of neuropsychiatric conditions. The initiative’s latest phase of research analyzed human brains at the single-cell level instead of relying on bulk tissue samples as in previous efforts. “Single-cell analysis gives you the ability to really understand a condition in terms of cell-cell interactions, and how a condition might affect different cell types in very different ways,” says PsychENCODE chair Daniel Geschwind, professor of human genetics, neurology and psychiatry at the University of California, Los Angeles, who led the new autism study. Past work by Geschwind and others identified a “molecular signature” in tissue samples of autism brains, characterized by increased expression of immune signaling genes, decreased activity of synaptic and neuronal genes, and a reduction in the regional gene-expression patterns typically seen across the cortex. The first single-cell analysis—involving cells from 15 autistic and 16 non-autistic people, and published in 2019—hinted at a role for microglia and excitatory neurons in layer 2/3 of the cortex. The new study confirms these previous findings and expands autism’s molecular signature to include a subtype of interneurons and layer 5/6 excitatory neurons, which project to other cortical areas. It also adds gene-expression changes, such as heightened immune responses in oligodendrocytes, cells that help produce the myelin sheath insulating the central nervous system. “That suggests there may be something going on broadly with connectivity in autism,” Geschwind says. © 2024 Simons Foundation

Keyword: Autism; Epigenetics
Link ID: 29371 - Posted: 06.26.2024

By Gina Kolata and Pam Belluck A committee of independent advisers to the Food and Drug Administration voted unanimously on Monday that the benefits outweigh the risks of the newest experimental drug for Alzheimer’s disease. Alzheimer’s afflicts more than six million Americans. It has no cure, and there is no treatment or lifestyle modification that can restore memory loss or reverse cognitive decline. The drug, made by Eli Lilly, is donanemab. It modestly slowed cognitive decline in patients in the early stages of the disease but also had significant safety risks, including swelling and bleeding in the brain. The committee concluded, though, that the consequences of Alzheimer’s are so dire that even a modest benefit can be worthwhile. The F.D.A. usually follows the advice of the agency’s advisory committees but not always. The drug is based on a long-held hypothesis that Alzheimer’s disease begins when rough hard balls of amyloid, a protein, pile up in patients’ brains, followed by a cascade of reactions leading to the death of neurons. The idea is to treat Alzheimer’s by attacking amyloid, clearing it from the brain. Two similar amyloid-fighting drugs were approved recently: Leqembi, made by Eisai and Biogen, was approved last year. That drug’s risks and modest benefits are similar to those of donanemab. Aduhelm, made by Biogen, is the other drug and was approved in 2021 but was discontinued because there was insufficient evidence that it could benefit patients. Donanemab was expected to be approved earlier this year, but in March, the F.D.A. decided that, instead, it would require donanemab to undergo the scrutiny of an independent advisory committee, a surprise to Eli Lilly. © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29354 - Posted: 06.11.2024

Hannah Devlin Science correspondent A 10-minute brain scan could detect dementia several years before people develop noticeable symptoms, a study suggests. Scientists used a scan of “resting” brain activity to identify whether people would go on to develop dementia, with an estimated 80% accuracy up to nine years before people received a diagnosis. If the findings were confirmed in a larger cohort, the scan could become a routine procedure in memory clinics, scientists said. “We’ve known for a long time that the function of the brain starts to change many years before you get dementia symptoms,” said Prof Charles Marshall, who led the work at Queen Mary University of London. “This could help us to be more precise at identifying those changes using an MRI scan that you could do on any NHS scanner.” The research comes as a new generation of Alzheimer’s drugs are on the horizon. The UK’s Medicines and Healthcare products Regulatory Agency (MHRA) is assessing lecanemab, made by Eisai and Biogen, and donanemab, made by Eli Lilly, and both drugs are widely expected to be licensed this year. “Predicting who is going to get dementia in the future will be vital for developing treatments that can prevent the irreversible loss of brain cells that causes the symptoms of dementia,” Marshall said. The researchers used functional MRI (fMRI) scans from 1,100 UK Biobank volunteers to detect changes in the brain’s “default mode network” (DMN). The scan measures correlations in brain activity between different regions while the volunteer lies still, not doing any particular task. The network, which reflects how effectively different regions are communicating with each other, is known to be particularly vulnerable to Alzheimer’s disease. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Brain imaging
Link ID: 29349 - Posted: 06.08.2024

By Elissa Welle The traditional story of Alzheimer’s disease casts two key proteins in starring roles—each with clear stage directions: Plaques of sticky amyloid beta protein accumulate outside neurons as the condition unfolds, and tangles of tau protein gum up the insides of the cells. But it may be time for a rewrite. Amyloid beta, too, coalesces inside neurons and seems to mark them for early death, according to research posted on a preprint server last November. In brain slices from people with Alzheimer’s, but not in those from age-matched controls, cells containing intracellular amyloid beta decreased in number as the disease progressed. At first, the result appeared to be a mistake, says study investigator Alessia Caramello, a postdoctoral researcher in the UK Dementia Research Institute. Intracellular amyloid beta is “nowhere to be found” in most discussions of Alzheimer’s disease, she says. “It’s never mentioned. Never ever.” Instead, the field has long focused on the buildup of amyloid beta outside the cell. But even before those plaques form, there seems to be another pathological event, she says—namely intracellular amyloid—“Why not look at it?” The work from Caramello and her colleagues is not the first to suggest that amyloid beta, or Abeta for short, wreaks havoc inside neurons, not just in the extracellular space between them. This “inside-out” hypothesis, as it has been called, has implications for how scientists understand Alzheimer’s disease. In particular, it could help to account for some big mysteries around the condition—such as why the extent of amyloid beta plaques in the brain doesn’t always correlate with symptoms, why neurons die and why treatments to lessen plaques marginally slow down, but do not halt, the disease. “It just puts a totally different spin on how you need to address this,” says Gunnar Gouras, professor of experimental neurology at Lund University and a proponent of the inside-out hypothesis. “It’s really a cell biological, neurobiological issue that is a bit more complex. And we need to also study this instead of just saying, ‘Abeta is bad; we’ve got to get rid of it.’” © 2024 Simons Foundation

Keyword: Alzheimers
Link ID: 29335 - Posted: 06.02.2024

By Ben Casselman Long before people develop dementia, they often begin falling behind on mortgage payments, credit card bills and other financial obligations, new research shows. A team of economists and medical experts at the Federal Reserve Bank of New York and Georgetown University combined Medicare records with data from Equifax, the credit bureau, to study how people’s borrowing behavior changed in the years before and after a diagnosis of Alzheimer’s or a similar disorder. What they found was striking: Credit scores among people who later develop dementia begin falling sharply long before their disease is formally identified. A year before diagnosis, these people were 17.2 percent more likely to be delinquent on their mortgage payments than before the onset of the disease, and 34.3 percent more likely to be delinquent on their credit card bills. The issues start even earlier: The study finds evidence of people falling behind on their debts five years before diagnosis. “The results are striking in both their clarity and their consistency,” said Carole Roan Gresenz, a Georgetown University economist who was one of the study’s authors. Credit scores and delinquencies, she said, “consistently worsen over time as diagnosis approaches, and so it literally mirrors the changes in cognitive decline that we’re observing.” The research adds to a growing body of work documenting what many Alzheimer’s patients and their families already know: Decision-making, including on financial matters, can begin to deteriorate long before a diagnosis is made or even suspected. People who are starting to experience cognitive decline may miss payments, make impulsive purchases or put money into risky investments they would not have considered before the disease. “There’s not just getting forgetful, but our risk tolerance changes,” said Lauren Hersch Nicholas, a professor at the University of Colorado School of Medicine who has studied dementia’s impact on people’s finances. “It might seem suddenly like a good move to move a diversified financial portfolio into some stock that someone recommended.” © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29334 - Posted: 06.02.2024

By Elie Dolgin The COVID-19 pandemic didn’t just reshape how children learn and see the world. It transformed the shape of their eyeballs. As real-life classrooms and playgrounds gave way to virtual meetings and digital devices, the time that children spent focusing on screens and other nearby objects surged — and the time they spent outdoors dropped precipitously. This shift led to a notable change in children’s anatomy: their eyeballs lengthened to better accommodate short-vision tasks. Study after study, in regions ranging from Europe to Asia, documented this change. One analysis from Hong Kong even reported a near doubling in the incidence of pathologically stretched eyeballs among six-year-olds compared with pre-pandemic levels1. This elongation improves the clarity of close-up images on the retina, the light-sensitive layer at the back of the eye. But it also makes far-away objects appear blurry, leading to a condition known as myopia, or short-sightedness. And although corrective eyewear can usually address the issue — allowing children to, for example, see a blackboard or read from a distance — severe myopia can lead to more-serious complications, such as retinal detachment, macular degeneration, glaucoma and even permanent blindness. Rates of myopia were booming well before the COVID-19 pandemic. Widely cited projections in the mid-2010s suggested that myopia would affect half of the world’s population by mid-century (see ‘Rising prevalence’), which would effectively double the incidence rate in less than four decades2 (see ‘Affecting every age’). Now, those alarming predictions seem much too modest, says Neelam Pawar, a paediatric ophthalmologist at the Aravind Eye Hospital in Tirunelveli, India. “I don’t think it will double,” she says. “It will triple.” © 2024 Springer Nature Limited

Keyword: Vision; Development of the Brain
Link ID: 29329 - Posted: 05.29.2024

By Laura Sanders It’s a bit like seeing a world in a grain of sand. Except the view, in this case, is the exquisite detail inside a bit of human brain about half the size of a grain of rice. Held in that minuscule object is a complex collective of cells, blood vessels, intricate patterns and biological puzzles. Scientists had hints of these mysteries in earlier peeks at this bit of brain (SN: 6/29/21). But now, those details have been brought into new focus by mapping the full landscape of some 57,000 cells, 150 million synapses and their accompanying 23 centimeters of blood vessels, researchers report in the May 10 Science. The full results, the scientists hope, may lead to greater insights into how the human brain works. “We’re going in and looking at every individual connection attached to every cell — a very high level of detail,” says Viren Jain, a computational neuroscientist at Google Research in Mountain View, Calif. The big-picture goal of brain mapping efforts, he says, is “to understand how human brains work and what goes wrong in various kinds of brain diseases.” The newly mapped brain sample was removed during a woman’s surgery for epilepsy, so that doctors could reach a deeper part of the brain. The bit, donated with the woman’s consent, was from the temporal lobe of the cortex, the outer part of the brain involved in complex mental feats like thinking, remembering and perceiving. This digital drawing of a person's head shows the brain inside. An arrow points to the bottom left side of the brain. After being fixed in a preservative, the brain bit was sliced into almost impossibly thin wisps, and then each slice was imaged with a high-powered microscope. Once these views were collected, researchers used computers to digitally reconstruct the three-dimensional objects embedded in the piece of brain. © Society for Science & the Public 2000–2024

Keyword: Brain imaging; Development of the Brain
Link ID: 29324 - Posted: 05.25.2024

By Angie Voyles Askham Some questions about neurons, such as how they give rise to behavior, are tricky to answer when those cells are embedded within their natural milieu. “Is residence in a nervous system sufficient to allow synapses to form?” says Kristin Baldwin, professor of genetics and development at Columbia University. “Are synapses that we can see sufficient to allow communication? And is synaptic communication sufficient to actually endow an animal with a set of behaviors that would be appropriate for it?” The best way to answer those questions is to put the cells in a new environment where their extrinsic and intrinsic influences can be teased apart, says Xin Jin, assistant professor of neuroscience at the Scripps Research Institute. For a long time, Jin says, that new environment was the unnatural setting of a petri dish. But two new studies that make use of chimeric mice—animals with both mouse and rat cells in their brain—point to another option: One demonstrates how rat stem cells can restore a mouse’s ability to smell, whereas the other shows how rat stem cells can give rise to a forebrain in mice that would otherwise lack one. The studies were published last month in Cell. Because rat brains are larger than mouse brains and develop at a different rate, the chimeras enable researchers to probe the competing forces of a cell’s intrinsic programming and its external environment. The work opens up doors for new research and the ability to explore the origins of species-specific cellular behaviors, says Jin, who was not involved in either study. “It’s sort of a fundamental ‘nature versus nurture,’” says Baldwin, who led one of the new studies. © 2024 Simons Foundation

Keyword: Development of the Brain
Link ID: 29312 - Posted: 05.18.2024

By Carissa Wong Researchers have mapped a tiny piece of the human brain in astonishing detail. The resulting cell atlas, which was described today in Science1 and is available online, reveals new patterns of connections between brain cells called neurons, as well as cells that wrap around themselves to form knots, and pairs of neurons that are almost mirror images of each other. The 3D map covers a volume of about one cubic millimetre, one-millionth of a whole brain, and contains roughly 57,000 cells and 150 million synapses — the connections between neurons. It incorporates a colossal 1.4 petabytes of data. “It’s a little bit humbling,” says Viren Jain, a neuroscientist at Google in Mountain View, California, and a co-author of the paper. “How are we ever going to really come to terms with all this complexity?” The brain fragment was taken from a 45-year-old woman when she underwent surgery to treat her epilepsy. It came from the cortex, a part of the brain involved in learning, problem-solving and processing sensory signals. The sample was immersed in preservatives and stained with heavy metals to make the cells easier to see. Neuroscientist Jeff Lichtman at Harvard University in Cambridge, Massachusetts, and his colleagues then cut the sample into around 5,000 slices — each just 34 nanometres thick — that could be imaged using electron microscopes. Jain’s team then built artificial-intelligence models that were able to stitch the microscope images together to reconstruct the whole sample in 3D. “I remember this moment, going into the map and looking at one individual synapse from this woman’s brain, and then zooming out into these other millions of pixels,” says Jain. “It felt sort of spiritual.” When examining the model in detail, the researchers discovered unconventional neurons, including some that made up to 50 connections with each other. “In general, you would find a couple of connections at most between two neurons,” says Jain. Elsewhere, the model showed neurons with tendrils that formed knots around themselves. “Nobody had seen anything like this before,” Jain adds. © 2024 Springer Nature Limited

Keyword: Brain imaging; Development of the Brain
Link ID: 29304 - Posted: 05.14.2024