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 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

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 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 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