By Cordula Hölig, Brigitte Röder, Ramesh Kekunnaya Growing up in poverty or experiencing any adversity, such as abuse or neglect, during early childhood can put a person at risk for poor health, including mental disorders, later in life. Although the underlying mechanisms are poorly understood, some studies have shown that adverse early childhood experience leaves persisting (and possibly irreversible) traces in brain structure. As neuroscientists who are investigating sensitive periods of human brain development, we agree: safe and nurturing environments are a prerequisite for healthy brain development and lifelong well-being. Thus, preventing early childhood adversity undoubtedly leads to healthier lives. Poverty and adversity can cause changes in brain development. Harms can come from exposure to violence or toxins or a lack of nutrition, caregiving, perceptual and cognitive stimulation or language interaction. Neuroscientists have demonstrated that these factors crucially influence human brain development. Advertisement We don’t know whether these changes are reversed by more favorable circumstances later in life, however. Investigating this question in humans is extremely difficult. For one, multiple biological and psychological factors through which poverty and adversity affect brain development are hard to disentangle. That’s because they often occur together: a neglected child often experiences a lack of caregiving simultaneously with malnutrition and exposure to physical violence. Secondly, a clear beginning and end of an adverse experience is hard to define. Finally, it is almost impossible to fully reverse harsh environments in natural settings because most of the time it is impossible to move children out of their families or communities.. © 2023 Scientific American

Keyword: Development of the Brain; Learning & Memory
Link ID: 28783 - Posted: 05.13.2023

Scientists at the National Institutes of Health have identified new genetic risk factors for two types of non-Alzheimer’s dementia. These findings were published in Cell Genomics and detail how researchers identified large-scale DNA changes, known as structural variants, by analyzing thousands of DNA samples. The team discovered several structural variants that could be risk factors Lewy body dementia (LBD) and frontotemporal dementia (FTD). The project was a collaborative effort between scientists at the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA) at NIH. Structural variants have been implicated in a variety of neurological disorders. Unlike more commonly studied mutations, which often affect one or a few DNA building blocks called nucleotides, structural variants represent at least 50 but often hundreds, or even thousands, of nucleotides at once, making them more challenging to study. “If you imagine that our entire genetic code is a book, a structural variant would be a paragraph, page, or even an entire chapter that has been removed, duplicated, or inserted in the wrong place,” said Sonja W. Scholz, M.D., Ph.D., investigator in the neurogenetics branch of NINDS and senior author of this study. By combining cutting-edge computer algorithms capable of mapping structural variations across the whole genome with machine learning, the research team analyzed whole-genome data from thousands of patient samples and several thousand unaffected controls. A previously unknown variant in the gene TCPN1 was found in samples from patients with LBD, a disease, that like Parkinson’s disease, is associated with abnormal deposits of the protein alpha-synuclein in the brain. This variant, in which more than 300 nucleotides are deleted from the gene, is associated with a higher risk for developing LBD. While this finding is new for LBD, TCPN1 is a known risk factor for Alzheimer’s disease, which could mean that this structural variant plays a role in the broader dementia population.

Keyword: Alzheimers; Genes & Behavior
Link ID: 28775 - Posted: 05.10.2023

Sara Reardon For the second time, an experimental drug has been shown to reduce the cognitive decline associated with Alzheimer’s disease. On 3 May, pharmaceutical company Eli Lilly announced in a press release that its monoclonal antibody donanemab slowed mental decline by 35% for some participants in a 1,736-person trial — a rate comparable to that for competitor drug lecanemab. But researchers warn that until the full results are published, questions remain as to the drug’s clinical usefulness, as well as whether the modest benefit outweighs the risk of harmful side effects. Like lecanemab, donanemab targets amyloid protein, which is thought to cause dementia by accumulating in the brain and damaging neurons. The trial results provide strong evidence that amyloid is a key driver of Alzheimer’s, says Jeffrey Cummings, a neuroscientist at the University of Nevada, Las Vegas. “These are transformative in an enormously important way from a scientific point of view,” he adds. “They’re terrific.” But Marsel Mesulam, a neurologist at Northwestern University in Chicago, is more cautious. “The results that are described are extremely significant and impressive, but clinically their significance is doubtful,” he says, adding that the modest effect suggests that factors other than amyloid contribute to Alzheimer’s disease progression. “We’re heading to a new era — there’s room to cheer, but it’s an era that should make us all very sober, realizing that there will be no single magic bullet.” In the press release, Eli Lilly said that people with mild Alzheimer’s who received donanemab showed 35% less clinical decline over 18 months than did those who received a placebo, and 40% less decline in their ability to perform daily tasks. The company, based in Indianapolis, Indiana, says that it will present the full results at a conference in July and publish them in a peer-reviewed journal. It plans to apply for approval by the US Food and Drug Administration (FDA) in the next two months. Promising treatments © 2023 Springer Nature Limited

Keyword: Alzheimers
Link ID: 28773 - Posted: 05.06.2023

By Sofia Quaglia With a large blade resembling a bread knife—but without the jagged edges—Stephanie Forkel slices through the human brain lying in front of her on the dissection table. A first-year university student, Forkel is clad in an apron and protective gear. It’s her first day working in the morgue at a university hospital in Munich, Germany, where the brains of people who’ve donated their bodies to science are examined for research. Her contact lenses feel dry because of the dense formaldehyde hanging in the air. But that’s not the only reason she squints a little harder. When she looks down at the annotated brain diagram in the textbook she’s supposed to use for reference, the real human brain in front of her looks nothing like the illustrated one. That was Forkel’s first eureka moment: The standard reference shape of the brain and real brains were actually vastly divergent. As she continued her studies, she confirmed that, indeed, “every individual brain looked very different,” she recounts decades later. A growing body of research now confirms there are plenty of physical dissimilarities between individual brains, particularly when it comes to white matter—the material nestled beneath the much-prized gray matter. And it’s not just anatomical. White matter hosts connections between the brain’s sections, like a city’s streets and avenues. So behavioral patterns can arise from even small physical differences in white matter, according to a late 2022 Science paper penned by Forkel and a colleague.1 Forkel is now one of a host of researchers probing subtle differences in white matter to better understand the extent of its role in making us who we are—including how much white matter dictates variations between people’s everyday behavior, and whether it’s implicated in how some patients recover better than others from life-threatening brain injuries. © 2023 NautilusNext Inc.,

Keyword: Development of the Brain
Link ID: 28762 - Posted: 05.03.2023

By Jaya Padmanabhan Speaking two languages provides the enviable ability to make friends in unusual places. A new study suggests that bilingualism may also come with another benefit: improved memory in later life. Studying hundreds of older patients, researchers in Germany found that those who reported using two languages daily from a young age scored higher on tests of learning, memory, language and self-control than patients who spoke only one language. The findings, published in the April issue of the journal Neurobiology of Aging, add to two decades of work suggesting that bilingualism protects against dementia and cognitive decline in older people. “It’s promising that they report that early and middle-life bilingualism has a beneficial effect on cognitive health in later life,” said Miguel Arce Rentería, a neuropsychologist at Columbia University who was not involved in the study. “This would line up with the existing literature.” In recent years, scientists have gained a greater understanding of bilingualism and the aging brain, though not all their findings have aligned. Some have found that if people who have fluency in two languages develop dementia, they’ll develop it at a later age than people who speak one language. But other research has shown no clear benefit from bilingualism. Neuroscientists hypothesize that because bilingual people switch fluidly between two languages, they may be able to deploy similar strategies in other skills — such as multitasking, managing emotions and self-control — that help delay dementia later on. The new study tested 746 people age 59 to 76. Roughly 40 percent of the volunteers had no memory problems, while the others were patients at memory clinics and had experienced confusion or memory loss. © 2023 The New York Times Company

Keyword: Alzheimers; Language
Link ID: 28761 - Posted: 04.29.2023

Nicola Davis Science correspondent From loud snores to twitching paws, dogs often appear to have a penchant for a good snooze. But researchers have said elderly canines with dementia appear to spend less time slumbering than those with healthy brains – mirroring patterns seen in humans. It has long been known that people with dementia can experience sleep problems, including finding it harder to get to sleep. Researchers have also found changes in the brainwaves of people with dementia during sleep – including decreased slow brain waves that occur during non-rapid eye movement deep sleep. These are important in memory consolidation and appear to be linked to the activity of the brain’s system for clearing away waste. Now it seems sleep impairment may occur in dogs experiencing a condition similar to dementia in humans. “Changes in sleep habits should be expected in older dogs, and could be a harbinger of decline in cognition,” said Prof Natasha Olby, senior author of a study at North Carolina State University. Writing in the journal Frontiers in Veterinary Science, Olby and colleagues reported on their study of 28 dogs aged between 10 and 16 years old. The canines’ brainwaves were recorded by electroencephalogram (EEG) while the dogs took a two-hour afternoon nap. The researchers also assessed owners’ answers to a questionnaire and each dog’s performance on a range of problem-solving, memory and attention tasks, to provide a score indicating whether the dog had, or was at risk of, canine dementia. Twenty of the dogs were deemed to have cognitive impairment, with this judged to be severe in eight of them. Combining their data, the team found dogs with higher dementia scores took longer to fall asleep and spent less time sleeping. © 2023 Guardian News & Media Limited

Keyword: Alzheimers; Sleep
Link ID: 28760 - Posted: 04.29.2023

By Laurie McGinley — When Rebecca Chopp was diagnosed with early-stage Alzheimer’s disease, she and her husband did the only thing that seemed to make sense: They went to their favorite Mexican restaurant, held each other in a back booth and drank margaritas. And cried. After a while, they helped each other back across the street to their home. Chopp, at 67, was chancellor of the University of Denver, at the pinnacle of a career powered by a daunting intellect and relentless work. She was also an ordained minister, prolific author and former president of Swarthmore College and Colgate University. Sometimes, Chopp thought of herself as a brain with a body attached. The changes were subtle: Chopp was sleeping more. She got lost on the way to the doctor. Then came the diagnosis. (Joanna Kulesza/For The Washington Post ) Now, she was crushed, facing the loss of that beautiful mind. She worried she would soon be an empty shell, drooling and unkempt, a burden to the people she loved. “There is a sense that when you are diagnosed, you are immediately going to descend into madness,” Chopp said. When she relinquished the job she loved, Chopp fell into deep despair, confounded by the prescription given to her by an empathetic doctor: “Live with joy!” She had nightmares about going insane. But, eventually, she began to push back against the darkness. Chopp has mild cognitive impairment, a condition that involves subtle changes in thinking and memory and that, in most cases, leads to Alzheimer’s dementia, a fatal neurodegenerative disease that affects more than 6.7 million Americans. Using diet, exercise and joy to slow Alzheimer’s For years, there was little doctors could do for people with Alzheimer’s, even at a very early stage. Now, changes are coming in how the disease is diagnosed and treated, and patients with mild cognitive impairment are at the center of the efforts. Lacking a cure, scientists are trying desperately to delay the worst phase of the illness.

Keyword: Alzheimers
Link ID: 28752 - Posted: 04.26.2023

By Emily Underwood The ability to set a goal and pursue it without getting derailed by temptations or distractions is essential to nearly everything we do in life, from finishing homework to driving safely in traffic. It also places complex demands on the brain, requiring skills like working memory — the ability to keep small amounts of information in mind to perform a task — as well as impulse control and being able to rapidly adapt when rules or circumstances change. Taken together, these elements add up to something researchers call executive function. We all struggle with executive function sometimes, for example when we’re stressed or don’t get enough sleep. But in teenagers, these powers are still a work in progress, contributing to some of the contradictory behaviors and lapses in judgment — “My honor roll student did what on TikTok?” — that baffle many parents. This erratic control can be dangerous, especially when teens make impulsive choices. But that doesn’t mean the teen brain is broken, says Beatriz Luna, a developmental cognitive neuroscientist at the University of Pittsburgh and coauthor of a review on the maturation of one aspect of executive function, called cognitive control, in the 2015 Annual Review of Neuroscience. Adolescents have all the basic neural circuitry needed for executive function and cognitive control, Luna says. In fact, they have more than they need — what’s lacking is experience, which over time will strengthen some neural pathways and weaken or eliminate others. This winnowing serves an important purpose: It tailors the brain to help teens handle the demands of their unique, ever-changing environments and to navigate situations their parents may never have encountered. Luna’s research suggests that teens’ inconsistent cognitive control is key to becoming independent, because it encourages them to seek out and learn from experiences that go beyond what they’ve been actively taught. © 2023 Annual Reviews

Keyword: Development of the Brain; Attention
Link ID: 28751 - Posted: 04.26.2023

By R. Douglas Fields Dazzling intricacies of brain structure are revealed every day, but one of the most obvious aspects of brain wiring eludes neuroscientists. The nervous system is cross-wired, so that the left side of the brain controls the right half of the body and vice versa. Every doctor relies upon this fact in performing neurological exams, but when I asked my doctor last week why this should be, all I got was a shrug. So I asked Catherine Carr, a neuroscientist at the University of Maryland, College Park. “No good answer,” she replied. I was surprised — such a fundamental aspect of how our brain and body are wired together, and no one knew why? Nothing that we know of stops the right side of the brain from connecting with the right side of the body. That wiring scheme would seem much simpler and less prone to errors. In the embryonic brain, the crossing of the wires across the midline — an imaginary line dividing the right and left halves of the body — requires a kind of molecular “traffic cop” to somehow direct the growing nerve fibers to the right spot on the opposite side of the body. Far simpler just to keep things on the same side. Yet this neural cross wiring is ubiquitous in the animal kingdom — even the neural connections in lowly nematode worms are wired with left-right reversal across the animal’s midline. And many of the traffic cop molecules that direct the growth of neurons in these worms do the same in humans. For evolution to have conserved this arrangement so doggedly, surely there’s some benefit to it, but biologists still aren’t certain what it is. An intriguing answer, however, has come from the world of mathematics. The key to that solution lies in exactly how neural circuits are laid out within brain tissue. Neurons that make connections between the brain and the body are organized to create a virtual map in the cerebral cortex. If a neuroscientist sticks an electrode into the brain and finds that neurons there receive input from the thumb, for example, then neurons next to it in the cerebral cortex will connect to the index finger. This mapping phenomenon is called somatotopy, Greek for “body mapping,” but it’s not limited to the physical body. The 3D external world we perceive through vision and our other senses is mapped onto the brain in the same way. All Rights Reserved © 2023

Keyword: Laterality; Development of the Brain
Link ID: 28749 - Posted: 04.22.2023

Jon Hamilton Boys born to mothers who got COVID-19 while pregnant appear nearly twice as likely as other boys to be diagnosed with subtle delays in brain development. That's the conclusion of a study of more than 18,000 children born at eight hospitals in Eastern Massachusetts. Nearly 900 of the children were born to mothers who had COVID during their pregnancy. In the study, boys, but not girls, were more likely to be diagnosed with a range of developmental disorders in the first 18 months of life. These included delays in speech and language, psychological development and motor function, as well as intellectual disabilities. In older children, these differences are often associated with autism spectrum disorder, says Dr. Roy Perlis, a co-author of the study and a psychiatrist at Massachusetts General Hospital. But for the young children in this study, "it's way too soon to reliably diagnose autism," Perlis says. "All we can hope to detect at this point are more subtle sorts of things like delays in language and speech, and delays in motor milestones." The study, which relied on an analysis of electronic health records, was published in March in the journal JAMA Network Open. The finding is just the latest to suggest that a range of maternal infections can alter fetal brain development, especially in male offspring. For example, studies have found links between infections like influenza and cytomegalovirus, and disorders like autism and schizophrenia. "Male fetuses are known to be more vulnerable to maternal infectious exposures during pregnancy," says Dr. Andrea Edlow, the study's lead author and a maternal-fetal medicine specialist at Massachusetts General Hospital. © 2023 npr

Keyword: Development of the Brain; Sexual Behavior
Link ID: 28743 - Posted: 04.18.2023

by Sarah DeWeerdt Many papers about autism-linked genes note that the genes are expressed throughout both the central and the peripheral nervous systems. The proportion of such prolific genes may be as high as two-thirds, according to one 2020 analysis. Yet few studies delve into what those genes are actually doing outside the brain. That’s starting to change. Although autism is typically thought of as a brain condition, a critical mass of researchers has started to investigate how the condition alters neurons elsewhere in the body. Their work — part of a broader trend in neuroscience to look beyond the brain — hints that the role of the peripheral nervous system in autism is, well, anything but peripheral: Neuronal alterations outside the brain may help to explain a host of the condition’s characteristic traits. Much of the research so far focuses on touch and the workings of the gut, but there is increasing interest in other sensory and motor neurons, as well as the autonomic nervous system, which orchestrates basic body functions such as heartbeat, blood pressure, breathing and digestion. It’s difficult to pinpoint whether some autism traits arise in the peripheral nervous system or the central nervous system; in many cases, complex feedback loops link the two. “Your nervous system doesn’t know that we’ve divided it that way,” says Carissa Cascio, associate professor of psychiatry and behavioral sciences at Vanderbilt University in Nashville, Tennessee. But at least some peripheral changes may offer novel treatment targets. And drugs that act in the peripheral nervous system could also prove more effective and have fewer side effects than brain-based therapies, says Julia Dallman, associate professor of biology at the University of Miami in Coral Gables, Florida. © 2023 Simons Foundation

Keyword: Autism
Link ID: 28739 - Posted: 04.15.2023

By Azeen Ghorayshi Morénike Giwa Onaiwu was shocked when day care providers flagged some concerning behaviors in her daughter, Legacy. The toddler was not responding to her name. She avoided eye contact, didn’t talk much and liked playing on her own. But none of this seemed unusual to Dr. Onaiwu, a consultant and writer in Houston. “I didn’t recognize anything was amiss,” she said. “My daughter was just like me.” Legacy was diagnosed with autism in 2011, just before she turned 3. Months later, at the age of 31, Dr. Onaiwu was diagnosed as well. Autism, a neurodevelopmental disorder characterized by social and communication difficulties as well as repetitive behaviors, has long been associated with boys. But over the past decade, as more doctors, teachers and parents have been on the lookout for early signs of the condition, the proportion of girls diagnosed with it has grown. In 2012, the Centers for Disease Control and Prevention estimated that boys were 4.7 times as likely as girls to receive an autism diagnosis. By 2018, the ratio had dipped to 4.2 to 1. And in data released by the agency last month, the figure was 3.8 to 1. In that new analysis, based on the health and education records of more than 226,000 8-year-olds across the country, the autism rate in girls surpassed 1 percent, the highest ever recorded. More adult women like Dr. Onaiwu are being diagnosed as well, raising questions about how many young girls continue to be missed or misdiagnosed. “I think we just are getting more aware that autism can occur in girls and more aware of the differences,” said Catherine Lord, a psychologist and autism researcher at the University of California, Los Angeles. © 2023 The New York Times Company

Keyword: Autism; Sexual Behavior
Link ID: 28737 - Posted: 04.12.2023

Alison Abbott When neurologist Reisa Sperling stepped up to receive her lifetime achievement award at an international Alzheimer’s conference last December, she was more excited about the future than about celebrating the past. What thrilled Sperling, who won the award for her work on clinical trials of Alzheimer’s treatments, was a sense of hope, which has been conspicuously missing from research into the disease for many years. Most other attendees felt the same. Just a few months before the meeting, researchers had announced that an antibody drug called lecanemab clearly lowered the amount of amyloid protein plaques — a tell-tale sign of the disease — in the brains of participants in a clinical trial, and slowed their cognitive decline. Sperling, who runs a laboratory at Harvard Medical School in Boston, Massachusetts, was buoyant as she gripped the microphone tightly. After spending more than 30 frustrating years in Alzheimer’s research, she said, there was finally proof that she and her colleagues were on the right track. “But still, it isn’t enough,” she said. In the trial, treatment led to a 25% slowing of decline, enough to give participants a few extra months of independent living1. “But actually conquering a destructive disease that affects tens of millions of people worldwide is a different story,” she says. What’s more, lecanemab, marketed in the United States as Leqembi, makes for a tough treatment regime. It has to be infused through a vein by a nursing professional. And because the drug can cause potentially life-threatening brain swelling and bleeds, people taking it have to be monitored regularly.

Keyword: Alzheimers
Link ID: 28736 - Posted: 04.12.2023

By Amber Dance Isabelle Lousada was in her early 30s when she collapsed at her Philadelphia wedding in 1995. A London architect, she had suffered a decade of mysterious symptoms: tingling fingers, swollen ankles, a belly distended by her enlarged liver. The doctors she first consulted suggested she had chronic fatigue syndrome or that she’d been partying and drinking too hard. But her new brother-in-law, a cardiologist, felt that something else must be going on. A fresh series of doctor’s visits led, finally, to the proper diagnosis: Malformed proteins had glommed together inside Lousada’s bloodstream and organs. Those giant protein globs are called amyloid, and the diagnosis was amyloidosis. Amyloid diseases that affect the brain, such as Alzheimer’s and Parkinson’s diseases, receive the lion’s share of attention from medical professionals and the press. In contrast, amyloid diseases that affect other body parts are less familiar and rarely diagnosed conditions, says Gareth Morgan, a biochemist at Boston University Chobanian & Avedisian School of Medicine. Physicians may struggle to recognize and distinguish them, especially in early stages. Treatment options have also been limited — Lousada, now CEO of the nonprofit Amyloidosis Research Consortium in Newton, Massachusetts, was fortunate to survive thanks to a stem cell transplant that is too grueling or unsuitable for many with amyloidosis. Several new medications have come out in the last five years — and these, Lousada says, “have been real game-changers.” But although these therapies can block the formation of new, damaging amyloid, they can’t dissolve the amyloid that’s already built up. The body has natural processes to do so, but these are often too slow to clear years’ worth of built-up amyloid, especially in older individuals. And so patients still deal with amyloid clogging their organs, and people still die of amyloidosis, even if they survive longer than they once did. © 2023 Annual Reviews

Keyword: Alzheimers; Parkinsons
Link ID: 28731 - Posted: 04.09.2023

Visual: Andrew Bret Wallis/The Image Bank via Getty Images By Lina Tran At 25, Dasha Kiper moved in with a 98-year-old man. She’d just left a graduate program in clinical psychology; Mr. Kessler was a Holocaust survivor in the early stages of Alzheimer’s disease, whose son had hired Kiper as a live-in caregiver. One day, Mr. Kessler clambers onto a chair to replace the battery in a smoke detector. When he ignores her instructions to come down, Kiper loses her cool. She shouts that he’s incapable of changing the battery and doing much of anything for himself. Later, Kiper is filled with remorse. She should have known better than to yell at a nonagenarian with dementia. This is the focus of Kiper’s “Travelers to Unimaginable Lands: Stories of Dementia, the Caregiver, and the Human Brain” — not the mind of the patient, but the caregiver. Often, the spouses, children, and loved ones of people living with dementia succumb to arguing or pleading with their patients, despite reason. “We want to reestablish a shared reality,” Kiper writes. “It’s not cruelty but desperation that drives us to confront them with the truth.” Caregivers aren’t mere observers to cognitive decline but the “invisible victims” of dementia disorders, Kiper writes. They traverse warped realities that operate under different rules of time and memory. One caregiver says, referring to a famous case study by neurologist and author Oliver Sacks, it’s “like being an anthropologist on Mars.” But a caregiver’s slip-up isn’t necessarily the result of character flaws or a lapse in compassion. Rather, Kiper shows the healthy brain is riddled with cognitive biases that impede the work of caring for a person with an impaired mind. This takes a heavy toll. “People always ask about the patient,” one exasperated woman tells Kiper, after recounting how her husband, who doesn’t recognize her, takes to locking her out of their apartment each night. She starts carrying a spare key to let herself in after he falls asleep. “Let me tell you something, the patient is fine; it’s the caregiver who’s going crazy.”

Keyword: Alzheimers; Stress
Link ID: 28728 - Posted: 04.09.2023

ByJennifer Couzin-Frankel A class of Alzheimer’s drugs that aims to slow cognitive decline, including the antibody lecanemab that was granted accelerated approval in the United States in January, can cause brain shrinkage, researchers report in a new analysis. Although scientists and drug developers have documented this loss of brain volume in clinical trial participants for years, the scientific review, published yesterday in Neurology, is the first to look at data across numerous studies. It also links the brain shrinkage to a better known side effect of the drugs, brain swelling, which often presents without symptoms. “We don’t fully know what these changes might imply,” says Jonathan Jackson, a cognitive neuroscientist at Massachusetts General Hospital. But, “These data are extremely concerning, and it’s likely these changes are detrimental.” The analysis, which found that trial participants taking these Alzheimer’s drugs often developed more brain shrinkage than when they were on a placebo, alarmed Scott Ayton, a neuroscientist at the Florey Institute of Neuroscience and Mental Health in Melbourne, Australia, who led the work. “We’re talking about the possibility of brain damage” from treatment, says Ayton, who was invited by Eisai to join an advisory board on lecanemab’s rollout in Australia if the drug is approved there. “I find it very peculiar that these data, which are very important, have been completely ignored by the field.” A spokesperson for Eisai suggested there are benign theories for the brain shrinkage, too. The company said that although participants in its pivotal trial did experience “greater cortical volume loss on lecanemab relative to placebo,” those reductions may be due to antibody clearing the protein beta amyloid from the brain, and reducing inflammation. © 2023 American Association for the Advancement of Science.

Keyword: Alzheimers; Brain imaging
Link ID: 28721 - Posted: 03.29.2023

By Emily Underwood Many of our defining traits — including the languages we speak and how we connect with others — can be traced back at least in part to our earliest experiences. Although our brains remain malleable throughout our lives, most neuroscientists agree that the changes that occur in the womb and in the first few years of life are among the most consequential, with an outsize effect on our risk of developmental and psychiatric conditions. “Early on in life, the brain is still forming itself,” says Claudia Lugo-Candelas, a clinical psychologist at Columbia University and coauthor of an overview of the prenatal origins of psychiatric illness in the Annual Review of Clinical Psychology. Starting from a tiny cluster of stem cells, the brain develops into a complex organ of roughly 100 billion neurons and trillions of connections in just nine months. Compared to the more subtle brain changes that occur later in life, Lugo-Candelas says, what happens in utero and shortly after birth “is like building the house, versus finishing the deck.” But just how this process unfolds, and why it sometimes goes awry, has been a hard mystery to crack, largely because so many of the key events are difficult to observe. The first magnetic resonance imaging (MRI) scans of baby and fetal brains were taken back in the early 1980s, and doctors seized on the tool to diagnose major malformations in brain structure. But neuroimaging tools that can capture the baby brain’s inner workings in detail and spy on fetal brain activity in pregnant moms are much newer developments. Today, this research, coupled with long-term studies that follow thousands of individual children for years, is giving scientists new insights into how the brain develops. These advances have propelled researchers to a different stage than they were in even five years ago, says Damien Fair, a neuroscientist at the University of Minnesota who studies developmental conditions like autism and attention deficit hyperactivity disorder (ADHD). © 2023 Annual Reviews

Keyword: Development of the Brain; ADHD
Link ID: 28718 - Posted: 03.25.2023

By Emily Anthes The prevalence of autism spectrum disorder in American children rose between 2018 and 2020, continuing a long-running trend, according to a study released by the Centers for Disease Control and Prevention on Thursday. In 2020, an estimated one in 36 8-year-olds had autism, up from one in 44 in 2018. The prevalence was roughly 4 percent in boys and 1 percent in girls. The rise does not necessarily mean that autism has become more common among children, and it could stem from other factors, such as increased awareness and screening. “I have a feeling that this is just more discovery,” said Catherine Lord, a professor of psychiatry at the University of California, Los Angeles medical school, who was not involved in the research. “The question is what’s happening next to these kids, and are they getting services?” The rise was especially sharp among Black, Hispanic, and Asian or Pacific Islander children. For the first time, autism was significantly more prevalent among 8-year-olds in these groups than in white children, who have traditionally been more likely to receive autism diagnoses. “These patterns might reflect improved screening, awareness and access to services among historically underserved groups,” the researchers wrote. But why the prevalence in these children has surpassed that in white children is an open question that requires more investigation, Dr. Lord said. An accompanying study, also published on Thursday, suggests that the pandemic may have disrupted or delayed the detection of autism in younger children. © 2023 The New York Times Company

Keyword: Autism
Link ID: 28717 - Posted: 03.25.2023

Jon Hamilton Mora Leeb places some pieces into a puzzle during a local puzzle tournament. The 15-year-old has grown up without the left side of her brain after it was removed when she was very young. Seth Leeb In most people, speech and language live in the brain's left hemisphere. Mora Leeb is not most people. When she was 9 months old, surgeons removed the left side of her brain. Yet at 15, Mora plays soccer, tells jokes, gets her nails done, and, in many ways, lives the life of a typical teenager. "I can be described as a glass-half-full girl," she says, pronouncing each word carefully and without inflection. Her slow, cadence-free speech is one sign of a brain that has had to reorganize its language circuits. Yet to a remarkable degree, Mora's right hemisphere has taken on jobs usually done on the left side. It's an extreme version of brain plasticity, the process that allows a brain to modify its connections to adapt to new circumstances. Brain plasticity is thought to underlie learning, memory, and early childhood development. It's also how the brain revises its circuitry to help recover from a brain injury — or, in Mora's case, the loss of an entire hemisphere. Scientists hope that by understanding the brains of people like Mora, they can find ways to help others recover from a stroke or traumatic brain injury. They also hope to gain a better understanding of why very young brains are so plastic. Sometime in the third trimester of Ann Leeb's pregnancy, the child she was carrying had a massive stroke on the left side of her brain. No one knew it at the time. © 2023 npr

Keyword: Development of the Brain; Epilepsy
Link ID: 28714 - Posted: 03.23.2023

Heidi Ledford A mouse’s brain (red and blue) hosts a human astrocyte (green) that arose from transplanted neural stem cells.Credit: Liu et al./Cell (2023) In a technical “tour de force”, researchers have analysed multiple traits of individual cells to pinpoint those that give rise to crucial components of the human brain. The analysis, published on 16 March in Cell1, uses a combination of protein and RNA analysis to painstakingly purify and classify individual stem cells and their close relatives isolated from human brains. Researchers then injected different types of cell into mice and monitored the cells as they divided and their progeny took on specialized roles in the brain. The hope is that this study, and others like it, will illuminate how such developmental programmes go awry in neurological diseases — and how they can be harnessed to create new therapies. “The census of stem and progenitor cells in the developing human brain is really just beginning,” says Arnold Kriegstein, a developmental neuroscientist at the University of California, San Francisco, who was not involved in the research. “This work offers a nice window into some of that complexity.” The brain is an intricate symphony of different cells, each of which performs essential functions. Star-shaped cells known as astrocytes, for example, are important for supporting metabolism in neurons, and loss of astrocyte function is linked to neurodegenerative conditions such as Alzheimer’s disease. Oligodendrocytes are cells that create a protective, insulating sheath around the connections between neurons. When they are damaged — as in diseases such as multiple sclerosis — communication between neurons slows or stops altogether. © 2023 Springer Nature Limited

Keyword: Development of the Brain
Link ID: 28707 - Posted: 03.18.2023