Melinda Wenner Moyer Like many paediatricians, Dani Dumitriu braced herself for the impact of the SARS-CoV-2 coronavirus when it first surged in her wards. She was relieved when most newborn babies at her hospital who had been exposed to COVID-19 seemed to do just fine. Knowledge of the effects of Zika and other viruses that can cause birth defects meant that doctors were looking out for problems. But hints of a more subtle and insidious trend followed close behind. Dumitriu and her team at the NewYork–Presbyterian Morgan Stanley Children’s Hospital in New York City had more than two years of data on infant development — since late 2017, they had been analysing the communication and motor skills of babies up to six months old. Dumitriu thought it would be interesting to compare the results from babies born before and during the pandemic. She asked her colleague Morgan Firestein, a postdoctoral researcher at Columbia University in New York City, to assess whether there were neurodevelopmental differences between the two groups. A few days later, Firestein called Dumitriu in a panic. “She was like, ‘We’re in a crisis, I don’t know what to do, because we not only have an effect of a pandemic, but it’s a significant one,’” Dumitriu recalled. She was up most of that night, poring over the data. The infants born during the pandemic scored lower, on average, on tests of gross motor, fine motor and communication skills compared with those born before it (both groups were assessed by their parents using an established questionnaire)1. It didn’t matter whether their birth parent had been infected with the virus or not; there seemed to be something about the environment of the pandemic itself. Dumitriu was stunned. “We were like, oh, my God,” she recalled. “We’re talking about hundreds of millions of babies.” Although children have generally fared well when infected with SARS-CoV-2, preliminary research suggests that pandemic-related stress during pregnancy could be negatively affecting fetal brain development in some children. Moreover, frazzled parents and carers might be interacting differently or less with their young children in ways that could affect a child’s physical and mental abilities.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 28152 - Posted: 01.12.2022

Mir Jalil Razavi Weiying Dai The human brain has been called the most complex object in the known universe. And with good reason: It has around 86 billion neurons and several hundred thousand miles of axon fibers connecting them. Unsurprisingly, the process of brain folding that results in the brain’s characteristic bumps and grooves is also highly complex. Despite decades of speculation and research, the underlying mechanism behind this process remains poorly understood. As biomechanics and computer science researchers, we have spent several years studying the mechanics of brain folding and ways to visualize and map the brain, respectively. Figuring out this complexity may help researchers better diagnose and treat developmental brain disorders such as lissencephaly, or smooth brain, and epilepsy. Because many neurological disorders emerge at the early stages of development, understanding how brain folding works can provide useful insights into normal and pathological brain function. The mechanics of brain folding The brain is made of two layers. The outer layer, called the cerebral cortex, is composed of folded gray matter made up of small blood vessels and the spherical cell bodies of billions of neurons. The inner layer is composed of white matter, consisting mostly of the neurons’ elongated tails, called myelinated axons. When a story fascinates you, remember: Your donations make it possible Illustration of cross section of brain showing axonal pathways transitioning from gray matter into white matter. In recent years, researchers have shown that mechanics, or the forces that objects exert on one another, play an important role in the growth and folding of the brain. © 2010–2021, The Conversation US, Inc.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28119 - Posted: 12.18.2021

by Chloe Williams In June 2020, cannabidiol hit what has become a familiar hurdle in fragile X research: Like many previous drug candidates, it missed its primary target in clinical testing. Among 109 young people with fragile X syndrome who took the drug and 101 who took a placebo, researchers saw no meaningful difference in a rating of social avoidance. A secondary analysis factored into the trial’s original design offered a glimmer of hope, though. A subset of 91 participants showed marked improvement on the same measure after treatment with the drug, according to unpublished findings. Among that group, the gene underlying fragile X syndrome, called FMR1, is awash with methyl groups, which block its expression of the protein FMRP. By contrast, the remaining participants have only partially methylated copies of the gene and may make more FMRP. “Looking at methylation was pretty important to find that subgroup that had the most optimal response,” says Randi Hagerman, medical director of the MIND Institute at the University of California, Davis, who led one of the trial sites. The subgroup’s improvements meet only the minimum threshold for one measure of statistical significance — they have a p-value of 0.02 — and the results await replication, something the company running the trials, Zynerba Pharmaceuticals, is working on. But the trial’s design reflects a fundamental shift in how researchers are trying to advance drug development for fragile X syndrome, one of the leading inherited causes of intellectual disability and autism. © 2021 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28003 - Posted: 09.25.2021

by Rachel Zamzow The X chromosome holds stronger-than-expected genetic sway over the structure of several brain regions, a new study finds. The X-linked genes that may underlie this oversized influence have ties to autism and intellectual disability. “There were already hints that the X chromosome was likely to be conspicuous, with how involved it is with the brain,” says lead investigator Armin Raznahan, chief of the section on developmental neurogenomics at the U.S. National Institute of Mental Health. Many X chromosome genes — including those at the root of several autism-related conditions, such as fragile X syndrome and Rett syndrome — are expressed in the brain, for example. But the new findings suggest that the X chromosome, despite containing only 5 percent of the human genome, has a privileged role in shaping the brain — one that may be particularly relevant to developmental conditions. What’s more, this influence may be stronger in men than in women, the study shows. “What they’re showing is X is fundamentally different,” says David Glahn, professor of psychology at Harvard University, who was not involved in the new study. “It’s off the scale.” Research over the past decade has linked genetic variation to shifts in brain features, such as overall size or patterns of connectivity between regions, Glahn says. But “the X chromosome and the Y chromosome are fundamentally understudied,” because including them requires extra analytical legwork, he says. © 2021 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 8: Hormones and Sex
Link ID: 27992 - Posted: 09.15.2021

By Laura Sanders Clumps of brain cells grown from the stem cells of two people with a neurological syndrome show signs of the disorder. The results, published August 23 in Nature Neuroscience, suggest that personalized brain organoids could be powerful tools to understand complex disorders. Researchers are eager to create brain organoids, human stem cells coaxed into becoming 3-D blobs of brain cells, because of their ability to mimic human brains in the lab (SN: 2/20/18). In the current study, researchers grew two kinds of brain organoids. One kind, grown from healthy people’s stem cells, produced complex electrical activity that echoed the brain waves a full-sized brain makes. These waves, created by the coordinated firing of many nerve cells, are part of how the brain keeps information moving (SN: 3/13/18). The researchers also grew organoids using cells from a 25-year-old woman and a 5-year-old girl with Rett syndrome, a developmental disorder marked by seizures, autism and developmental lags. Rett syndrome is thought to be caused by changes in a gene called MECP2, mutations that the lab-grown organoids carried as well. These organoids looked like those grown from healthy people, but behaved differently in some ways. Their nerve cells fired off signals that were too synchronized and less varied. Some of the brain waves these organoids produced are reminiscent of a brain having a seizure, in which a bolus of electrical activity scrambles normal brain business. © Society for Science & the Public 2000–2021.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27976 - Posted: 09.04.2021

Amanda Heidt Scientists have discovered two types of glial cells in the brains of adult mice—an astrocyte and an oligodendrocyte progenitor cell—after nudging neural stem cells to rise from dormancy, according to a study published June 10 in Science. The results suggest new roles for glial cells, best known for providing support to neurons, and could prompt a better understanding of how brains remain plastic into adulthood, when the vast majority of neurons no longer undergo cell division. This study is “a very important addition to the whole story about these fascinating [stem] cells that exist in the adult brain of rodents that have the capacity to generate new cells,” says Arturo Alvarez-Buylla, a developmental neuroscientist at the University of California, San Francisco, who was not involved in the work. “Understanding adult stem cells is fundamental to really know the kinds of plasticity that exist after the developmental period is over.” Most mammalian brain cells, be they neurons or glia, are generated during embryonic development, and reservoirs of stem cells become largely, if not entirely, dormant in adulthood. The small trickle of activity that is left can help the brain respond to change, sometimes by generating new neurons to help with learning or by producing cells in response to injury or disease. One pool exists in the brains of adult humans and mice, in an area called the ventricular-subventricular zone (V-SVZ). The walls of the two lateral ventricles, cavities filled with cerebrospinal fluid, are lined with stem cells, and along these walls, the cells have a regional identity—where a stem cell lies on the wall dictates what it differentiates into. This feature has been well-characterized for neuronal subtypes, which are synthesized within discrete domains on the lateral wall. Glial cells are known to be generated at low levels along the septal wall, but the specific subtypes remain unknown because the cells along this wall generally remain inactive. © 1986–2021 The Scientist.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 27921 - Posted: 07.24.2021

Tanya T. Nguyen, M.D., Dilip V. Jeste, M.D. In James Hilton’s 1933 novel Lost Horizons, Shangri-La was a magical utopia where people lived well beyond 100 years. But now, less than a century later, it seems we are well on our way to making Hilton’s vision a reality. The US Census Bureau reported in 2020 that the average life expectancy has increased from 47 in 1900 to over 80 years today, while the number of people over age 60 exceeds children under 15 for the first time ever. By 2060, the average lifespan will approach 90 years. Astonishingly, more than half of the babies born today will live to age 100 and beyond, which will make Hilton’s seemingly far-fetched vision come to pass. One might think that people living longer would represent an enormous, thrilling milestone. But unfortunately, aging is rarely perceived that way. The increase in older people—metaphorically termed a “silver tsunami” since the 1980s—has economic implications, including unimaginable healthcare costs. Certain segments of western culture sadly equate aging with such “d” words as degeneration, decline, disability, diseases, dementia, depression, and death. Policy makers and economists are outspoken in their fear that spending money on older people’s care will mean less money for children and younger adults, who represent the future. This attitude—commonly labeled ageism—is analogous to such phenomena as sexism, racism, and bias against certain sexual orientations. Ageism has made many older people feel guilty about living longer and becoming a potential burden. They think—and are encouraged by society to think—that aging is an incurable disease. © 2021 The Dana Foundation.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27911 - Posted: 07.17.2021

Philip M. Boffey I was astonished to learn while writing a column on the brain-computer interface in 2019 that patients with amyotrophic lateral sclerosis (ALS), whose brain signals were fed into a computer, could control a complex robotic arm, having it pick up a pitcher and pour water into a glass, just by thinking about it. So you can imagine my surprise when I learned that scientists have achieved comparably difficult tasks—not with signals from a human brain—but simply from a clump of stem calls in a Petri dish. The achievement is clearly described in Alan Alda’s Clear+Vivid podcast featuring Alysson Muotri, a Brazilian citizen who is director of the stem cell program at University of California, San Diego, where much of this pioneering work was performed. The podcast is a useful complement to a more comprehensive report issued on April 8 by the National Academies of Sciences, Engineering, and Medicine. As Alda’s introduction explains, Muotri uses factors that drive skin cells to revert to stem cells and then become brain tissues that self-organize, forming “brain organoids in a dish. Muotri, who has a personal interest because he has a son with autism, hopes to learn how early brain development can change course in conditions like autism and epilepsy—and how our brains differ from those of our evolutionary? cousins, the Neanderthals. Although some people call what he has created “brains” or “mini-brains” in a dish, Muotri is more circumspect, describing them as “brain organoids.” © 2021 The Dana Foundation.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27886 - Posted: 07.03.2021

Christopher M. Filley One of the most enduring themes in human neuroscience is the association of higher brain functions with gray matter. In particular, the cerebral cortex—the gray matter of the brain's surface—has been the primary focus of decades of work aiming to understand the neurobiological basis of cognition and emotion. Yet, the cerebral cortex is only a few millimeters thick, so the relative neglect of the rest of the brain below the cortex has prompted the term “corticocentric myopia” (1). Other regions relevant to behavior include the deep gray matter of the basal ganglia and thalamus, the brainstem and cerebellum, and the white matter that interconnects all of these structures. On page 1304 of this issue, Zhao et al. (2) present compelling evidence for the importance of white matter by demonstrating genetic influences on structural connectivity that invoke a host of provocative clinical implications. Insight into the importance of white matter in human behavior begins with its anatomy (3–5) (see the figure). White matter occupies about half of the adult human brain, and some 135,000 km of myelinated axons course through a wide array of tracts to link gray matter regions into distributed neural networks that serve cognitive and emotional functions (3). The human brain is particularly well interconnected because white matter has expanded more in evolution than gray matter, which has endowed the brain of Homo sapiens with extensive structural connectivity (6). The myelin sheath, white matter's characteristic feature, appeared late in vertebrate evolution and greatly increased axonal conduction velocity. This development enhanced the efficiency of distributed neural networks, expanding the transfer of information throughout the brain (5). Information transfer serves to complement the information processing of gray matter, where neuronal cell bodies, synapses, and a variety of neurotransmitters are located (5). The result is a brain with prodigious numbers of both neurons and myelinated axons, which have evolved to subserve the domains of attention, memory, emotion, language, perception, visuospatial processing, executive function (5), and social cognition (7). © 2021 American Association for the Advancement of Science.

Related chapters from BN: Chapter 18: Attention and Higher Cognition; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 14: Attention and Higher Cognition; Chapter 13: Memory and Learning
Link ID: 27862 - Posted: 06.19.2021

Andrew Anthony David Eagleman, 50, is an American neuroscientist, bestselling author and presenter of the BBC series The Brain, as well as co-founder and chief executive officer of Neosensory, which develops devices for sensory substitution. His area of speciality is brain plasticity, and that is the subject of his new book, Livewired, which examines how experience refashions the brain, and shows that it is a much more adaptable organ than previously thought. For the past half-century or more the brain has been spoken of in terms of a computer. What are the biggest flaws with that particular model? It’s a very seductive comparison. But in fact, what we’re looking at is three pounds of material in our skulls that is essentially a very alien kind of material to us. It doesn’t write down memories, the way we think of a computer doing it. And it is capable of figuring out its own culture and identity and making leaps into the unknown. I’m here in Silicon Valley. Everything we talk about is hardware and software. But what’s happening in the brain is what I call livewire, where you have 86bn neurons, each with 10,000 connections, and they are constantly reconfiguring every second of your life. Even by the time you get to the end of this paragraph, you’ll be a slightly different person than you were at the beginning. In what way does the working of the brain resemble drug dealers in Albuquerque? It’s that the brain can accomplish remarkable things without any top-down control. If a child has half their brain removed in surgery, the functions of the brain will rewire themselves on to the remaining real estate. And so I use this example of drug dealers to point out that if suddenly in Albuquerque, where I happened to grow up, there was a terrific earthquake, and half the territory was lost, the drug dealers would rearrange themselves to control the remaining territory. It’s because each one has competition with his neighbours and they fight over whatever territory exists, as opposed to a top-down council meeting where the territory is distributed. And that’s really the way to understand the brain. It’s made up of billions of neurons, each of which is competing for its own territory. © 2021 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 15: Language and Lateralization
Link ID: 27855 - Posted: 06.16.2021

Michael Marshall In her laboratory in Barcelona, Spain, Miki Ebisuya has built a clock without cogs, springs or numbers. This clock doesn’t tick. It is made of genes and proteins, and it keeps time in a layer of cells that Ebisuya’s team has grown in its lab. This biological clock is tiny, but it could help to explain some of the most conspicuous differences between animal species. Animal cells bustle with activity, and the pace varies between species. In all observed instances, mouse cells run faster than human cells, which tick faster than whale cells. These differences affect how big an animal gets, how its parts are arranged and perhaps even how long it will live. But biologists have long wondered what cellular timekeepers control these speeds, and why they vary. A wave of research is starting to yield answers for one of the many clocks that control the workings of cells. There is a clock in early embryos that beats out a regular rhythm by activating and deactivating genes. This ‘segmentation clock’ creates repeating body segments such as the vertebrae in our spines. This is the timepiece that Ebisuya has made in her lab. “I’m interested in biological time,” says Ebisuya, a developmental biologist at the European Molecular Biology Laboratory Barcelona. “But lifespan or gestation period, they are too long for me to study.” The swift speed of the segmentation clock makes it an ideal model system, she says. © 2021 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 10: Biological Rhythms and Sleep
Link ID: 27790 - Posted: 04.28.2021

by Jessica Jiménez, Mark Zylka Mice and rats typically give birth to 6 to 12 animals per litter. Some scientists treat this as a benefit, because a large number of animals can be produced with a small number of matings. In reality, though, this is of no benefit at all, especially when you consider a fact that is well known in the toxicology field: Animals within a litter are more similar to one another than animals between litters. Herein lies what is known as the ‘litter effect.’ Anyone who uses multiple animals from a small number of litters to increase sample size is making a serious mistake. The similarities within individual litters will heavily skew the results. Our goal in writing this article, and an accompanying peer-reviewed paper on this topic, is to raise awareness about the litter effect and to encourage researchers who study neurodevelopmental conditions to control for it in future work. Like many scientists who use rodents to study autism and related conditions, we were oblivious to the litter effect and its impact on research. However, we now recognize that it is essential to control for the litter effect whenever a rodent autism model is studied, be it a mouse with a gene mutation or an environmental exposure. It is essential because the litter effect can lead to erroneous conclusions that negatively influence the rigor and reproducibility of scientific research. Indeed, false positives, or the incorrect identification of a significant effect, increase as fewer litters are sampled. Conversely, litter-to-litter variation adds ‘noise’ to the data that can mask true treatment or genetic effects. This is concerning because most phenotypes associated with rodent models of autism are remarkably small, and they are often difficult to reproduce between labs. © 2021 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 8: Hormones and Sex
Link ID: 27789 - Posted: 04.28.2021

by Grace Huckins Autism-linked mutations in the CUL3 gene may alter brain structure by disrupting the ‘skeletons’ of neurons, according to a new study. Like all cells, neurons contain long strands of protein that help them keep their shape. These strands, collectively called a cytoskeleton, also help ferry substances within cells and enable developing cells to migrate through the brain. Mice engineered to have a CUL3 mutation that resembles one seen in an autistic person show atypical expression of a variety of cytoskeleton proteins, the new work shows. These mice exhibit some autism-like social behaviors — for instance, unlike wildtype mice, they display no preference for a novel mouse over a familiar one. In addition, various cortical regions in the CUL3 mice are smaller than in wildtype mice, and their cortices are, on the whole, thinner. The brain and behavioral differences observed in these mice may be linked to cytoskeletal abnormalities, says lead investigator Lilia Iakoucheva, associate professor of psychiatry at the University of California, San Diego. Mutations in CUL3 could lead to cytoskeletal changes via RhoA, an enzyme linked to autism, Iakoucheva says. RhoA carries out some of the effects of mutations in KCTD13, an autism-related gene that works with CUL3, according to past work by her team. The new study represents an important step forward in understanding the link between Rho enzymes and autism, says Froylan Calderón de Anda, research group leader at the Center for Molecular Neurobiology Hamburg in Germany, who was not involved in the work. “Little by little, we are adding to this puzzle.” © 2021 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27776 - Posted: 04.17.2021

By Pam Belluck Reports about the mysterious Covid-related inflammatory syndrome that afflicts some children and teenagers have mostly focused on physical symptoms: rash, abdominal pain, red eyes and, most seriously, heart problems like low blood pressure, shock and difficulty pumping. Now, a new report shows that a significant number of young people with the syndrome also develop neurological symptoms, including hallucinations, confusion, speech impairments and problems with balance and coordination. The study of 46 children treated at one hospital in London found that just over half — 24 — experienced such neurological symptoms, which they had never had before. Those patients were about twice as likely as those without neurological symptoms to need ventilators because they were “very unwell with systemic shock as part of their hyperinflammatory state,” said an author of the study, Dr. Omar Abdel-Mannan, a clinical research fellow at University College London’s Institute of Neurology. Patients with neurological symptoms were also about twice as likely to require medication to improve the heart’s ability to squeeze, he said. The condition, called Multisystem Inflammatory Syndrome in Children (MIS-C), typically emerges two to six weeks after a Covid infection, often one that produces only mild symptoms or none at all. The syndrome is rare, but can be very serious. The latest data from the Centers for Disease Control and Prevention reports 3,165 cases in 48 states, Puerto Rico and the District of Columbia, including 36 deaths. The new findings strengthen the theory that the syndrome is related to a surge of inflammation triggered by an immune response to the virus, Dr. Abdel-Mannan said. For the children in the report, the neurological symptoms mostly resolved as the physical symptoms were treated. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27773 - Posted: 04.14.2021

by Angie Voyles Askham Sluggish fetal head growth toward the end of the second trimester foretells poor performance on tests of cognition, language and fine motor skills at age 2, according to a new international study. By the time a child shows developmental delays, which are common in autism, “a lot of other things have already happened” to put her on that track, says Hao Huang, associate professor of radiology at the University of Pennsylvania in Philadelphia, who was not involved in the study. If clinicians could predict such delays in advance, they could start behavioral interventions early, during the period when a child’s brain is most responsive to treatment, he says. The new study offers a step toward that goal, identifying a potential biomarker of atypical development in routine ultrasound scans taken at 20 to 25 weeks of gestation. Researchers analyzed the scans — performed more frequently than usual during 3,598 pregnancies at six international sites — to measure how fetal head circumference changed over time. “[Change in] head circumference is a very nice proxy of growth, particularly brain growth,” says study investigator José Villar, professor of perinatal medicine at the University of Oxford in the United Kingdom. Fetal head growth follows one of five paths, Villar and his colleagues found. Each path is associated with a different outcome on cognitive and behavioral tests when the child is 2 years old. © 2021 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27766 - Posted: 04.10.2021

By Alla Katsnelson New monthly payments in the pandemic relief package have the potential to lift millions of American children out of poverty. Some scientists believe the payments could change children’s lives even more fundamentally — via their brains. It’s well established that growing up in poverty correlates with disparities in educational achievement, health and employment. But an emerging branch of neuroscience asks how poverty affects the developing brain. Over the past 15 years, dozens of studies have found that children raised in meager circumstances have subtle brain differences compared with children from families of higher means. On average, the surface area of the brain’s outer layer of cells is smaller, especially in areas relating to language and impulse control, as is the volume of a structure called the hippocampus, which is responsible for learning and memory. These differences don’t reflect inherited or inborn traits, research suggests, but rather the circumstances in which the children grew up. Researchers have speculated that specific aspects of poverty — subpar nutrition, elevated stress levels, low-quality education — might influence brain and cognitive development. But almost all the work to date is correlational. And although those factors may be at play to various degrees for different families, poverty is their common root. A continuing study called Baby’s First Years, started in 2018, aims to determine whether reducing poverty can itself promote healthy brain development. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 27763 - Posted: 04.08.2021

By Lisa Sanders, M.D. The 35-year-old man rose abruptly from the plastic chair in the waiting room at the Health Sciences Center Emergency Department in Winnipeg, Manitoba. He lurched toward the door, arms held stiffly before him as if warding off something only he could see. “I gotta get out of here,” he muttered. His eyes looked unfocused as he glanced at the family he didn’t seem to recognize. His mother hurried to his side. “It’s OK, Sean,” she murmured in his ear. “We’re here with you.” She took him over to his seat. And then, just as suddenly, he was back to normal, back to the man his family knew and loved. This was why Sean was in the E.D. that day. He had been completely healthy until the day before, when his brother-in-law found him wandering through the house, confused. He didn’t seem to know where he was, or even who he was. But by the time the ambulance reached the community hospital near their home, the confusion had cleared, and he seemed fine. The doctors in the E.D. ordered a few tests and, when they were unrevealing, sent him home. Only a few hours later, it happened again. That’s when they brought him here, to the biggest hospital in the city. By the time they arrived, the bizarre episode had subsided. A second attack in the waiting room lasted only a few minutes, so when the E.D. doctors saw him, he was fine. These doctors also wanted to send him home, but the mother was adamant. Her 30-year-old daughter, Andrea, was admitted to another hospital in the city just three months earlier. Andrea had episodes of confusion, too. And she died in that hospital 12 days later. No one understood what her daughter had or why she died, the mother told the doctors. She wasn’t about to let the same thing happen to her son. Re-enacting His Sister’s Symptoms? And so Sean was admitted for observation. Over the next two days, he had many of these strange episodes. He would try to leave the unit. He wouldn’t answer questions; he didn’t even seem to hear them. He looked afraid. And then it would be over. He was seen by specialists in internal medicine and neurology. He had an M.R.I., a spinal tap and many blood tests. When none of those tests provided an answer, the doctors worried that he had been so emotionally traumatized by his sister’s sudden death that he developed psychological symptoms, something known as conversion disorder. He was transferred to the psychiatric unit for further evaluation. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27735 - Posted: 03.17.2021

By Rachel Nuwer The ability to link language to the world around us is a crowning feature of our species. For very young infants, it is not yet about learning the meaning of words like “cat” or “dog.” Rather, the acoustic signals in speech help foster infants' fundamental cognitive capacities, including the formation of categories of objects, such as cats or dogs. The sounds that activate this key step in development can come not just from human language but also from vocalizations made by nonhuman primates. A new study shows that babies do not use just any natural sound to build cognition, however. While primate calls and human language pass the test, birdsongs do not. “By tracing the link from language to cognition and how it’s built up with babies’ experiences with objects in the world, we get to see what are the components of this quintessential human ability to go beyond the here and now,” says Sandra Waxman, a developmental scientist at Northwestern University and senior author of the findings, which were published today in PLOS ONE. “Asking how broad that earliest link is helps to answer questions about our evolutionary legacy.” By three or four months of age, infants can categorize objects—from toys and food to pets and people—based on commonalities those objects share. This ability is boosted if the objects are presented while the infants are listening to language. The new findings build on previous work Waxman and her colleagues conducted about which sounds outside of the realm of human speech support infants’ ability to categorize objects. In past studies, they found that sequences of pure tones and backward speech do not help infants under six months of age to categorize objects, whereas listening to vocalizations from nonhuman primates—specifically, lemurs—does..” © 2021 Scientific American,

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 13: Memory and Learning
Link ID: 27731 - Posted: 03.13.2021

By Kelly Servick Put human stem cells in a lab dish with the right nutrients, and they’ll do their best to form a little brain. They’ll fail, but you’ll get an organoid: a semiorganized clump of cells. Organoids have become a powerful tool for studying brain development and disease, but researchers assumed these microscopic blobs only mirror a brain’s prenatal development—its earliest and simplest stages. A study today reveals that with enough time, organoid cells can take on some of the genetic signatures that brain cells display after birth, potentially expanding the range of disorders and developmental stages they can recreate. “Things that, before I saw this paper, I would have said you can’t do with organoids … actually, maybe you can,” says Madeline Lancaster, a developmental geneticist at the Medical Research Council’s Laboratory of Molecular Biology. For example, Lancaster wasn’t optimistic about using organoids to study schizophrenia, which is suspected to emerge in the brain after birth, once neural communication becomes more complex. But she now wonders whether cells from a person with this disorder—once “reprogrammed” to a primitive, stem cell state and coaxed to mature within a brain organoid—could reveal important cellular differences underlying the condition. Stanford University neurobiologist Sergiu Pașca has been making brain organoids for about 10 years, and his team has learned that some of these tissue blobs can thrive in a dish for years. In the new study, they teamed up with neurogeneticist Daniel Geschwind and colleagues at the University of California, Los Angeles (UCLA), to analyze how the blobs changed over their life spans. © 2021 American Association for the Advancement of Science.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27705 - Posted: 02.23.2021

Ariana Remmel Researchers have created tiny, brain-like ‘organoids’ that contain a gene variant harboured by two extinct human relatives, Neanderthals and Denisovans. The tissues, made by engineering human stem cells, are far from being true representations of these species’ brains — but they show distinct differences from human organoids, including size, shape and texture. The findings, published1 in Science on 11 February, could help scientists to understand the genetic pathways that allowed human brains to evolve. Can lab-grown brains become conscious? “It’s an extraordinary paper with some extraordinary claims,” says Gray Camp, a developmental biologist at the University of Basel in Switzerland, whose lab last year reported2 growing brain organoids that contained a gene common to Neanderthals and humans. The latest work takes the research further by looking at gene variants that humans lost in evolution. But Camp remains sceptical about the implications of the results, and says the work opens more questions that will require investigation. Humans are more closely related to Neanderthals and Denisovans than to any living primate, and some 40% of the Neanderthal genome can still be found spread throughout living humans. But researchers have limited means to study these ancient species’ brains — soft tissue is not well preserved, and most studies rely on inspecting the size and shape of fossilized skulls. Knowing how the species’ genes differ from humans’ is important because it helps researchers to understand what makes humans unique — especially in our brains. © 2021 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27687 - Posted: 02.13.2021