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

By James Gorman Dogs go through stages in their life, just as people do, as is obvious to anyone who has watched their stiff-legged, white-muzzled companion rouse themselves to go for one more walk. Poets from Homer to Pablo Neruda have taken notice. As have folk singers and story tellers. Now science is taking a turn, in the hope that research on how dogs grow and age will help us understand how humans age. And, like the poets before them, scientists are finding parallels between the two species. Their research so far shows that dogs are similar to us in important ways, like how they act during adolescence and old age, and what happens in their DNA as they get older. They may be what scientists call a “model” for human aging, a species that we can study to learn more about how we age and perhaps how to age better. Most recently, researchers in Vienna have found that dogs’ personalities change over time. They seem to mellow in the same way that most humans do. The most intriguing part of this study is that like people, some dogs are just born old, which is to say, relatively steady and mature, the kind of pup that just seems ready for a Mr. Rogers cardigan. “That’s professor Spot, to you, thank you, and could we be a little neater when we pour kibble into my dish?” Mind you, the Vienna study dogs were all Border collies, so I’m a little surprised that any of them were mature. That would suggest a certain calm, a willingness to tilt the head and muse that doesn’t seem to fit the breed, with its desperate desire to be constantly chasing sheep, geese, children or Frisbees. Another recent paper came to the disturbing conclusion that the calculus of seven dog years for every human year isn’t accurate. To calculate dog years, you must now multiply the natural logarithm of a dog’s age in human years by 16 and then add 31. Is that clear? It’s actually not as hard as it sounds, as long as you have a calculator or internet access. For example the natural log of 6 is 1.8, roughly, which, multiplied by 16 is about 29, which, plus 31, is 60. OK, it’s not that easy, even with the internet. © 2020 The New York Times Company

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 4: Development of the Brain
Link ID: 27574 - Posted: 11.10.2020

By Laura Sanders Nearly 2,000 years ago, a cloud of scorching ash from Mount Vesuvius buried a young man as he lay on a wooden bed. That burning ash quickly cooled, turning some of his brain to glass. This confluence of events in A.D. 79 in the town of Herculaneum, which lay at the western base of the volcano, preserved the usually delicate neural tissue in a durable, glassy form. New scrutiny of this tissue has revealed signs of nerve cells with elaborate tendrils for sending and receiving messages, scientists report October 6 in PLOS ONE. That the young man once possessed these nerve cells, or neurons, is no surprise; human brains are packed with roughly 86 billion neurons (SN: 8/7/19). But samples from ancient brains are sparse. Those that do exist have become a soaplike substance or mummified, says Pier Paolo Petrone, a biologist and forensic anthropologist at the University of Naples Federico II in Italy. But while studying the Herculaneum site, Petrone noticed something dark and shiny inside this man’s skull. He realized that those glassy, black fragments “had to be the remains of the brain.” Petrone and colleagues used scanning electron microscopy to study glassy remains from both the man’s brain and spinal cord. The researchers saw tubular structures as well as cell bodies that were the right sizes and shapes to be neurons. In further analyses, the team found layers of tissue wrapped around tendrils in the brain tissue. This layering appears to be myelin, a fatty substance that speeds signals along nerve fibers. The preserved tissue was “something really astonishing and incredible,” Petrone says, because the conversion of objects to glass, a process called vitrification, is relatively rare in nature. “This is the first ever discovery of ancient human brain remains vitrified by hot ash during a volcanic eruption.” © Society for Science & the Public 2000–2020.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27558 - Posted: 10.31.2020

The plant compound apigenin improved the cognitive and memory deficits usually seen in a mouse model of Down syndrome, according to a study by researchers at the National Institutes of Health and other institutions. Apigenin is found in chamomile flowers, parsley, celery, peppermint and citrus fruits. The researchers fed the compound to pregnant mice carrying fetuses with Down syndrome characteristics and then to the animals after they were born and as they matured. The findings raise the possibility that a treatment to lessen the cognitive deficits seen in Down syndrome could one day be offered to pregnant women whose fetuses have been diagnosed with Down syndrome through prenatal testing. The study appears in the American Journal of Human Genetics. Down syndrome is a set of symptoms resulting from an extra copy or piece of chromosome 21. The intellectual and developmental disabilities accompanying the condition are believed to result from decreased brain growth caused by increased inflammation in the fetal brain. Apigenin is not known to have any toxic effects, and previous studies have indicated that it is an antioxidant that reduces inflammation. Unlike many compounds, it is absorbed through the placenta and the blood brain barrier, the cellular layer that prevents potentially harmful substances from entering the brain. Compared to mice with Down symptoms whose mothers were not fed apigenin, those exposed to the compound showed improvements in tests of developmental milestones and had improvements in spatial and olfactory memory. Tests of gene activity and protein levels showed the apigenin-treated mice had less inflammation and increased blood vessel and nervous system growth. Guedj, F. et al. Apigenin as a candidate prenatal treatment for Trisomy 21: effects in human amniocytes and the Ts1Cje mouse model. American Journal of Human Genetics. 2020.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 4: Development of the Brain
Link ID: 27546 - Posted: 10.24.2020

Catherine Offord Overactivation of the brain’s immune cells, called microglia, may play a role in cognitive impairments associated with Down syndrome, according to research published today (October 6) in Neuron. Researchers in Italy identified elevated numbers of the cells in an inflammation-promoting state in the brains of mice with a murine version of the syndrome as well as in postmortem brain tissue from people with the condition. The team additionally showed that drugs that reduce the number of activated microglia in juvenile mice could boost the animals’ performance on cognitive tests. “This is a fabulous study that gives a lot of proof of principle to pursuing some clinical trials in people,” says Elizabeth Head, a neuroscientist at the University of California, Irvine, who was not involved in the work. “The focus on microglial activation, I thought, was very novel and exciting,” she adds, noting that more research will be needed to see how the effects of drugs used in the study might translate from mice to humans. Down syndrome is caused by an extra copy of part or all of human chromosome 21, and is the most commonly occurring chromosomal condition in the US. Children with Down syndrome often experience cognitive delays compared to typically developing children, although there’s substantial variation and the effects are usually mild or moderate. People with the syndrome also have a higher risk of certain medical conditions, including Alzheimer’s disease. © 1986–2020 The Scientist.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27537 - Posted: 10.21.2020

By Elizabeth Svoboda After a 3-year-old named Matthew started having one seizure after another, his worried parents learned he had a chronic brain condition that was causing the convulsions. They faced an impossible decision: allow the damaging seizures to continue indefinitely, or allow surgeons to remove half of their son’s brain. They chose the latter. When Matthew emerged from surgery, he couldn’t walk or speak. But bit by bit, he remastered speech and recaptured his lost milestones. The moment one side of his brain was removed, the remainder set itself to the colossal task of re-forging lost neural connections. This gut-level renovation was so successful that no one who meets Matthew today would guess that half his brain is gone. Stanford neuroscientist David Eagleman is obsessed with probing the outer limits of this kind of neural transformation — and harnessing it to useful ends. We’ve all heard that our brains are more plastic than we think, that they can adapt ingeniously to changed conditions, but in “Livewired: The Inside Story of the Ever-Changing Brain,” Eagleman tackles this topic with fresh élan and rigor. He shows not just how we can direct our own neural remodeling on a cellular level, but how such remodeling — a process he calls “livewiring” — alters the core of who we are. “Our machinery isn’t fully preprogrammed, but instead shapes itself by interacting with the world,” Eagleman writes. “You are a different person than you were at this time last year, because the gargantuan tapestry of your brain has woven itself into something new.”

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 15: Language and Lateralization
Link ID: 27515 - Posted: 10.10.2020

By Macarena Carrizosa, Sophie Bushwick A new system called PiVR creates working artificial environments for small animals such as zebra fish larvae and fruit flies. Developers say the system’s affordability could help expand research into animal behavior. © 2020 Scientific American

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 7: Vision: From Eye to Brain
Link ID: 27505 - Posted: 10.07.2020

In an article published in Nature Genetics, researchers confirm that about 14% of all cases of cerebral palsy, a disabling brain disorder for which there are no cures, may be linked to a patient’s genes and suggest that many of those genes control how brain circuits become wired during early development. This conclusion is based on the largest genetic study of cerebral palsy ever conducted. The results led to recommended changes in the treatment of at least three patients, highlighting the importance of understanding the role genes play in the disorder. The work was largely funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “Our results provide the strongest evidence to date that a significant portion of cerebral palsy cases can be linked to rare genetic mutations, and in doing so identified several key genetic pathways involved,” said Michael Kruer, M.D., a neurogeneticist at Phoenix Children’s Hospital and the University of Arizona College of Medicine - Phoenix and a senior author of the article. “We hope this will give patients living with cerebral palsy and their loved ones a better understanding of the disorder and doctors a clearer roadmap for diagnosing and treating them.” Cerebral palsy affects approximately one in 323 children(link is external) in the United States. Signs of the disorder appear early in childhood resulting in a wide range of permanently disabling problems with movement and posture, including spasticity, muscle weakness, and abnormal gait. Nearly 40% of patients need some assistance with walking. In addition, many patients may also suffer epileptic seizures, blindness, hearing and speech problems, scoliosis, and intellectual disabilities.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27494 - Posted: 09.28.2020

By Lisa Friedman WASHINGTON — The Trump administration has rejected scientific evidence linking the pesticide chlorpyrifos to serious health problems, directly contradicting federal scientists’ conclusions five years ago that it can stunt brain development in children. The Environmental Protection Agency’s assessment of the pesticide, which is widely used on soybeans, almonds, grapes and other crops, is a fresh victory for chemical makers and the agricultural industry, as well as the latest in a long list of Trump administration regulatory rollbacks. In announcing its decision, the E.P.A. said on Tuesday that “despite several years of study, the science addressing neurodevelopmental effects remains unresolved.” However, in making its finding, the agency excluded several epidemiological studies, most prominently one conducted at Columbia University, that found a correlation between prenatal exposure to chlorpyrifos and developmental disorders in toddlers. As a result, the assessment may be the first major test of the Trump administration’s intention, often referred to as its “secret science” proposal, to bar or give less weight to scientific studies that can’t or don’t publicly release their underlying data. This controversial policy would eliminate many studies that track the effects of exposure to substances on people’s health over long periods of time, because the data often includes confidential medical records of the subjects, scientists have said. © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27485 - Posted: 09.25.2020