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by Angie Voyles Askham . Many problems associated with fragile X syndrome stem from a leak in mitochondria, organelles that act as the power stations of the cell, a new study suggests1. Stopping this leak eases some of the autism-like traits of mice that model the syndrome. “The paper is very solid,” says John Jay Gargus, director of the Center for Autism Research and Translation at the University of California, Irvine, who was not involved in the study. And because mitochondrial energy deficiency is seen in other forms of autism, the findings may be relevant beyond fragile X syndrome, Gargus says. Fragile X syndrome results from mutations in the FMR1 gene, which lead to a loss of the protein FMRP. Without FMRP, cells have immature dendritic spines — the bumps along a neuron’s arms that receive input from other neurons — and produce other proteins in excess. These differences are thought to contribute to the syndrome’s characteristic traits, such as developmental delay, intellectual disability and, often, autism. The new study shows that a leak in the mitochondrial membrane, possibly caused by the lack of FMRP, may drive the affected cells’ immaturity and excess protein production. The leak affects a cell’s metabolism, causing it to produce energy quickly but not efficiently, says lead researcher Elizabeth Jonas, professor of internal medicine and neuroscience at Yale University. All cells start out with mitochondrial leaks; the rapid energy production these leaks allow may be useful in early development. As typical cells mature and efficiency becomes more important than speed, however, they seem to close the leaks, Jonas says. Because cells with a fragile X mutation cannot close their leaks, they remain in an immature state. © 2020 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: 27466 - Posted: 09.12.2020

When it comes to brain cells, one size does not fit all. Neurons come in a wide variety of shapes, sizes, and contain different types of brain chemicals. But how did they get that way? A new study in Nature suggests that the identities of all the neurons in a worm are linked to unique members of a single gene family that control the process of converting DNA instructions into proteins, known as gene expression. The results of this study could provide a foundation for understanding how nervous systems have evolved in many other animals, including humans. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “The central nervous systems of all animals, from worms to humans, are incredibly intricate and highly ordered. The generation and diversity of a plethora of neuronal cell types is driven by gene expression,” said Robert Riddle, Ph.D., program director at NINDS. “So, it is surprising and exciting to consider that the cell diversity we see in the entire nervous system could come from a just a single group of genes.” Researchers led by Oliver Hobert, Ph.D., professor of biochemistry and molecular biophysics at Columbia University in New York City and graduate student Molly B. Reilly, wanted to know how brain cells in the C. elegans worm got their various shapes and functions. For these experiments, the researchers used a genetically engineered worm in which individual neurons were color coded. In addition, coding sequences for green fluorescence protein were inserted into homeobox genes, a highly conserved set of genes known to play fundamental roles in development. Homeobox gene expression patterns were determined by examining the patterns of the glowing fluorescent marker.

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 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 27428 - Posted: 08.20.2020

By Simon Makin New research could let scientists co-opt biology's basic building block—the cell—to construct materials and structures within organisms. A study, published in March in Science and led by Stanford University psychiatrist and bioengineer Karl Deisseroth, shows how to make specific cells produce electricity-carrying (or blocking) polymers on their surfaces. The work could someday allow researchers to build large-scale structures within the body or improve brain interfaces for prosthetic limbs. In the medium term, the technique may be useful in bioelectric medicine, which involves delivering therapeutic electrical pulses. Researchers in this area have long been interested in incorporating polymers that conduct or inhibit electricity without damaging surrounding tissues. Stimulating specific cells—to intervene in a seizure, for instance—is much more precise than flooding the whole organism with drugs, which can cause broad side effects. But current bioelectric methods, such as those using electrodes, still affect large numbers of cells indiscriminately. The new technique uses a virus to deliver genes to desired cell types, instructing them to produce an enzyme (Apex2) on their surface. The enzyme sparks a chemical reaction between precursor molecules and hydrogen peroxide, infused in the space between cells; this reaction causes the precursors to fuse into a polymer on the targeted cells. “What's new here is the intertwining of various emerging fields in one application,” says University of Florida biomedical engineer Kevin Otto, who was not involved in the research but co-authored an accompanying commentary in Science. “The use of conductive polymers assembled [inside living tissue] through synthetic biology, to enable cell-specific interfacing, is very novel.” © 2020 Scientific American

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 27411 - Posted: 08.11.2020

by Chloe Williams A new atlas lays bare how neuronal connections, or synapses, change from birth to old age in mice1. The ‘synaptome’ may help researchers investigate how mutations linked to autism affect these connections at different stages of life. Synapses are the junctions where information is transferred between cells, and they are integral to functions such as learning, behavior and movement. Autism is linked to several mutations that alter synaptic proteins. In 2018, researchers created the first synaptome of the mouse brain, mapping billions of synapses and sorting them into types based on their size, shape and composition2. The map revealed that synapse subtypes have distinct distributions in the brain, suggesting they have specific functions. This synaptome mapped the mouse brain only at one point in time, however. In the new work, the team charted five billion synapses in mice at 10 different ages, revealing how synapses change in number, structure and molecular makeup throughout life. “It’s the first time anybody’s ever done that in any species,” says Seth Grant, professor of molecular neuroscience at the University of Edinburgh in Scotland, who led the research. To create the atlas, the team engineered mice to express fluorescent markers of different colors on two proteins — PSD95 and SAP102 — that frequently line the signal-receiving end of excitatory synapses, which make up the preponderance of synapses in the brain. Mutations in these proteins have been linked to autism, schizophrenia and intellectual disability. © 2020 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: 27402 - Posted: 08.06.2020

Ian Sample Science editor Doctors in France have reported what they believe to be the first proven case of Covid-19 being passed on from a pregnant woman to her baby in the womb. The newborn boy developed inflammation in the brain within days of being born, a condition brought on after the virus crossed the placenta and established an infection prior to birth. He has since made a good recovery. The case study, published in Nature Communications, follows the birth of a number of babies with Covid-19 who doctors suspect contracted the virus in the womb. Until now, they have not been able to rule out the possibility that the babies were infected during or soon after delivery. “Unfortunately there is no doubt about the transmission in this case,” said Daniele De Luca, medical director of paediatrics and neonatal critical care at the Antoine Béclère hospital in Paris. “Clinicians must be aware that this may happen. It’s not common, that’s for sure, but it may happen and it must be considered in the clinical workout.” The 23-year-old mother was admitted to the hospital on 24 March with a fever and severe cough after contracting coronavirus late in the third trimester. She tested positive for Covid-19 shortly her arrival. Three days after the woman was admitted, monitoring of the baby revealed signs of distress and doctors performed an emergency caesarean with the mother under general anaesthetic. The baby was immediately isolated in a neonatal intensive care unit and intubated because he was affected by the general anaesthetic. © 2020 Guardian News & Media Limited

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: 27366 - Posted: 07.15.2020

by Angie Voyles Askham An experimental drug prevents seizures and improves memory in a mouse model of fragile X syndrome, according to a new study1. The drug selectively blocks an enzyme that is overactive in the brains of people with fragile X and could offer a potential treatment for the condition. “It’s truly a novel target,” says co-lead investigator Mark Bear, professor of neuroscience at the Massachusetts Institute of Technology. Fragile X syndrome is characterized by intellectual disability, seizures, hyperactivity and, in one out of three people, autism. It results from mutations that diminish the gene FMR1’s production of FMRP, a protein that limits the synthesis of other proteins at synapses, where neurons exchange chemical messages. Without FMRP, according to one leading theory, proteins build up at synapses and disrupt this signaling, leading to fragile X’s outward signs. The new drug helps put the brakes on protein buildup by blocking a specific form of an enzyme called glycogen synthase kinase 3 (GSK3), which plays an important role during brain development. Previous trials have prevented protein buildup by blocking a different target, the mGluR5 receptor, which helps control protein production in neurons. But those drugs have failed in clinical trials because people have experienced adverse side effects and built up a tolerance to chronic dosing. The drug to block GSK3, called BRD0705, may result in fewer side effects because it is highly selective. The enzyme comes in two forms, known as alpha and beta, and BRD0705 blocks only the former. The findings should stimulate more research on GSK3 alpha, which has not been studied as well as its counterpart, researchers say. © 2020 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: 27355 - Posted: 07.11.2020

By Veronique Greenwood Planarians have unusual talents, to say the least. If you slice one of the tiny flatworms in half, the halves will grow back, giving you two identical worms. Cut a flatworm’s head in two, and it will grow two heads. Cut an eye off a flatworm — it will grow back. Stick an eye on a flatworm that lacks eyes — it’ll take root. Pieces as small as one-279th of a flatworm will turn into new, whole flatworms, given the time. This process of regeneration has fascinated scientists for more than 200 years, prompting myriad zany, if somewhat macabre, experiments to understand how it is possible for a complex organism to rebuild itself from scratch, over and over and over again. In a paper published Friday in Science, researchers revealed a tantalizing glimpse into how the worms’ nervous systems manage this feat. Specialized cells, the scientists report, point the way for neurons stretching from newly grown eyes to the brain of the worm, helping them connect correctly. The research suggests that cellular guides hidden throughout the planarian body may make it possible for the worm’s newly grown neurons to retrace their steps. Gathering these and other insights from the study of flatworms may someday help scientists interested in helping humans regenerate injured neurons. María Lucila Scimone, a researcher at M.I.T.’s Whitehead Institute for Biomedical Research, first noticed these cells while studying Schmidtea mediterranea, a planarian common to bodies of freshwater in Southern Europe and North Africa. During another experiment, she noted that they were expressing a gene involved in regeneration. The team looked more closely and realized that some of the regeneration-related cells were positioned at key branching points in the network of nerves between the worms’ eyes and their brains. When the researchers transplanted an eye from one animal to another, the neurons growing from the new eye always grew toward these cells. When the nerve cells reached their target, they kept growing along the route that would take them to the brain. Removing those cells meant the neurons got lost and did not reach the brain. © 2020 The New York Times Company

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 13: Memory and Learning; Chapter 7: Vision: From Eye to Brain
Link ID: 27340 - Posted: 07.01.2020

Amber Dance They told Marcelle Girard her baby was dead. Back in 1992, Girard, a dentist in Gatineau, Canada, was 26 weeks pregnant and on her honeymoon in the Dominican Republic. When she started bleeding, physicians at the local clinic assumed the baby had died. But Girard and her husband felt a kick. Only then did the doctors check for a fetal heartbeat and realize the baby was alive. The couple was medically evacuated by air to Montreal, Canada, then taken to the Sainte-Justine University Hospital Center. Five hours later, Camille Girard-Bock was born, weighing just 920 grams (2 pounds). Babies born so early are fragile and underdeveloped. Their lungs are particularly delicate: the organs lack the slippery substance, called surfactant, that prevents the airways from collapsing upon exhalation. Fortunately for Girard and her family, Sainte-Justine had recently started giving surfactant, a new treatment at the time, to premature babies. After three months of intensive care, Girard took her baby home. Today, Camille Girard-Bock is 27 years old and studying for a PhD in biomedical sciences at the University of Montreal. Working with researchers at Sainte-Justine, she’s addressing the long-term consequences of being born extremely premature — defined, variously, as less than 25–28 weeks in gestational age. Families often assume they will have grasped the major issues arising from a premature birth once the child reaches school age, by which time any neurodevelopmental problems will have appeared, Girard-Bock says. But that’s not necessarily the case. Her PhD advisers have found that young adults of this population exhibit risk factors for cardiovascular disease — and it may be that more chronic health conditions will show up with time.

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: 27279 - Posted: 06.04.2020

By Laura Sanders The heart has its own “brain.” Now, scientists have drawn a detailed map of this little brain, called the intracardiac nervous system, in rat hearts. The heart’s big boss is the brain, but nerve cells in the heart have a say, too. These neurons are thought to play a crucial role in heart health, helping to fine-tune heart rhythms and perhaps protecting people against certain kinds of heart disease. But so far, this local control system hasn’t been mapped in great detail. To make their map, systems biologist James Schwaber at Thomas Jefferson University in Philadelphia and colleagues imaged male and female rat hearts with a method called knife-edge scanning microscopy, creating detailed pictures of heart anatomy. Those images could then be built into a 3-D model of the heart. The scientists also plucked out individual neurons and measured the amount of gene activity within each cell. These measurements helped sort the heart’s neurons into discrete groups. Most of these neuron clusters dot the top of the heart, where blood vessels come in and out. Some of these clusters spread down the back of the heart, and were particularly abundant on the left side. With this new view of the individual clusters, scientists can begin to study whether these groups have distinct jobs. The comprehensive, 3-D map of the heart’s little brain could ultimately lead to targeted therapies that could treat or prevent heart diseases, the authors write online May 26 in iScience. © Society for Science & the Public 2000–2020.

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 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27274 - Posted: 06.03.2020

Jordana Cepelewicz In the 1990s, an army of clones invaded Germany. Within a decade, they had spread to Italy, Croatia, Slovakia, Hungary, Sweden, France, Japan and Madagascar — wreaking havoc in rivers and lakes, rice paddies and swamps; in waters warm and cold, acidic and basic. The culprits: six-inch-long, lobster-like creatures called marbled crayfish. Scientists suspect that sometime around 1995, a genetic mutation allowed a pet crayfish to reproduce asexually, giving rise to a new, all-female species that could make clones of itself from its unfertilized eggs. Deliberately or accidentally, some of these mutants were released from aquariums into the wild, where they rapidly multiplied into the millions, threatening native waterways species and ecosystems. But their success is strange. “All marbled crayfish which exist today derive from a single animal,” said Günter Vogt, a biologist at Heidelberg University. “They are all genetically identical.” Ordinarily, the absence of genetic diversity makes a population exceedingly vulnerable to the vagaries of its environment. Yet the marbled crayfish have managed to thrive around the globe. A closer look reveals that the crayfishes’ uniformity is only genome-deep. According to studies conducted by Vogt and others in the mid-2000s, these aquatic clones actually vary quite a bit in their color, size, behavior and longevity. Which means that something other than their genes is inspiring that diversity. Common sense tells us that if it’s not nature, it’s nurture: environmental influences that interact with an animal’s genome to generate different outcomes for various traits. But that’s not the whole story. New research on crayfish and scores of other organisms is revealing an important role for a third, often-overlooked source of variation and diversity — a surprising foundation for what makes us unique that begins in the first days of an embryo’s development: random, intrinsic noise. All Rights Reserved © 2020

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: 27139 - Posted: 03.24.2020

By Perri Klass, M.D. When you talk about sibling issues, everyone takes it personally. Whether it’s birth order and the supposed advantages of being the oldest (or youngest, or middle), or the question of having (or being) the favorite child, people tend to respond immediately with their own sometimes very individual and emotional stories. What I want to talk about today are sibling sex ratios — having a sibling of the other sex versus growing up in all-boy or all-girl sibling configurations. The most evocative phrase I’ve seen for this is “family constellations,” which I like because it suggests that there are lots of interesting — and even beautiful — arrangements, but that differences are real. But let’s take one step further back: Are there actually parents, or parent pairs, who are more likely to conceive boys or girls? Does the five-daughter family (from “Pride and Prejudice” or “Fiddler on the Roof”) or the seven-son setup (“Seven Brides for Seven Brothers”) just reflect five (or seven) random rolls of the dice, or is there actually something going on from an evolutionary point of view? The evolutionary theory, which has been advanced to explain sex ratio, goes back to Darwin, but was fully formulated in 1930 by a British scientist named Ronald Fisher, who made the argument that if individuals vary in the sex ratio among their offspring (that is, some are more likely to produce more males or more females), the reproductive advantage in a population will always lie with the rarer sex, and thus the sex ratio will equilibrate toward 1:1. After all, Fisher argued, half of the genetic material of the next generation must come by way of those who tend to produce males, and half from those who tend to produce females. But are there such tendencies? I’ve heard people say that having boys “runs in the family,” or that their cousins are almost all girls, that’s the “family pattern.” But a very large study of 4.7 million births in Sweden published in February in the journal Proceedings of the Royal Society argues that there is no evidence of a genetic tendency toward one sex or the other, or a family tendency. © 2020 The New York Times Company

Related chapters from BN: Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 13: Memory and Learning
Link ID: 27108 - Posted: 03.10.2020

By Simon Makin Neuroscientists understand much about how the human brain is organized into systems specialized for recognizing faces or scenes or for other specific cognitive functions. The questions that remain relate to how such capabilities arise. Are these networks—and the regions comprising them—already specialized at birth? Or do they develop these sensitivities over time? And how might structure influence the development of function? “This is an age-old philosophical question of how knowledge is organized,” says psychologist Daniel Dilks of Emory University. “And where does it come from? What are we born with, and what requires experience?” Dilks and his colleagues addressed these questions in an investigation of neural connectivity in the youngest humans studied in this context to date: 30 infants ranging from six to 57 days old (with an average age of 27 days). Their findings suggest that circuit wiring precedes, and thus may guide, regional specialization, shedding light on how knowledge systems emerge in the brain. Further work along these lines may provide insight into neurodevelopmental disorders such as autism. In the study, published Monday in Proceedings of the National Academy of Sciences USA, the researchers looked at two of the best-studied brain networks dedicated to a particular visual function—one that underlies face recognition and another that processes scenes. The occipital face area and fusiform face area selectively respond to faces and are highly connected in adults, suggesting they constitute a face-recognition network. The same description applies to the parahippocampal place area and retrosplenial complex but for scenes. All four of these areas are in the inferior temporal cortex, which is behind the ear in humans. © 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 13: Memory and Learning; Chapter 7: Vision: From Eye to Brain
Link ID: 27088 - Posted: 03.03.2020

By Viviane Callier In 1688 Irish philosopher William Molyneux wrote to his colleague John Locke with a puzzle that continues to draw the interest of philosophers and scientists to this day. The idea was simple: Would a person born blind, who has learned to distinguish objects by touch, be able to recognize them purely by sight if he or she regained the ability to see? The question, known as Molyneux’s problem, probes whether the human mind has a built-in concept of shapes that is so innate that such a blind person could immediately recognize an object with restored vision. The alternative is that the concepts of shapes are not innate but have to be learned by exploring an object through sight, touch and other senses, a process that could take a long time when starting from scratch. An attempt was made to resolve this puzzle a few years ago by testing Molyneux's problem in children who were congenitally blind but then regained their sight, thanks to cataract surgery. Although the children were not immediately able to recognize objects, they quickly learned to do so. The results were equivocal. Some learning was needed to identify an object, but it appeared that the study participants were not starting completely from scratch. Lars Chittka of Queen Mary University of London and his colleagues have taken another stab at finding an answer, this time using another species. To test whether bumblebees can form an internal representation of objects, Chittka and his team first trained the insects to discriminate spheres and cubes using a sugar reward. The bees were trained in the light, where they could see but not touch the objects that were isolated inside a closed petri dish. Then they were tested in the dark, where they could touch but not see the spheres or cubes. The researchers found that the invertebrates spent more time in contact with the shape they had been trained to associate with the sugar reward, even though they had to rely on touch rather than sight to discriminate the objects. © 2020 Scientific American

Related chapters from BN: Chapter 10: Vision: From Eye to Brain; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 13: Memory and Learning
Link ID: 27061 - Posted: 02.21.2020

Timothy Bella The headaches had become so splitting for Gerardo Moctezuma that the pain caused him to vomit violently. The drowsiness that came with it had intensified for months. But it wasn’t until Moctezuma, 40, fainted without explanation at a soccer match in Central Texas last year that he decided to figure out what was going on. When Jordan Amadio looked down at his MRI results, the neurosurgeon recognized — but almost couldn’t believe — what looked to be lodged in Moctezuma’s brain. As he opened up Moctezuma’s skull during an emergency surgery in May 2019, he was able to confirm what it was that had uncomfortably set up shop next to the man’s brain stem: a tapeworm measuring about an inch-and-a-half. “It’s very intense, very strong, because it made me sweat too, sweat from the pain,” Moctezuma said to KXAN. The clear and white parasite came from tapeworm larva that Amadio believes Moctezuma, who moved from Mexico to the U.S. 14 years before his diagnosis, might have had in his brain for more than a decade undetected. His neurological symptoms had intensified due to his neurocysticercosis, which was the direct result of the tapeworm living in his brain. The cyst would trigger hydrocephalus, an accumulation of cerebrospinal fluid that increased pressure to the skull to the point that the blockage and pain had become life-threatening. “It’s a remarkable case where a patient came in and, if he had not been treated urgently, he would have died from tremendous pressure in the brain,” Amadio, attending neurosurgeon at the Ascension Seton Brain and Spine Institute in Austin, told The Washington Post on Thursday night.

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System; Chapter 13: Memory and Learning
Link ID: 27013 - Posted: 02.01.2020

Madeline Andrews, Aparna Bhaduri, Arnold Kriegstein What was going on with our brain organoids? As neuroscientists, we use these three-dimensional clusters of cells grown in petri dishes to learn more about how the human brain works. Researchers culture various kinds of organoids from stem cells – cells that have the potential to become one of many different cell types found throughout the body. We use chemical signals to direct stem cells to produce brain-like cells that together resemble certain structural aspects of a real brain. While they are not “brains in a dish” – organoids cannot function or think independently – the idea is that organoid models let scientists see developmental processes that may yield insights into how the human brain works. If researchers better understand normal development, we may be able to understand when and how things go wrong in diseases. When we recently compared our lab’s organoid cells to normal brain cells, we were surprised to find that they didn’t look as similar as we’d expected. Our brain organoids, each the size of a few millimeters, were stressed out. Our investigation into why has important implications for this popular new method since many labs are using it to study brain function and neurological disease. Without accurate models of the brain, scientists will not be able to work toward disease treatments. Our lab is particularly interested in the human cerebral cortex – the brain’s bumpy exterior – because it is so different in human beings than it is in any other species. The human cortex is proportionally bigger than in our closest living relatives, the great apes, containing more and different types of cells. It’s the source of many unique human abilities, including our cognitive capacity. © 2010–2020, 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: 27011 - Posted: 01.31.2020

By Neuroskeptic A new neuroscience paper bears the remarkable title of Life without a brain. Although the title is somewhat misleading, this is still a rather interesting report about a unique rat who functioned extremely well despite having a highly abnormal brain. This case sheds new light on a number of famous examples of humans born with similar abnormalities. According to the authors of the new paper, Ferris et al., the rat in question was called R222 and it was discovered unexpectedly during testing as part of a batch of rats taking part in an experiment. R222 didn't actually have no brain, but it had a highly abnormal brain anatomy. Its brain was actually twice the size of a normal rat's, but much of it consisted of empty, fluid-filled space. The cerebral cortex was limited to a thin sheet surrounding the fluid spaces, although the total cortical volume was - surprisingly given the images shown above - only slightly less than normal - 575 μL vs. the normal ~615 μL. Despite the grossly abnormal appearance of R222's brain, the rat seemed to suffer no major impairments. Ferris et al. say that "R222’s general health, appearance and body weight were no different from the other rats in the cohort." The rodent's motor skills and memory function were within the normal range, although it did seem to be highly anxious. © 2020 Kalmbach Media Co.

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: 27009 - Posted: 01.31.2020

Jordana Cepelewicz Part of the brain’s allure for scientists is that it is so deeply personal — arguably the core of who we are and what makes us human. But that fact also renders a large share of imaginable experiments on it monstrous, no matter how well intended. Neuroscientists have often had to swallow their frustration and settle for studying the brains of experimental animals or isolated human neurons kept alive in flat dishes — substitutes that come with their own ethical, practical and conceptual limitations. A new world of possibilities opened in 2008, however, when researchers learned how to create cerebral organoids — tiny blobs grown from human stem cells that self-organize into brainlike structures with electrically active neurons. Though no bigger than a pea, organoids hold enormous promise for improving our understanding of the brain: They can replicate aspects of human development and disease once thought impossible to observe in the laboratory. Scientists have already used organoids to make discoveries about schizophrenia, autism spectrum disorders and the microcephaly caused by the Zika virus. Yet the study of brain organoids can also be fraught with ethical dilemmas. “In order for it to be a good model, you want it to be as human as possible,” said Hank Greely, a law professor at Stanford University who specializes in ethical and legal issues in the biosciences. “But the more human it gets, the more you’re backing into the same sorts of ethics questions that are the reasons why you can’t just use living humans.” In the popular imagination, fueled by over-the-top descriptions of organoids as “mini-brains,” these questions often center on whether the tissue might become conscious and experience its unnatural existence as torture. The more immediate, realistic concerns that trouble experts are less sensational but still significant. It also doesn’t help that the study of organoids falls into an odd gap between other areas of research, complicating formal ethical oversight. Still, no one wants to see brain organoids’ potential discarded lightly. All Rights Reserved © 2020

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 1: Introduction: Scope and Outlook
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 20:
Link ID: 27007 - Posted: 01.29.2020

One day, a scientist in Craig Ferris’s lab was scanning the brains of very old rats when he found that one could see, hear, smell, and feel just like the other rats, but it was walking around with basically no brain—and likely had been since birth. This rat, named R222, did have a brain. But its brain, affected by a condition called hydrocephalus, had compressed and collapsed as it filled with fluid, and many of the functions that would ordinarily be carried out in the brain had relocalized to areas that weren’t taken over by fluid. This provided the tools for Ferris, a psychology professor at Northeastern, to investigate how powerful the brain remains, even when tight on space. This, he says, might even influence the ever-present goal of machine learning: How small can you be and still get the job done? Pretty small, it turns out, at least in R222’s case, but this efficient use of space is dependent on the brain’s capacity to reorganize. This ability, known as neuroplasticity, is a widely documented phenomenon, but such an extreme example was rare, says Ferris. In R222’s case, he says, the processing of visual input “was distributed over much of the remaining brain, and the same thing with smell and touch.” What at first the scans suggested to be a brainless rat was actually a rat with a brain that had been pushed out of the way and flattened like a pancake—and kept working. ©2020 Technology Networks

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: 26998 - Posted: 01.27.2020

Children as young as 6 years old who underwent fetal surgery to repair a common birth defect of the spine are more likely to walk independently and have fewer follow-up surgeries, compared to those who had traditional corrective surgery after birth, according to researchers funded by the National Institutes of Health. The study appears in Pediatrics. The procedure corrects myelomeningocele, the most serious form of spina bifida, a condition in which the spinal column fails to close around the spinal cord. With myelomeningocele, the spinal cord protrudes through an opening in the spine and may block the flow of spinal fluid and pull the brain into the base of the skull, a condition known as hindbrain herniation. In 2011, the Management of Myelomeningocele study, funded by NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), found that by 12 months of age, children who had fetal surgery required fewer surgical procedures to divert, or shunt, fluid away from the brain. By 30 months, the fetal surgery group was more likely to walk without crutches or other devices. For the current study, NICHD-funded researchers re-evaluated children from the original trial when they were 6 to 10 years old. Of the 161 children who took part in the follow-up study, 79 had been assigned to prenatal surgery and 82 had been assigned to traditional surgery. Children in the prenatal surgery group walked independently more often than those in the traditional surgery group (93% vs. 80%). Those in the prenatal surgery group also had fewer shunt placements for hydrocephalus, or fluid buildup in the brain (49% vs. 85%), and fewer shunt replacements (47% vs. 70%). The group also scored higher on a measure of motor skills. The two groups did not differ significantly in a test measuring communication ability, daily living skills, and social interaction skills.

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: 26993 - Posted: 01.25.2020

By Simon Makin Knowing how the human brain develops is critical to understanding how things can go awry in neurodevelopmental disorders, from intellectual disability and epilepsy to schizophrenia and autism. But between the fact that researchers cannot poke around inside growing human brains and the inadequacies of animal models, scientists currently do not fully understand the process. “We know a bit about the early stages because [the situation is] very similar to what happens in rodents,” says psychiatrist Sergiu Paşca of Stanford University. “But everything beyond the second trimester [of pregnancy] and soon after birth is poorly understood.” Enter the invention of brain “organoids”: cells grown in 3-D clusters in the lab and designed to mimic the composition of the organ’s tissue. The technology recently reached the point where specific brain regions can be modelled for sufficiently long periods to allow researchers to study their development. Paşca and his colleagues have now used organoid models of parts of the human forebrain—the seat of higher cognitive abilities such as complex thought, perception and voluntary movement—to peer into how gene activity drives brain development. “The work brings new understanding of how, as the brain is formed, distinct regulatory regions of the genome are used to execute specific tasks—for example, the generation of specific types of neurons,” says neuroscientist Paola Arlotta of Harvard University, who was not involved in the new study. The researchers used their findings to map genes associated with certain disorders to specific cell types at specific stages, giving insight into the origins of conditions such as autism and schizophrenia. © 2020 Scientific American,

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: 26991 - Posted: 01.25.2020