Links for Keyword: Development of the Brain

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By Kerri Smith, Cole Skinner was hanging from a wall above an abandoned quarry when he heard a car pull up. He and his friends bolted, racing along a narrow path on the quarry’s edge and hopping over a barbed-wire fence to exit the grounds. The chase is part of the fun for Skinner and his friend Alex McCallum-Toppin, both 15 and pupils at a school in Faringdon, UK. The two say that they seek out places such as construction sites and disused buildings—not to get into trouble, but to explore. There are also bragging rights to be earned. “It’s just something you can say: ‘Yeah, I’ve been in an abandoned quarry’,” says McCallum-Toppin. “You can talk about it with your friends.” Science has often looked at risk-taking among adolescents as a monolithic problem for parents and the public to manage or endure. When Eva Telzer, a neuroscientist at the University of North Carolina in Chapel Hill, asks family, friends, undergraduates or researchers in related fields about their perception of teenagers, “there’s almost never anything positive,” she says. “It’s a pervasive stereotype.” But how Alex and Cole dabble with risk—considering its social value alongside other pros and cons—is in keeping with a more complex picture emerging from neuroscience. Adolescent behaviour goes beyond impetuous rebellion or uncontrollable hormones, says Adriana Galván, a neuroscientist at the University of California, Los Angeles. “How we define risk-taking is going through a shift.” © 2018 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25350 - Posted: 08.18.2018

Decca Aitkenhead Annual media coverage of August’s exam results has traditionally conformed to an unwritten rule that all photos must show euphoric teenagers celebrating multiple A*s. This year, the images may tell a different story. Radical reforms to GCSEs are widely predicted to produce disappointment, and many teenagers are bracing themselves for the worst. Parents may be unsympathetic, however, if their 15- or 16-year-old spent the exam year ignoring all their wise advice to revise, and instead lay in bed until lunchtime and partied all night with friends. Even if the exam results turn out to be good, many will wonder why their teenager took so many risks with their future. Sarah-Jayne Blakemore looks barely older than a teenager herself. The award-winning professor of cognitive neuroscience at University College London is, in fact, 44 and has made the study of the adolescent brain her life’s work. She has been critical of the very existence of GCSEs, arguing that they impose “enormous stress” on teenagers at a time when their brains are going through huge change. “Until about 15 or 20 years ago,” she says, “we just didn’t know that the brain develops at all within the teenage years.” Until then, it was assumed that teenage behaviour was almost entirely down to hormonal changes in puberty, but brain scans and psychological experiments have now found that adolescence is a critical period of neurological change, much of which is responsible for the unique characteristics of adolescent behaviour. Far from being a defective or inferior version of an adult brain, the adolescent mind is both unique and – to Blakemore – beautiful. “Teenagers,” she says tenderly, “are brilliant.” © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25348 - Posted: 08.18.2018

by Lindsey Bever It was a solution no parent wants to hear: To get rid of a brain tumor and stop their young son's seizures, surgeons would need to cut out one-sixth of his brain. But for Tanner Collins, it was the best option. A slow-growing tumor was causing sometimes-daily seizures, and medications commonly used to treat them did not seem to be working, his father said. But removing a portion of his brain was no doubt risky. That region — the right occipital and posterior temporal lobes — is important for facial recognition, and, without it, Tanner's parents wondered if he would recognize them. Tanner, who was 6 at the time, underwent surgery at the University of Pittsburgh Medical Center's Children's Hospital. Although his brain has had to work to adapt since then, he's had no major problems. Other than some visual impairment, Tanner, now 12, said he's “perfectly fine.” “As far as I’m concerned, I’m a perfectly normal 12-year-old boy,” Tanner said. Tanner's case was published Tuesday in the scientific journal Cell Reports, explaining how the 12-year-old's brain learned to adapt after a part largely responsible for visual processing was taken out. Marlene Behrmann, a cognitive neuroscientist and lead author of the paper, said Tanner was one of the first pediatric patients studied over the past several years in her laboratory at Carnegie Mellon University to determine the extent to which a child's brain can reorganize itself after certain sections are surgically removed. In Tanner's case, she said, surgeons took out his right occipital and posterior temporal lobes, which made up about one-third of the right hemisphere of his brain. © 1996-2018 The Washington Post

Related chapters from BN8e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Memory, Learning, and Development
Link ID: 25287 - Posted: 08.03.2018

Ashley Yeager Neuroscientist Gavin Clowry didn’t intend to grow a miniature human brain in a rat pup. But a few months ago, that’s essentially what happened. “We were astonished when we saw it,” recalls the faculty member at Newcastle University in the UK. Clowry and his colleagues had derived human neural stem cells from induced pluripotent stem cells, diffused them into a 3-D gel, and transplanted the gel into the young rats’ brains to test the cells’ ability to survive. A month later, much to the team’s surprise, the human cells had formed columns of tightly packed progenitor cells surrounded by immature neurons. “They looked like organoids,” says Clowry, who published the results in May. Organoids are tiny collections of tissue made from cells that self-organize into 3-D structures that mimic the anatomy of fully formed organs. Clowry attributes the unexpected development of the human brain organoids to the complex environment of the rat’s brain, where diverse cell types interact to keep neurons operating. That’s not to say cerebral organoids can’t also be grown in a dish. Scientists published the first description of lab-grown, human brain organoids in 2013. But even cultured mini-brains appear to benefit from an in vivo environment. Clowry’s study appeared in the literature just three weeks after a paper from Fred “Rusty” Gage and his colleagues at the Salk Institute for Biological Studies in La Jolla, California, described how they had transplanted lab-grown human brain organoids into the brains of mice and watched as the animals’ native blood vessels and immune cells infiltrated the organoids. Gage’s team also noted that the cells in the implanted organoids were sending and receiving signals to and from the mice’s native nerve cells. As Clowry and his colleagues would later observe in rat brains, the organoids were being integrated into the animals’ brains. © 1986 - 2018 The Scientist

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25284 - Posted: 08.02.2018

by Bethany Brookshire An astonishing number of things that scientists know about brains and behavior are based on small groups of highly educated, mostly white people between the ages of 18 and 21. In other words, those conclusions are based on college students. College students make a convenient study population when you’re a researcher at a university. It makes for a biased sample, but one that’s still useful for some types of studies. It would be easy to think that for studies of, say, how the typical brain develops, a brain is just a brain, no matter who’s skull its resting in. A biased sample shouldn’t really matter, right? Wrong. Studies heavy in rich, well-educated brains may provide a picture of brain development that’s inaccurate for the American population at large, a recent study found. The results provide a strong argument for scientists to pay more attention to who, exactly, they’re studying in their brain imaging experiments. It’s “a solid piece of evidence showing that those of us in neuroimaging need to do a better job thinking about our sample, where it’s coming from and who we can generalize our findings to,” says Christopher Monk, who studies psychology and neuroscience at the University of Michigan in Ann Arbor. The new study is an example of what happens when epidemiology experiments — studies of patterns in health and disease — crash into studies of brain imaging. “In epidemiology we think about sample composition a lot,” notes Kaja LeWinn, an epidemiologist at the University of California in San Francisco. Who is in the study, where they live and what they do is crucial to finding out how disease patterns spread and what contributes to good health. But in conversations with her colleagues in psychiatry about brain imaging, LeWinn realized they weren’t thinking very much about whose brains they were looking at. Particularly when studying healthy populations, she says, there was an idea that “a brain is a brain is a brain.” |© Society for Science & the Public 2000 - 2018

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25197 - Posted: 07.12.2018

Laura Sanders I’m making my way through my third round of breastfeeding a newborn and taking stock of how things are going. Some aspects are definitely easier: My milk came in really quickly (a perk of being a repeat lactator), the fancy breastfeeding baby holds are no longer mysterious to me and I already own all of the weird pillows I need to prop up my tiny baby. But one thing isn’t easier this time around: the bone-crushing, mind-numbing exhaustion. Just like my other two, this sweet baby seems to eat all the time. All day. All night. Sometimes multiple times an hour, especially in the witching hours of the evening. This frequency got me curious about the biology of newborns’ stomachs. Just how small are they? Are they so microscopic that one can hold only enough sustenance to keep my newborn satisfied for a thousandth of a second? Birth educators and medical professionals often use a marble to illustrate the size of a newborn’s stomach, a tiny orb that holds about 5 to 7 milliliters of liquid. But that small estimate has come into question. A 2008 review published in the Journal of Human Lactation points out that there aren’t many solid studies on the size of the infant stomach, and some of the ones that do exist come to different conclusions. Another review of existing studies concluded that the average newborn stomach is slightly smaller than a Ping-Pong ball and can hold about 20 milliliters, or about two-thirds of an ounce. © Society for Science and the Public

Related chapters from BN8e: 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, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 25189 - Posted: 07.10.2018

Sukanya Charuchandra At times a predominant layer of the developing brain, the subplate disappears in the adult human brain—or so researchers believed. In findings published in Cell Stem Cell on June 21, scientists propose that neurons from the human subplate, which underlies the tissue that will become the cortex, relocate into the cortex. The researchers found high levels of a protein, known to help cells migrate into the cortex, in stem cell–derived subplate neurons. These relocated subplate cells may be associated with neurological diseases. “A lot of the genes associated with autism are first expressed in the subplate,” M. Zeeshan Ozair, a coauthor on the paper, says in a statement. “And if subplate neurons don’t die but instead become part of the cortex, they will carry those mutations with them.” M.Z. Ozair et al., “hPSC modeling reveals that fate selection of cortical deep projection neurons occurs in the subplate,” Cell Stem Cell, doi:10.1016/j.stem.2018.05.024, 2018. © 1986 - 2018 The Scientist Magazine

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25146 - Posted: 06.27.2018

Jennifer Ouellette Gerardo Ortiz remembers well the time in 2010 when he first heard his Indiana University colleague John Beggs talk about the hotly debated “critical brain” hypothesis, an attempt at a grand unified theory of how the brain works. Ortiz was intrigued by the notion that the brain might stay balanced at the “critical point” between two phases, like the freezing point where water turns into ice. A condensed matter physicist, Ortiz had studied critical phenomena in many different systems. He also had a brother with schizophrenia and a colleague who suffered from epilepsy, which gave him a personal interest in how the brain works, or doesn’t. Ortiz promptly identified one of the knottier problems with the hypothesis: It’s very difficult to maintain a perfect tipping point in a messy biological system like the brain. The puzzle compelled him to join forces with Beggs to investigate further. Ortiz’s criticism has beleaguered the theory ever since the late Danish physicist Per Bak proposed it in 1992. Bak suggested that the brain exhibits “self-organized criticality,” tuning to its critical point automatically. Its exquisitely ordered complexity and thinking ability arise spontaneously, he contended, from the disordered electrical activity of neurons. Bak’s canonical example of a self-organized critical system is a simple sandpile. If you drop individual grains of sand on top of a sandpile one by one, each grain has a chance of causing an avalanche. Bak and colleagues showed that those avalanches will follow a “power law,” with smaller avalanches occurring proportionally more frequently than larger ones. So if there are 100 small avalanches in which 10 grains slide down the side of the sandpile during a given period, there will be 10 larger avalanches involving 100 grains in the same period, and just one large avalanche involving 1,000 grains. When a huge avalanche collapses the whole pile, the base widens, and the sand begins to pile up again until it returns to its critical point, where, again, avalanches of any size may occur. The sandpile is incredibly complex, with millions or billions of tiny elements, yet it maintains an overall stability. All Rights Reserved © 2018

Related chapters from BN8e: Chapter 6: Evolution of the Brain and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25137 - Posted: 06.25.2018

Veronique Greenwood The question most of genetics tries to answer is how genes connect to the traits we see. One person has red hair, another blonde hair; one dies at age 30 of Huntington’s disease, another lives to celebrate a 102nd birthday. Knowing what in the vast expanse of the genetic code is behind traits can fuel better treatments and information about future risks and illuminate how biology and evolution work. For some traits, the connection to certain genes is clear: Mutations of a single gene are behind sickle cell anemia, for instance, and mutations in another are behind cystic fibrosis. But unfortunately for those who like things simple, these conditions are the exceptions. The roots of many traits, from how tall you are to your susceptibility to schizophrenia, are far more tangled. In fact, they may be so complex that almost the entire genome may be involved in some way, an idea formalized in a theory put forward last year. Starting about 15 years ago, geneticists began to collect DNA from thousands of people who shared traits, to look for clues to each trait’s cause in commonalities between their genomes, a kind of analysis called a genome-wide association study (GWAS). What they found, first, was that you need an enormous number of people to get statistically significant results — one recent GWAS seeking correlations between genetics and insomnia, for instance, included more than a million people. Second, in study after study, even the most significant genetic connections turned out to have surprisingly small effects. The conclusion, sometimes called the polygenic hypothesis, was that multiple loci, or positions in the genome, were likely to be involved in every trait, with each contributing just a small part. (A single large gene can contain several loci, each representing a distinct part of the DNA where mutations make a detectable difference.) All Rights Reserved © 2018

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25134 - Posted: 06.25.2018

Richard Harris One of the enduring mysteries of biology is why so much of the DNA in our chromosomes appears to be simply junk. In fact, about half of the human genome consists of repetitive bits of DNA that cut and paste themselves randomly into our chromosomes, with no obvious purpose. A study published Thursday finds that some of these snippets may actually play a vital role in the development of embryos. The noted biologist Barbara McClintock, who died in 1992, discovered these odd bits of DNA decades ago in corn, and dubbed them "jumping genes." (She won a Nobel prize for that finding in 1983.) McClintock's discovery stimulated generations of scientists to seek to understand this bizarre phenomenon. Some biologists have considered these weird bits of DNA parasites, since they essentially hop around our chromosomes and infect them, sometimes disrupting genes and leaving illness in their wake. But Miguel Ramalho-Santos, a biologist at the University of California, San Francisco, doesn't like that narrative. "It seemed like a waste of this real estate in our genome — and in our cells — to have these elements and not have them there for any particular purpose," Ramalho-Santos says. "So we just asked a very simple question: Could they be doing something that's actually beneficial?" He and his colleagues focused on a jumping gene called LINE-1; all told, copies of it make up a whopping 20 percent of our entire DNA. Ramalho-Santos' lab studies embryos, so the team wondered whether LINE-1 played any role in prompting a single fertilized egg to develop into an embryo. © 2018 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25130 - Posted: 06.23.2018

By Jon Cohen Until now, researchers wanting to understand the Neanderthal brain and how it differed from our own had to study a void. The best insights into the neurology of our mysterious, extinct relatives came from analyzing the shape and volume of the spaces inside their fossilized skulls. But a recent marriage of three hot fields—ancient DNA, the genome editor CRISPR, and "organoids" built from stem cells—offers a provocative, if very preliminary, new option. At least two research teams are engineering stem cells to include Neanderthal genes and growing them into "minibrains" that reflect the influence of that ancient DNA. None of this work has been published, but Alysson Muotri, a geneticist at the University of California, San Diego (UCSD) School of Medicine, described his group's Neanderthal organoids for the first time this month at a UCSD conference called Imagination and Human Evolution. His team has coaxed stem cells endowed with Neanderthal DNA into pea-size masses that mimic the cortex, the outer layer of real brains. Compared with cortical minibrains made with typical human cells, the Neanderthal organoids have a different shape and differences in their neuronal networks, including some that may have influenced the species's ability to socialize. "We're trying to recreate Neanderthal minds," Muotri says. Muotri focused on one of approximately 200 protein-coding genes that differ between Neanderthals and modern humans. Known as NOVA1, it plays a role in early brain development in modern humans and also is linked to autism and schizophrenia. Because it controls splicing of RNA from other genes, it likely helped produce more than 100 novel brain proteins in Neanderthals. Conveniently, just one DNA base pair differs between the Neanderthal gene and the modern human one. © 2018 American Association for the Advancement of Science.

Related chapters from BN8e: 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, Learning, and Development
Link ID: 25116 - Posted: 06.21.2018

By Sara Goudarzi The presidents of the National Academies of Sciences, Engineering, and Medicine issued a statement Wednesday advocating for the U.S. Department of Homeland Security to stop separating migrant families. The statement cites research that indicates endangerment of those involved. Last week the American Psychological Association released a letter opposing the Trump administration’s policy of taking immigrant children from their parents at the border. Under the zero-tolerance immigration policy, since May more than 2,300 immigrant children—some of them babies—have been forcibly separated from their parents attempting to enter the U.S. from Mexico. Also Wednesday, as the backlash and public outcry continue to grow, Pres. Donald Trump said he would sign an executive order to stop separating families at the order. It was unclear when children already separated might be reunited with their families. But even if reunited soon, medical experts say the effects of separation can potentially last a lifetime. Scientific American spoke with Alan Shapiro, assistant clinical professor in pediatrics at Albert Einstein College of Medicine, about the effects of separation trauma and other health and mental consequences of breaking up families. Shapiro is also senior medical director for Community Pediatric Programs (CPP), a collaboration between the Children’s Hospital at Montefiore in New York City and the Children’s Health Fund, and medical director and co-founder of Terra Firma, a partnership that provides medical and legal services to immigrant children. © 2018 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25115 - Posted: 06.21.2018

By Jan Hoffman One in seven high school students reported misusing prescription opioids, one of several disturbing results in a nationwide survey of teenagers that revealed a growing sense of fear and despair among youth in the United States. The numbers of teenagers reporting “feelings of sadness or hopelessness,” suicidal thoughts, and days absent from school out of fear of violence or bullying have all risen since 2007. The increases were particularly pointed among lesbian, gay and bisexual high school students. Nationally, 1 in 5 students reported being bullied at school; 1 in 10 female students and 1 in 28 male students reported having been physically forced to have sex. “An adolescent’s world can be bleak,” said Dr. Jonathan Mermin, an official with the Centers for Disease Control and Prevention, which conducted the survey and analyzed the data. “But having a high proportion of students report they had persistent feelings of hopelessness and 17 percent considering suicide is deeply disturbing.” In 2017, 31 percent of students surveyed said they had such feelings, while 28 percent said so in 2007. In 2017, nearly 14 percent of students had actually made a suicide plan, up from 11 percent in 2007. The Youth Risk Behavior Survey is given every two years to nearly 15,000 students in high schools in 39 states, and poses questions about a wide array of attitudes and activities. The report did offer some encouraging trends, suggesting that the overall picture for adolescents is a nuanced one. Compared to a decade ago, fewer students reported having had sex, drinking alcohol or using drugs like cocaine, heroin or marijuana. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 15: Brain Asymmetry, Spatial Cognition, and Language
Link ID: 25098 - Posted: 06.18.2018

By Clyde Haberman For nine frustrating years, Lesley and John Brown tried to conceive a child but failed because of her blocked fallopian tubes. Then in late 1977, this English couple put their hopes in the hands of two men of science. Thus began their leap into the unknown, and into history. On July 25, 1978, the Browns got what they had long wished for with the arrival of a daughter, Louise, a baby like no other the world had seen. She came into being through a process of in vitro fertilization developed by Robert G. Edwards and Patrick Steptoe. Her father’s sperm was mixed with her mother’s egg in a petri dish, and the resulting embryo was then implanted into the womb for normal development. Louise was widely, glibly and incorrectly called a “test-tube baby.” The label was enough to throw millions of people into a moral panic, for it filled them with visions of Dr. Frankenstein playing God and throwing the natural order of the universe out of kilter. The reality proved far more benign, maybe best captured by Grace MacDonald, a Scottish woman who in January 1979 gave birth to the second in vitro baby, a boy named Alastair. Nothing unethical was at work, she told the BBC in 2003. “It’s just nature being given a helping hand.” In this installment of its video documentaries, Retro Report explores how major news stories of the past shape current events by harking back to Louise Brown’s birth. If anything, more modern developments in genetics have raised the moral, ethical and political stakes. But the fundamental questions are essentially what they were in the 1970s with the advent of in vitro fertilization: Are these welcome advances that can only benefit civilization? Or are they incursions into an unholy realm, one of “designer babies,” with potentially frightening consequences? In vitro fertilization, or I.V.F., is by now broadly accepted, though it still has objectors, including the Roman Catholic Church. Worldwide, the procedure has produced an estimated six million babies, and is believed to account for 3 percent of all live births in some developed countries. Designer-baby fears have proved in the main to be “overblown,” said Dr. Paula Amato, a professor of obstetrics and gynecology at Oregon Health & Science University in Portland. “We have not seen it with I.V.F. in general,” she told Retro Report. “We have not seen it with P.G.D.” © 2018 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25077 - Posted: 06.11.2018

Mark Brown Arts correspondent Teenagers are being damaged by the British school system because of early start times and exams at 16 when their brains are going through enormous change, a leading neuroscientist has said. Sarah-Jayne Blakemore said it was only in recent years that the full scale of the changes that take place in the adolescent brain has been discovered. “That work has completely revolutionised what we think about this period of life,” she said. Blakemore, a professor in cognitive neuroscience at University College London, told the Hay festival that teenagers were unfairly mocked and demonised for behaviour they had no control over, whether that was moodiness, excessive risk-taking, bad decision making or sleeping late. The changes in the brain were enormous, she said, with substantial rises in white matter and a 17% fall in grey matter, which affects decision making, planning and self-awareness. All parents know that teenagers would sleep late if they could but it is all to do with brain changes, she said. “It is not because they are lazy, it is because they go through a period of biological change where melatonin, which is the hormone humans produce in the evenings and makes us feel sleepy, is produced a couple of hours later than it is in childhood or adulthood.” They are then forced to go to school when their brain says they should still be sleeping. That is then exacerbated at weekends when teenagers try to catch up by sleeping until lunchtime – what Blakemore called “social jetlag”. © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 10: Biological Rhythms and Sleep
Link ID: 25035 - Posted: 05.30.2018

By Jim Daley The organizer, a group of cells in the embryo that directs the developmental fates and morphogenesis of other embryonic cells, has been identified in human tissue for the first time, according to a study published today (May 23) in Nature. The discovery demonstrates that the organizer is evolutionarily conserved from amphibians to humans. “For many of us this was always the Holy Grail” of developmental biology, says Guillermo Oliver, the director of the Northwestern Feinberg School of Medicine’s Center for Vascular and Developmental Biology, who was not involved in the study. “The fact that now you can take stem cells and recapitulate those properties with the combination of actors reported here . . . is quite remarkable.” Rockefeller University embryologist Ali Brivanlou and colleagues report that when they grafted human stem cells that they’d treated with Wnt and Activin, two signaling proteins previously shown to be involved in organizer gene expression in other animals, into chick embryos, the grafted cells set off the developmental progress of the cells around them. The experiment establishes for the first time that the organizer exists in humans and that Wnt and Activin work in concert to make it possible for cells to direct embryonic development. S The search for the organizer, and with it the field of modern embryology, began nearly a century ago. Hilde Mangold, a PhD candidate in the lab of German zoologist Hans Spemann, wrote a dissertation in 1924 that described the organizer for the first time. Mangold and Spemann observed a distinct shape and morphology in some of the cells along the neural axis—the portion of the embryo that will become the central nervous system and one of the first structures to form during development—in a salamander embryo. When they grafted these cells from one embryo to another, the transplanted cells induced the formation of a second developmental axis in that embryo. Spemann would go on to receive the 1935 Nobel Prize in Physiology or Medicine for the discovery; Mangold died before then in an accident. © 1986-2018 The Scientist

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25021 - Posted: 05.25.2018

By Ashley Yeager Twenty years ago, Ilyce Randell and her husband received devastating news: their son Maxie, who was a little over four months old at the time, had Canavan disease. Maxie would never walk or talk, and he likely wouldn’t live past age 10. Not much could be done to help their son, the couple was told, though a geneticist offhandedly remarked that researchers were developing a gene therapy that might lessen Maxie’s symptoms or extend his life. But the Randells also learned that there was no funding available for a clinical trial on the gene therapy. Recently married, the couple contacted the same people they had invited to their wedding. Randell wrote a letter describing her son’s illness and included a photo of Maxie grinning. “That was my first fundraising campaign,” she says. It was also the start of Canavan Research Illinois, the Randell family’s foundation. Canavan disease is caused by mutations to the ASPA gene, which encodes an enzyme, aspartoacylase, that breaks down N-acetyl-L-aspartic acid. Without aspartoacylase, the acid builds up in the brain’s neurons and prevents their axons from being coated in fatty myelin sheaths. As a result, electrical signals don’t travel as efficiently from nerve cell to nerve cell. Neurons in the brain break down, leaving the organ spongy and leading to intellectual disabilities, loss of movement, abnormal muscle tone, and seizures, among other symptoms. In the first US trial of a gene therapy for Canavan, researchers tried encasing healthy copies of ASPA in liposomes and injecting them into the brain through an intraventricular catheter attached to a small, plastic, dome-shaped reservoir placed just beneath the scalp. The researchers injected the gene therapy into the reservoir, and it then diffused into the cerebrospinal fluid. In 1999, Maxie became one of 16 patients to receive the treatment. Maxie and his cohort showed some improvements in vision and movement, but the children weren’t cured. © 1986-2018 The Scientist

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25008 - Posted: 05.23.2018

By Diana Kwon When Eliza O’Neill was 3 years old, her parents, Glenn and Cara, noted that her development began to diverge from that of her peers. Their once fast-learning, gregarious child faced difficulties in school, and her improvements in areas such as social communication and speech began to slow. It took about six months and multiple visits to the doctor for Eliza to be diagnosed with Sanfilippo syndrome, a rare lysosomal storage disease in which sugar molecules called glycosaminoglycans build up in the central nervous system, destroying cells and eventually causing severe dementia, seizures, and a loss of mobility. The disease strikes between 1 and 9 out of 1,000,000 people, and most children affected do not survive beyond their teens. The diagnosis, which Eliza’s doctors made in July 2013, was like “a lightning bolt out of the sky,” Glenn recalls. “I didn’t even know that a disease as terrible as this could even exist.” In the weeks following Eliza’s diagnosis, the O’Neills combed the scientific literature looking for a way to save their daughter. Their research led them to a potential gene therapy for Sanfilippo under investigation at Nationwide Children’s Hospital (NCH) in Columbus, Ohio. At the time, the work was still in the preclinical stage, but “the data were amazing,” says Cara, a pediatrician. Once she found this study, she contacted Haiyan Fu, a scientist at NCH’s Center for Gene Therapy working on the experiments, who walked her through the research. “That was the first moment that I had a real solid hope in the science,” Cara recalls. © 1986-2018 The Scientist

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24990 - Posted: 05.18.2018

by Erin Blakemore Teenagers! They chew Tide Pods and have unprotected sex. They use social media we haven’t even heard of and are walking hormone machines. It’s easy to mock their outsize sense of self and their seemingly dumb decisions. But not so fast, says cognitive neuroscientist Sarah-Jayne Blakemore: The adolescent brain is nothing to laugh at. In “Inventing Ourselves: The Secret Life of the Teenage Brain,” Blake­more (no relation to the writer of this article) challenges adults to take teenagers and their growing brains seriously. Her book explains what’s happening inside those brains during the teen years — a complex period of neurological change that is fundamental to maturity. Blakemore breaks down the most up-to-date science on adolescent brain development. It turns out that much of what makes teenagers seem so, well, teenage is due not to their hormones but to their rapidly changing brain circuitry. The malleable mind continues to develop during adolescence, consolidating personality, preferences and behaviors. Some of those behaviors, including risk-taking and a tendency toward self-consciousness, may seem connected to peer pressure. But, Blakemore writes, they’re actually signs of brain development. With the help of data from studies that show the teenage brain in action, she connects brain development to all sorts of things, including self-control and depression. © 1996-2018 The Washington Post

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24975 - Posted: 05.15.2018

Hannah Devlin Scientists are preparing to create “miniature brains” that have been genetically engineered to contain Neanderthal DNA, in an unprecedented attempt to understand how humans differ from our closest relatives. In the next few months the small blobs of tissue, known as brain organoids, will be grown from human stem cells that have been edited to contain “Neanderthalised” versions of several genes. The lentil-sized organoids, which are incapable of thoughts or feelings, replicate some of the basic structures of an adult brain. They could demonstrate for the first time if there were meaningful differences between human and Neanderthal brain biology. “Neanderthals are the closest relatives to everyday humans, so if we should define ourselves as a group or a species it is really them that we should compare ourselves to,” said Prof Svante Pääbo, director of the genetics department at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, where the experiments are being performed. Pääbo previously led the successful international effort to crack the Neanderthal genome, and his lab is now focused on bringing Neanderthal traits back to life in the laboratory through sophisticated gene-editing techniques. The lab has already inserted Neanderthal genes for craniofacial development into mice (heavy-browed rodents are not anticipated), and Neanderthal pain perception genes into frogs’ eggs, which could hint at whether they had a different pain threshold to humans. Now the lab is turning its attention to the brain.

Related chapters from BN8e: 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, Learning, and Development
Link ID: 24971 - Posted: 05.13.2018