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Carl Zimmer For centuries, people have drawn the line between nature and nurture. In the nineteenth century, the English polymath Francis Galton cast nature-versus-nurture in scientific terms. He envisioned a battle between heredity and experience that shapes each of us. “When nature and nurture compete for supremacy…the former proves the stronger,” Galton wrote in 1874. Today, scientists can do something Galton couldn’t imagine: they can track the genes we inherit from our parents. They are gaining clues to how that genetic legacy influences many aspects of our experience, from our risk of developing cancer to our tendency to take up smoking. But determining exactly how any particular variation in DNA shapes the course of our life is proving far trickier than Galton would have guessed. There is no clean line between nature and nurture: How a particular variant acts, if at all, may depend on your environment. A study published on Thursday offers a striking new demonstration of this complexity. Genes may help determine how long children stay in school, the researchers found, but some of those genes operate at a distance — by influencing parents. The study was published in Science. The authors go on coin a new phrase for this effect: “genetic nurture.” To scientists accustomed to tracing the links between the genes you carry and the traits they govern, it’s a headspinning idea. A genetic variant may shape you not because it directly influences you, but because it changes those around you, noted Paige Harden, a psychologist at the University of Texas who co-authored a commentary on the new study: “Something is happening outside your own skin.” © 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: 24578 - Posted: 01.27.2018

Amy Maxmen A puzzle posed by segments of 'dark matter' in genomes — long, winding strands of DNA with no obvious functions — has teased scientists for more than a decade. Now, a team has finally solved the riddle. The conundrum has centred on DNA sequences that do not encode proteins, and yet remain identical across a broad range of animals. By deleting some of these ‘ultraconserved elements’, researchers have found that these sequences guide brain development by fine-tuning the expression of protein-coding genes. The results1, published on 18 January in Cell, might help researchers to better understand neurological diseases such as Alzheimer’s. They also validate the hypotheses of scientists who have speculated that all ultraconserved elements are vital to life — despite the fact that researchers knew very little about their functions. “People told us we should have waited to publish until we knew what they did. Now I’m like, dude, it took 14 years to figure this out,” says Gill Bejerano, a genomicist at Stanford University in California, who described ultraconserved elements in 20042. Bejerano and his colleagues originally noticed ultraconserved elements when they compared the human genome to those of mice, rats and chickens, and found 481 stretches of DNA that were incredibly similar across the species. That was surprising, because DNA mutates from generation to generation — and these animal lineages have been evolving independently for up to 200 million years. © 2018 Macmillan Publishers 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: 24547 - Posted: 01.20.2018

By JAN HOFFMAN The California case in which 13 siblings were found imprisoned at home earlier this week is shocking, but not without precedent. Lurid cases have come to light over the years of children locked in closets and basements, held captive by parents who have crumbled under the weight of drugs, extreme religious conviction, personality disorders or their own abusive backgrounds. The good news, trauma experts say, is that recovery is indeed possible. Victims can reclaim their lives. “The clinical data is encouraging,” said John A. Fairbank, co-director of the National Center for Child Traumatic Stress. “There are good treatments available for children seriously abused and traumatized.” In particular, said Dr. Fairbank, a professor of psychiatry and behavioral sciences at Duke, good results have been shown with a relatively short-term cognitive behavioral therapy tailored for trauma patients, an approach developed in the early 1990s but widely disseminated in the last 15 years. A significant hurdle to recovery for the California siblings and children in analogous situations, said psychologists, is that their captors were not stranger-kidnappers but their parents. “In doing the healing work, you look at what the patient’s support systems are, “ said Priscilla Dass-Brailsford, a trauma psychologist and an adjunct professor in the department of psychiatry at Georgetown University. “The biggest supports are parents and family. These kids don’t have that. The parents were the aggressors.” Experts interviewed for this article, who underscored that they had no direct knowledge of the California case, said that because the siblings’ primal assurance of unconditional love and safety had been ripped away, they would almost certainly struggle to trust and attach to future supportive figures. “The notion that this was done by parents increases a child’s helplessness and hopelessness,” said Nora J. Baladerian, a Los Angeles psychologist who often treats traumatized individuals. © 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: 24538 - Posted: 01.19.2018

By LAURA BEIL Millions of American children have been exposed to a parasite that could interfere with their breathing, liver function, eyesight and even intelligence. Yet few scientists have studied the infection in the United States, and most doctors are unaware of it. The parasites, roundworms of the genus Toxocara, live in the intestines of cats and dogs, especially strays. Microscopic eggs from Toxocara are shed in the animals’ feces, contaminating yards, playgrounds and sandboxes. These infectious particles cling to the hands of children playing outside. Once swallowed, the eggs soon hatch, releasing larvae that wriggle through the body and, evidence suggests, may even reach the brain, compromising learning and cognition. The Centers for Disease Control and Prevention periodically tracks positive tests for Toxocara through the National Health and Nutrition Examination Survey. The latest report, published in September in the journal Clinical Infectious Diseases, estimated that about 5 percent of the United States population — or about 16 million people — carry Toxocara antibodies in their blood, a sign they have ingested the eggs. But the risk is not evenly shared: Poor and minority populations are more often exposed. The rate among African Americans was almost 7 percent, according to the C.D.C. Among people living below the poverty line, the infection rate was 10 percent. The odds of a positive test rise with age, but it’s unknown whether this reflects recent infections or simply an accumulation of antibodies from past encounters. Dr. Peter Hotez, dean of the National School of Tropical Medicine at Baylor College of Medicine in Houston, calls Toxocara both one of the most common parasites in the country and arguably the most neglected. © 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: 24530 - Posted: 01.16.2018

By Meredith Wadman Chya* (pronounced SHY-a), who is not quite 10 years old, recently spent an unusual day at the University of Maryland School of Medicine in Baltimore. Part of the time she was in a "cool" brain scanner while playing video games designed to test her memory and other brain-related skills. At other points, she answered lots of questions about her life and health on an iPad. A slender Baltimore third grader who likes drawing, hip hop, and playing with her pet Chihuahua, Chya is one of more than 6800 children now enrolled in an unprecedented examination of teenage brain development. The Adolescent Brain Cognitive Development Study—or ABCD Study—will complete its 2-year enrollment period in September, and this month will release a trove of data from 4500 early participants into a freely accessible, anonymized database. Ultimately, the study aims to follow 10,000 children for a decade as they grow from 9- and 10-year-olds into young adults. Supported by the first chunk of $300 million pledged by several institutes at the National Institutes of Health (NIH) in Bethesda, Maryland, teams at 21 sites around the United States are regularly using MRI machines to record the structure and activity of these young brains. They're also collecting reams of psychological, cognitive, and environmental data about each child, along with biological specimens such as their DNA. In addition to providing the first standardized benchmarks of healthy adolescent brain development, this information should allow scientists to probe how substance use, sports injuries, screen time, sleep habits, and other influences may affect—or be affected by—a maturing brain. © 2017 American Association for the Advancement of Science.

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: 24488 - Posted: 01.04.2018

By C. CLAIBORNE RAY Q. Did cranial deformation as practiced by the ancient Mayans change or impair brain function? A. The famous slanted forehead that was apparently a mark of high rank among pre-Columbian Mayans was achieved by various forms of compression of the head in infancy. It is believed by many researchers to have had no significant effect on cranial capacity and how the brain worked, the conclusion of a 1989 study of skulls in The American Journal of Physical Anthropology. But there is no direct evidence to support this contention, no large study comparing brain development in living populations that do and do not practice head flattening. An extensive review article in the journal Anthropology in 2003 speculated that the practice of compression had the potential to damage the delicate developing frontal lobe, as is seen in certain conditions. The authors speculated that such damage could have impaired vision, object recognition, hearing ability, memory, attentiveness and concentration. These factors in turn might have contributed to behavior disorders and difficulty in learning new information. Still other researchers suggest that the diverging conclusions can be attributed to how the skull measurements are done. The compression may have affected the shape of the face more than the brain itself, they said. © 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: 24475 - Posted: 01.02.2018

Michaeleen Doucleff It's not every day that surgeons develop a new brain surgery that could save tens of thousands of babies, even a hundred thousand, each year. And it's definitely not every day that the surgery is developed in one of the world's poorest countries. But that's exactly what neurosurgeons from Boston and Mbale, Uganda, report Wednesday in the New England Journal of Medicine. The treatment is for a scary condition in which a baby's head swells up, almost like balloon. It's called hydrocephalus, or "water on the brain." But a more accurate description is "spinal fluid inside the brain." Inside our brains, there are four chambers that continually fill up and release spinal fluid. So their volume stays constant. In babies with hydrocephalus, the chambers don't drain properly. They swell up, putting pressure on the brain. If left untreated about half the children will die, and the others will be badly disabled. Traditionally doctors treat hydrocelphalus in the U.S. with what's called a shunt: They place a long tube in the baby's brain, which allows the liquid to drain into the child's stomach. © 2017 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: 24453 - Posted: 12.22.2017

/ By Carrie Arnold Jim and Ida Hall buried their daughter Jerra in a family plot at the bottom of a grassy rise. Several times a year, Jim Hall drives just over a mile from his home on North Main Street in the town of St. Louis, Michigan to Jerra’s headstone in the back corner of Oak Grove Cemetery in his 1997 Chevy pickup. In the 12 years since complications from a rare heart defect claimed the life of their brown-haired toddler, her family continues to cover her grave with stuffed animals (frogs were her favorite). Hall gently sweeps off the leaves and debris covering the childhood paraphernalia and wipes his callused hands on a pair of worn jeans, his tall frame stooped by grief. He stops and stares at the inscription: “Two years, two months, too little.” “We didn’t know what else to write,” he said. “When your daughter is born with a heart condition and doesn’t survive, you just wonder.” Jim Hall’s exposure to PBB as a child makes him valuable in the hunt for the answer to a burning scientific question: Can a father’s exposure to environmental toxins impact the health of his progeny? Jerra’s headstone sits where an umbrella of majestic oaks gives way to the dreadlocks of vines and grasses of a small wetland in the geographic center of Michigan’s Lower Peninsula, a little more than a mile from the chemical plant that once produced a toxic flame retardant called PBB, short for polybrominated biphenyl. Hall can’t help but think it may have killed his little girl. Copyright 2017 Undark

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: 24439 - Posted: 12.19.2017

By PAM BELLUCK As the first babies born with brain damage from the Zika epidemic become 2-year-olds, the most severely affected are falling further behind in their development and will require a lifetime of care, according to a study published Thursday by the Centers for Disease Control and Prevention. The study, the first to comprehensively assess some of the oldest Zika babies in Brazil, focused on 15 of the most disabled children born with abnormally small heads, a condition called microcephaly. At about 22 months old, these children had the cognitive and physical development of babies younger than 6 months. They could not sit up or chew, and they had virtually no language. “A child might be making those raspberry sounds, but they are not making even the sort of consonant sounds like ‘mama, baba, dada,’” said Dr. Georgina Peacock, an author of the study and the director of the division of human development and disability at the C.D.C.’s National Center on Birth Defects and Developmental Disabilities. It is unclear how many of the nearly 3,000 Brazilian Zika babies born with microcephaly will have outcomes as severe as the children in the study, but the experiences of doctors working in Brazil suggest it could be hundreds. “It’s heartbreaking,” the C.D.C. director, Dr. Brenda Fitzgerald, said in an interview. “We would expect that these children are going to require enormous amounts of work and require enormous amounts of care.” The new study, conducted with the Brazilian Ministry of Health and other organizations, evaluated children in Paraíba state, part of Brazil’s northeastern region, which became the epicenter of the Zika crisis. The researchers initially studied 278 babies born in Paraíba between October 2015 and the end of January 2016. Of those, 122 families agreed to participate in follow-up evaluations this year. The study released Thursday involves what were considered the most severe of those cases, Dr. Peacock said. © 2017 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: 24427 - Posted: 12.15.2017

Tina Hesman Saey PHILADELPHIA — Flat brains growing on microscope slides may have revealed a new wrinkle in the story of how the brain folds. Cells inside the brains contract, while cells on the outside grow and push outward, researchers at the Weizmann Institute of Science in Rehovot, Israel, discovered from working with the lab-grown brains, or organoids. This push and pull results in folds in the organoids similar to those found in full-size brains. Orly Reiner reported the results December 5 at the joint meeting of the American Society for Cell Biology and the European Molecular Biology Organization. Reiner and her colleagues sandwiched human brain stem cells between a glass microscope slide and a porous membrane. The apparatus allowed the cells access to nutrients and oxygen while giving the researchers a peek at how the organoids grew. The cells formed layered sheets that closed up at the edges, making the organoids resemble pita bread, Reiner said. Wrinkles began to form in the outer layers of the organoids about six days after the mini brains started growing. These brain organoids may help explain why people with lissencephaly — a rare brain malformation in which the ridges and folds are missing — have smooth brains. The researchers used the CRISPR/Cas9 gene-editing system to make a mutation in the LIS1 gene. People with lissencephaly often have mutations in that gene. Cells carrying the mutation didn’t contract or move normally, the team found. |© Society for Science & the Public 2000 - 2017.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 24421 - Posted: 12.14.2017

By PERRI KLASS, M.D. What does the child who can’t say goodbye to a parent without breaking down have in common with the child who is cripplingly terrified of dogs and the one who gets a bad stomach ache reliably on Monday morning? Anxieties and worries of all kinds are common in children, necessarily part of healthy development, but also, when they interfere with the child’s functioning, the most common pediatric mental health problems. From separation anxiety to social anxiety to school avoidance to phobias to generalized anxiety disorder, many children’s lives are at some point touched by anxiety that gets out of hand. “I often tell parents, anxiety and fears are totally a normal and healthy part of growing up,” said Dr. Sabrina Fernandez, an assistant professor of pediatrics at the University of California, San Francisco, who has written about strategies for primary care doctors to use in dealing with anxiety disorders. “I worry that it’s becoming something more when it interferes with the child’s ability to do their two jobs: to learn in school and to make friends.” Children whose lives are being seriously derailed by their anxieties often get psychotherapy or medication, or both. And a meta-analysis published in November in JAMA looked at the two best-studied treatments for anxiety disorders, cognitive behavioral therapy and psychotropic medication. The technique of a meta-analysis allows scientists to pull in a whole range of different studies, weight the results according to the size and rigor of the research, and then consider the wider array of data gleaned from multiple investigations. “We included panic disorder, social anxiety disorder, specific phobias, generalized anxiety disorder and separation anxiety,” said the lead author, Zhen Wang, an associate professor of health services research at the Mayo Clinic College of Medicine and Science (they did not include children with post-traumatic stress disorder or obsessive-compulsive disorder). The study looked at the effectiveness of treatments in reducing the symptoms of anxiety, and at ending the anxiety disorder state. And they also looked at any reports of adverse events associated with the treatments, from sleep disturbances to suicide. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 24416 - Posted: 12.11.2017

By Ruth Williams Two studies in Science today—one that focuses on prenatal development in humans, the other on infancy to old age—provide insights into the extent of DNA sequence errors that the average human brain cell accumulates over a lifetime. Together, they reveal that mutations become more common as fetuses develop, and over a lifetime a person may rack up more than 2,000 mutations per cell. “I think these are both very powerful technical papers, and they demonstrate how single-cell sequencing . . . can reliably detect somatic changes in the genomes of human neurons,” says neuroscientist Fred Gage of the Salk Institute in La Jolla who was not involved in either study. “What’s cool about [the papers] is that they show two different ways that one can look at somatic mutations in single human neurons . . . and yet they get consistent results,” says neuroscientist Michael McConnell of the University of Virginia School of Medicine. Cells of the human body acquire mutations over time, whether because of errors introduced during DNA replication or damage incurred during transcription and other cellular processes. But, until recent technological developments enabled whole genome sequencing from the miniscule quantities of DNA found inside single cells or small clones of the same cell, investigating the nature and extent of such somatic mutations—and the resulting tissue mosaicism—was practically impossible. © 1986-2017 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: 24412 - Posted: 12.09.2017

Seventeen million babies under the age of one are breathing toxic air, putting their brain development at risk, the UN children's agency has warned. Babies in South Asia were worst affected, with more than 12 million living in areas with pollution six times higher than safe levels. A further four million were at risk in East Asia and the Pacific. Unicef said breathing particulate air pollution could damage brain tissue and undermine cognitive development. Its report said there was a link to "verbal and non-verbal IQ and memory, reduced test scores, grade point averages among schoolchildren, as well as other neurological behavioural problems". The effects lasted a lifetime, it said. Delhi's air pollution is triggering a health crisis "As more and more of the world urbanises, and without adequate protection and pollution reduction measures, more children will be at risk in the years to come," Unicef said. It called for wider use of face masks and air filtering systems, and for children not to travel during spikes in pollution. Media captionSmog reduced visibility in Delhi to a few metres Last month hazardous smog began blanketing the Indian capital Delhi, prompting the Indian capital's chief minister Arvind Kejriwal to say the city had become a "gas chamber". Some schools in the city were closed but there was criticism when they re-opened, with parents accusing the authorities of disregarding their children's health. © 2017 BBC.

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: 24398 - Posted: 12.07.2017

By Ann Gibbons Ever since Alex Pollen was a boy talking with his neuroscientist father, he wanted to know how evolution made the human brain so special. Our brains are bigger, relative to body size, than other animals', but it's not just size that matters. "Elephants and whales have bigger brains," notes Pollen, now a neuroscientist himself at the University of California, San Francisco. Comparing anatomy or even genomes of humans and other animals reveals little about the genetic and developmental changes that sent our brains down such a different path. Geneticists have identified a few key differences in the genes of humans and apes, such as a version of the gene FOXP2 that allows humans to form words. But specifically how human variants of such genes shape our brain in development—and how they drove its evolution—have remained largely mysterious. "We've been a bit frustrated working so many years with the traditional tools," says neurogeneticist Simon Fisher, director of the Max Planck Institute for Psycholinguistics in Nijmegen, the Netherlands, who studies FOXP2. Now, researchers are deploying new tools to understand the molecular mechanisms behind the unique features of our brain. At a symposium at The American Society of Human Genetics here last month, they reported zooming in on the genes expressed in a single brain cell, as well as panning out to understand how genes foster connections among far-flung brain regions. Pollen and others also are experimenting with brain "organoids," tiny structured blobs of lab-grown tissue, to detail the molecular mechanisms that govern the folding and growth of the embryonic human brain. "We used to be just limited to looking at sequence data and cataloging differences from other primates," says Fisher, who helped organize the session. "Now, we have these exciting new tools that are helping us to understand which genes are important." © 2017 American Association for the Advancement of Science.

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: 24315 - Posted: 11.10.2017

By Sara B. Linker, Tracy A. Bedrosian, and Fred H. Gage For years, neurons in the brain were assumed to all carry the same genome, with differences in cell type stemming from epigenetic, transcriptional, and posttranscriptional differences in how that genome was expressed. But in the past decade, researchers have recognized an incredible amount of genomic diversity, in addition to other types of cellular variation that can affect function. Indeed, the human brain contains approximately 100 billion neurons, and we now know that there may be almost as many unique cell types. Our interest in this incredible diversity emerged from experiments that we initially labeled as failures. In 1995, we (F.H.G. and colleagues) found that a protein called fibroblast growth factor 2 (FGF2) is important for maintaining adult neural progenitor cells (NPCs) in a proliferative state in vitro. We could only expand NPCs by culturing them at high density, however, so we could not generate homogeneous populations of cells.1 Five years later, we identified a glycosylated form of the protein cystatin C (CCg) that, combined with FGF2, allowed us to isolate and propagate a very homogeneous population of NPCs—cells that would uniformly and exclusively differentiate into neurons.2 We compared gene expression of this homogeneous population of cells to that of rat stem cells and the oligodendrocytes, astroglia, and neurons derived from the NPCs. To our surprise and disappointment, the top nine transcripts that were unique to the NPC-derived population were all expressed components of long interspersed nuclear element-1, also known as LINE-1 or L1— an abundant retrotransposon that makes up about 20 percent of mammalian genomes. © 1986-2017 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: 24305 - Posted: 11.08.2017

BC's Hogan twins, featured in the documentary Inseparable, are unique in the world. Joined at the head, their brains are connected by a thalamic bridge which gives them neurological capabilities that researchers are only now beginning to understand. Still, they are like other Canadian ten-year-olds; they attend school, have a favourite pet and are part of a large, loving family determined to live each day to the fullest. Here are a few highlights: Craniopagus twins, joined at the head, are a rarity — one in 2.5 million. The vast majority do not survive 24 hours. Krista and Tatiana Hogan were born October 25, 2006, in Vancouver, B.C. A CT scan of the twins showed they could never be separated due to the risk of serious injury or death. The structure of the twins’ brains makes them unique in the world. Their brains are connected by a thalamic bridge, connecting the thalamus of one with that of the other. The thalamus acts like a switchboard relaying sensory and motor signals and regulating consciousness. Krista and Tatiana Hogan share the senses of touch and taste and even control one another’s limbs. Tatiana can see out of both of Krista’s eyes, while Krista can only see out of one of Tatiana’s. Tatiana controls three arms and a leg, while Krista controls three legs and an arm. They can also switch to self-control of their limbs. The twins say they know one another’s thoughts without having to speak. “Talking in our heads” is how they describe it. The girls are diabetic and have epilepsy. They take a regimen of pills, blood tests and need daily insulin injections. The twins go to a regular school and as of September 2017 have started Grade 6. Though academically delayed, they are learning to read, write and do arithmetic. ©2017 CBC/Radio-Canada.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 14: Attention and Consciousness
Link ID: 24288 - Posted: 11.04.2017

By BENOIT DENIZET-LEWIS The disintegration of Jake’s life took him by surprise. It happened early in his junior year of high school, while he was taking three Advanced Placement classes, running on his school’s cross-country team and traveling to Model United Nations conferences. It was a lot to handle, but Jake — the likable, hard-working oldest sibling in a suburban North Carolina family — was the kind of teenager who handled things. Though he was not prone to boastfulness, the fact was he had never really failed at anything. Not coincidentally, failure was one of Jake’s biggest fears. He worried about it privately; maybe he couldn’t keep up with his peers, maybe he wouldn’t succeed in life. The relentless drive to avoid such a fate seemed to come from deep inside him. He considered it a strength. Jake’s parents knew he could be high-strung; in middle school, they sent him to a therapist when he was too scared to sleep in his own room. But nothing prepared them for the day two years ago when Jake, then 17, seemingly “ran 150 miles per hour into a brick wall,” his mother said. He refused to go to school and curled up in the fetal position on the floor. “I just can’t take it!” he screamed. “You just don’t understand!” Jake was right — his parents didn’t understand. Jake didn’t really understand, either. But he also wasn’t good at verbalizing what he thought he knew: that going to school suddenly felt impossible, that people were undoubtedly judging him, that nothing he did felt good enough. “All of a sudden I couldn’t do anything,” he said. “I was so afraid.” His tall, lanky frame succumbed, too. His stomach hurt. He had migraines. “You know how a normal person might have their stomach lurch if they walk into a classroom and there’s a pop quiz?” he told me. “Well, I basically started having that feeling all the time.” © 2017 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 24174 - Posted: 10.11.2017

By Clare Wilson OUR braininess may have evolved thanks to gene changes that made our brain cells less sticky. The cortex is the thin, highly folded outer layer of our brains and it is home to some of our most sophisticated mental abilities, such as planning, language and complex thoughts. Around three millimetres thick, this layer is folded into an intricate pattern of ridges and valleys, which allows the cortex to be large, but still fit into a relatively small space. Many larger mammals, such as primates, dolphins and horses, have various patterns of folds in their cortex, but folds are rarer in smaller animals like mice. So far, we have only identified a few genetic mutations that contributed to the evolution of the human brain, including ones that boosted the number of cells in the cortex. One theory about how the cortex came to be folded is that it buckled as the layer of cells expanded. Daniel del Toro at the Max Planck Institute of Neurobiology in Munich, Germany, and colleagues wondered if some of the genetic changes in our brain’s evolution might have been about more than just an increasing number of cells. They investigated the genes for two molecules – FLRT1 and FLRT3 – which make developing brain cells stick to each other more. Human brain cells produce only a small amount of these compounds, while mice brain cells make lots. Del Toro’s team created mice embryos that lacked functioning FLRT1 and FLRT3 genes, which meant their cortex cells were only loosely attached to each other, like those of humans. © Copyright New Scientist Ltd.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 24153 - Posted: 10.05.2017

Anna Gorman Kerri De Nies received the news this spring from her son's pediatrician: Her chubby-cheeked toddler has a rare brain disorder. She'd never heard of the disease — adrenoleukodystrophy, or ALD — but soon felt devastated and overwhelmed. "I probably read everything you could possibly read online — every single website," De Nies says as she cradles her son, Gregory Mac Phee. "It's definitely hard to think about what could potentially happen. You think about the worst-case scenario." ALD is a genetic brain disorder depicted in the 1992 movie Lorenzo's Oil, which portrayed a couple whose son became debilitated by the disease. The most serious form of the illness typically strikes boys between the ages of 4 and 10. Most are diagnosed too late for treatment to be successful, and they often die before their 10th birthday. The more De Nies learned about ALD, the more she realized how fortunate the family was to have discovered Gregory's condition so early. Her son's blood was tested when he was about 10 months old. Dr. Florian Eichler, a neurologist at Massachusetts General Hospital, says newborn screening is a game changer for children with the ALD, because it allows doctors to keep a close eye on kids who test positive for an ALD mutation from the beginning. © 2017 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: 24147 - Posted: 10.05.2017

A tiny change—just one mutation—appears to have boosted the modern Zika virus’s ability to attack fetal brain cells, fueling the wave of birth defects involving microcephaly (small head size) that recently swept across the Americas. The findings are reported Thursday in Science. Researchers in China found that a single swap of amino acids—from serine to asparagine—on a structural protein of the Zika virus occurred a few months before the pathogen first took off in French Polynesia in 2013. The team’s results may begin to answer an outstanding question from the Zika epidemic: Why have Zika-related microcephaly and other brain abnormalities been seen in areas hard-hit by outbreaks in the past few years but not in the decades following the virus’s discovery in 1947? One theory is that the Zika–microcephaly connection previously flew under the radar because there were too few cases to see the link. Another leading theory is that something about the modern virus has changed, allowing it to infect brain cells more efficiently than its ancestors could. The new work suggests the latter is true. “This is a very good study and it gives a plausible explanation that is scientifically based,” says Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases at the U.S. National Institutes of Health. He adds that the results will be further strengthened if other groups replicate them. © 2017 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: 24121 - Posted: 09.29.2017