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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

Laura Sanders Frog brains get busy long before they’re fully formed. Just a day after fertilization, embryonic brains begin sending signals to far-off places in the body, helping oversee the layout of complex patterns of muscles and nerve fibers. And when the brain is missing, bodily chaos ensues, researchers report online September 25 in Nature Communications. The results, from brainless embryos and tadpoles, broaden scientists’ understanding of the types of signals involved in making sure bodies develop correctly, says developmental biologist Catherine McCusker of the University of Massachusetts Boston. Scientists are familiar with short-range signals among nearby cells that help pattern bodies. But because these newly described missives travel all the way from the brain to the far reaches of the body, they are “the first example of really long-range signals,” she says. Celia Herrera-Rincon of Tufts University in Medford, Mass., and colleagues came up with a simple approach to tease out the brain’s influence on the growing body. Just one day after fertilization, the scientists lopped off the still-forming brains of African clawed frog embryos. These embryos survive to become tadpoles even without brains, a quirk of biology that allowed the researchers to see whether the brain is required for the body’s development. The answer was a definite — and surprising — yes, Herrera-Rincon says. Long before the brain is mature, it’s already organizing and guiding organ behavior, she says. Brainless tadpoles had bungled patterns of muscles. Normally, muscle fibers form a stacked chevron pattern. But in tadpoles lacking a brain, this pattern didn’t form correctly. “The borders between segments are all wonky,” says study coauthor Michael Levin, also of Tufts University. “They can’t keep a straight line.” |© Society for Science & the Public 2000 - 2017.

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: 24109 - Posted: 09.25.2017

Daniel Cressey Many sharks are living much longer than was thought, according to a major review1 of studies on these important and often endangered top predators. This means that many estimates of how threatened particular species are — and decisions about whether they can be fished safely — could be based on faulty data. Scientists usually estimate how old sharks are by slicing through their spines and counting distinctive pairs of bands seen inside, which are often assumed to show age in the same way as the rings of a tree. But a growing number of cases are suggesting that the method can be problematic. For example, a 2014 study2 showed that sand tiger sharks (Carcharias taurus), which were thought to live for around two decades, can actually survive for up to twice that. And in 2007, researchers found3 that New Zealand porbeagle sharks (Lamna nasus) had been under-aged by an average of 22 years. To investigate the scale of the problem, fisheries researcher Alastair Harry of James Cook University in Townsville, Australia, reviewed evidence for age underestimation. He reports in Fish and Fisheries1 that of 53 populations of sharks and rays for which there are good data, 30% have probably had their ages underestimated (see graphic). “Current evidence points to it being systemic, rather than restricted to a few isolated cases,” says Harry. “We really can’t ignore it anymore.” © 2017 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: 24081 - Posted: 09.20.2017

By Michelle Roberts Health editor, BBC News online There is "surprisingly limited" evidence that light drinking during pregnancy poses any risk to the baby, say UK researchers. They reviewed all the available studies done on the topic since the 1950s and found no convincing proof that a drink or two a week is harmful. The Bristol University team stress this does not mean it is completely safe. They say women should avoid all alcohol throughout pregnancy "just in case", as per official guidelines. But women who have had small amounts to drink in pregnancy should be reassured that they are unlikely to have harmed their baby. The Chief Medical Officer for the UK, Prof Dame Sally Davies, updated her advice last year to advocate total abstinence. Before that, pregnant women had been told they could drink one or two units - equivalent to one or two small glasses of wine - a week. There is no proven safe amount that women can drink during pregnancy, although the risks of drinking heavily in pregnancy are well known. Getting drunk or binge drinking during pregnancy increases the risk of miscarriage and premature birth and can lead to mental and physical problems in the baby, called foetal alcohol syndrome. The risks associated with light drinking, however, are less clear. Dr Luisa Zuccolo and colleagues found 26 relevant studies on the topic. Their review found no overwhelming proof of harm - but, in seven of the studies, light drinking was associated, on average, with an 8% higher risk of having a small baby, compared with drinking no alcohol at all. The review, in BMJ Open, also notes it appeared to increase the risk of having a premature birth. © 2017 BBC.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 24057 - Posted: 09.12.2017

By Helen Thomson DON’T mind the gap. A woman has reached the age of 24 without anyone realising she was missing a large part of her brain. The case highlights just how adaptable the organ is. The discovery was made when the woman was admitted to the Chinese PLA General Hospital of Jinan Military Area Command in Shandong Province complaining of dizziness and nausea. She told doctors she’d had problems walking steadily for most of her life, and her mother reported that she hadn’t walked until she was 7 and that her speech only became intelligible at the age of 6. Doctors did a CAT scan and immediately identified the source of the problem – her entire cerebellum was missing (see scan, above). The space where it should be was empty of tissue. Instead it was filled with cerebrospinal fluid, which cushions the brain and provides defence against disease. The cerebellum – sometimes known as the “little brain” – is located underneath the two hemispheres. It looks different from the rest of the brain because it consists of much smaller and more compact folds of tissue. It represents about 10 per cent of the brain’s total volume but contains 50 per cent of its neurons. Although it is not unheard of to have part of your brain missing, either congenitally or from surgery, the woman joins an elite club of just nine people who are known to have lived without their entire cerebellum. A detailed description of how the disorder affects a living adult is almost non-existent, say doctors from the Chinese hospital, because most people with the condition die at a young age and the problem is only discovered on autopsy (Brain, doi.org/vh7). © Copyright New Scientist Ltd.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 24056 - Posted: 09.12.2017

Paul Martin Sir Patrick Bateson, who has died aged 79, was a scientist whose work advanced the understanding of the biological origins of behaviour. He will also be remembered as a man of immense warmth and kindness, whose success as a leader, teacher and administrator of science owed much to his collaborative spirit, generosity and good humour. He was a key figure in ethology – the biological study of animal behaviour. As well as being a conceptual thinker who revelled in painting the big theoretical picture, he was an accomplished experimental scientist. He published extensively, with more than 300 journal papers and several books to his name. His early research was on imprinting – a specialised form of early learning in which young animals rapidly learn about key features of their environment, such as the distinguishing characteristics of their parent or a desirable mate. He later worked with Gabriel Horn on unravelling the neurobiological mechanisms that underpin this learning. A related interest was the biology of mate choice, where he revealed how young animals could strike an optimal balance between outbreeding and inbreeding. His research achievements led to his election as fellow of the Royal Society in 1983. Another scientific focus was the role of play behaviour in the development of the individual. Studies with monkeys, cats and other species showed how experiences that are actively acquired through playing in early life help to build the physical, cognitive and social skills that are vital in later life. © 2017 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: 23962 - Posted: 08.16.2017

An experimental drug appears to slow the progression of Niemann-Pick disease type C1 (NPC1), a fatal neurological disease, according to results of a clinical study led by researchers at the National Institutes of Health. The study appears in The Lancet. NPC1 is a rare genetic disorder that primarily affects children and adolescents, causing a progressive decline in neurological and cognitive functions. The U.S. Food and Drug Administration has not approved any treatments for the condition. The drug, 2-hydroxypropyl-beta-cyclodextrin (VTS-270), is being tested under a cooperative research and development agreement, or CRADA, between NIH and Sucampo Pharmaceuticals, Inc. In April 2017, Sucampo acquired Vtesse Inc., which previously had been developing VTS-270. “The results are very encouraging and support continued development of VTS-270 for treating NPC1,” said Forbes D. Porter, M.D., Ph.D., clinical director at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the study’s senior author. “Compared to untreated patients we followed in an earlier study, participants who received VTS-270 scored better on a scale used to evaluate disease severity and progression, including elements such as speech, cognition and mobility.” The study was a phase 1/2a clinical trial designed to test the drug’s safety and effectiveness. A group of 14 participants, ranging from ages 4 to 23 years, received the experimental drug once a month at NIH for 12 to 18 months. Another group of three participants received the drug every two weeks for 18 months at Rush University Medical Center in Chicago.

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: 23952 - Posted: 08.12.2017

By Daniel Barron Conrad was 17 months old when Dave, his grandfather, was babysitting him at their home in Temple, Texas. The two had been playing in the pool and went inside for a break. Dave set to unloading dishes in the dishwasher, unaware that Conrad had snuck back outside. As he finished the dishes, Dave looked out the window and noticed something odd. There was what looked like a floating bundle of clothes in the swimming pool. It was his grandson. Fortunately, Conrad responded to cardiopulmonary resuscitation (CPR), but it’s unclear how long his lungs—and his brain—went without oxygen. Drowning is the second most common cause of accidental death in children to age four. As in Conrad’s case, CPR is fortunately very successful, with 66 percent of nearly drowned children surviving. But even when resuscitated, the seconds and minutes that the brain is deprived of oxygen come at a great cost. This type of damage is known as anoxic brain injury. Anoxic brain injury is a clinical term that indicates damage to the brain that occurs due to lack of oxygen. There is a spectrum of injury ranging from complete recovery to minor to widespread brain damage. Within this spectrum lies what is known as the disorders of consciousness, with the extent of damage being proportional to the loss of consciousness. In the case of nearly drowned children, the injury is frequently thought to be widespread. Nearly drowned children are labeled “minimally conscious” or even in a “persistent vegetative state” (with no consciousness) and the prevailing medical prognosis is grim: treatment and recovery is difficult if not impossible. © 2017 Scientific American,

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: 23926 - Posted: 08.08.2017

By Mitch Leslie If these sweltering summer days prompt you to reach for a cold drink, you can thank your hypothalamus, a region of the brain that helps us regulate body temperature and other internal conditions. But the region may fail us when we get older. A new study in mice suggests that the hypothalamus promotes aging, hastening physical and mental decline as its stem cells die off. “It’s a pretty stunning paper,” says Charles Mobbs, a neuroendocrinologist at the Icahn School of Medicine at Mount Sinai in New York City. The new aging mechanism “is totally novel and quite unexpected,” adds neuroendocrinologist Marianna Sadagurski of Wayne State University in Detroit, Michigan. Tucked away deep in the brain, the hypothalamus monitors and maintains our blood concentration, our body temperature, and other physiological variables. Researchers have also suspected that it plays a role in aging. The hypothalamus becomes inflamed as we get older, and 4 years ago a team led by neurodendocrinologist Dongsheng Cai of Albert Einstein College of Medicine in New York City showed that quelling this inflammation delays physical deterioration and boosts life span in mice. In the new study, the team turned its attention to the hypothalamus’s stem cells, which in young animals divide to produce replacements for dead and damaged cells. As mice get older, the scientists found, the number of stem cells in the hypothalamus plunges. By later ages they are “basically all gone,” Cai says. © 2017 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23886 - Posted: 07.27.2017

Sara Reardon Mice aged more slowly when injected with stem cells from the brains of newborns. Stem cells in the brain could be the key to extending life and slowing ageing. These cells — which are located in the hypothalamus, a region that produces hormones and other signalling molecules — can re­invigorate declining brain function and muscle strength in middle-aged mice, according to a study published on 26 July in Nature1. Previous studies have suggested that the hypothalamus is involved in ageing, but the latest research shows that stem cells in this region can slow the process. That makes sense, because the hypothalamus is involved in many bodily functions, including inflammation and appetite, says Dongsheng Cai, a neuroendocrinologist at Albert Einstein College of Medicine in New York City. In their study, Cai and his colleagues found that stem cells in the hypothalamus disappear as mice grow older. When the researchers injected their mice with viruses that destroy these cells, the animals seemed to grow older faster, experiencing declines in memory, muscle strength, endurance and coordination. They also died sooner than untreated mice of the same age. Next, the team injected stem cells taken from the hypothalami of newborn mice into the brains of middle-aged mice. After four months, these animals had better cognitive and muscular function than untreated mice of the same age. They also lived about 10% longer, on average. © 2017 Macmillan Publishers Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23885 - Posted: 07.27.2017

Carina Storrs In the late 1960s, a team of researchers began doling out a nutritional supplement to families with young children in rural Guatemala. They were testing the assumption that providing enough protein in the first few years of life would reduce the incidence of stunted growth. It did. Children who got supplements grew 1 to 2 centimetres taller than those in a control group. But the benefits didn't stop there. The children who received added nutrition went on to score higher on reading and knowledge tests as adolescents, and when researchers returned in the early 2000s, women who had received the supplements in the first three years of life completed more years of schooling and men had higher incomes1. “Had there not been these follow-ups, this study probably would have been largely forgotten,” says Reynaldo Martorell, a specialist in maternal and child nutrition at Emory University in Atlanta, Georgia, who led the follow-up studies. Instead, he says, the findings made financial institutions such as the World Bank think of early nutritional interventions as long-term investments in human health. Since the Guatemalan research, studies around the world — in Brazil, Peru, Jamaica, the Philippines, Kenya and Zimbabwe — have all associated poor or stunted growth in young children with lower cognitive test scores and worse school achievement2. A picture slowly emerged that being too short early in life is a sign of adverse conditions — such as poor diet and regular bouts of diarrhoeal disease — and a predictor for intellectual deficits and mortality. But not all stunted growth, which affects an estimated 160 million children worldwide, is connected with these bad outcomes. Now, researchers are trying to untangle the links between growth and neurological development. Is bad nutrition alone the culprit? What about emotional neglect, infectious disease or other challenges? © 2017 Macmillan Publishers Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23831 - Posted: 07.13.2017

Ewen Callaway For 18 months in the early 1980s, John Sulston spent his days watching worms grow. Working in twin 4-hour shifts each day, Sulston would train a light microscope on a single Caenorhabditis elegans embryo and sketch what he saw at 5-minute intervals, as a fertilized egg morphed into two cells, then four, eight and so on. He worked alone and in silence in a tiny room at the Medical Research Council Laboratory of Molecular Biology in Cambridge, UK, solving a Rubik's cube between turns at the microscope. “I did find myself little distractions,” the retired Nobel prize-winning biologist once recalled. His hundreds of drawings revealed the rigid choreography of early worm development, encompassing the births of precisely 671 cells, and the deaths of 111 (or 113, depending on the worm’s sex). Every cell could be traced to its immediate forebear and then to the one before that in a series of invariant steps. From these maps and others, Sulston and his collaborators were able to draw up the first, and so far the only, complete ‘cell-lineage tree’ of a multicellular organism1. Although the desire to record an organism’s development in such exquisite detail preceded Sulston by at least a century, the ability to do so in more-complex animals has been limited. No one could ever track the fates of billions of cells in a mouse or a human with just a microscope and a Rubik’s cube to pass the time. But there are other ways. Revolutions in biologists’ ability to edit genomes and sequence them at the level of a single cell have sparked a renaissance in cell-lineage tracing. © 2017 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: 23812 - Posted: 07.07.2017

Mike Mariani With its bright colors, anthropomorphic animal motif, and nautical-themed puzzle play mat, Dr. Kimberly Noble’s laboratory at Columbia University looks like your typical day care center—save for the team of cognitive neuroscientists observing kids from behind a large two-way mirror. The Neurocognition, Early Experience, and Development Lab is home to cutting-edge research on how poverty affects young brains, and I’ve come here to learn how Noble and her colleagues could soon definitively prove that growing up poor can keep a child’s brain from developing. Noble, a 40-year-old from outside of Philadelphia who discusses her work with a mix of enthusiasm and clinical restraint, is among the handful of neuroscientists and pediatricians who’ve seen increasing evidence that poverty itself—and not factors like nutrition, language exposure, family stability, or prenatal issues, as previously thought—may diminish the growth of a child’s brain. Now she’s in the middle of planning a five-year, nationwide study that could establish a causal link between poverty and brain development—and, in the process, suggest a path forward for helping our poorest children. It’s the culmination of years of work for Noble, who helped jump-start this fledgling field in the early 2000s when, as a University of Pennsylvania graduate student, she and renowned cognitive neuroscientist Martha Farah began exploring the observation that poor kids tended to perform worse academically than their better-off peers. They wanted to investigate the neurocognitive underpinnings of this relationship—to trace the long-standing correlation between socioeconomic status and academic performance back to specific parts of the brain. “There have been decades of work from social scientists, looking at socioeconomic disparities in broad cognitive outcomes—things like IQ or high school graduation rate,” she says. “But there’s no high school graduation part of the brain.” ©2017 Mother Jones and the Foundation for National Progress.

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: 23805 - Posted: 07.04.2017

Heidi Ledford By 13 weeks of gestation, human fetuses have developed a much more unusual immune system than previously thought. A human fetus in its second trimester is extraordinarily busy. It is developing skin and bones, the ability to hear and swallow, and working on its first bowel movement. Now, a study published on 14 June in Nature finds that fetuses are also acquiring a functioning immune system — one that can recognize foreign proteins, but is less inclined than a mature immune system to go on the attack (N. McGovern et al. Nature http://dx.doi.org/10.1038/nature22795; 2017). The results add to a growing body of literature showing that the fetal immune system is more active than previously appreciated. “In general textbooks, you see this concept of a non-responsive fetus is still prevailing,” says immunologist Jakob Michaelsson at the Karolinska Institute in Stockholm. But the fetal immune system is unique, he says. “It’s not just immature, it’s special.” A developing fetus is constantly exposed to foreign proteins and cells, which are transferred from the mother through the placenta. In humans, this exposure is more extensive than in many other mammals, says immunologist Mike McCune at the University of California, San Francisco. As a result, laboratory mice have proved a poor model for studying the developing human fetal immune system. But fully understanding that development could reveal the reasons for some miscarriages, as well as explain conditions such as pre-eclampsia, which is associated with abnormal immune responses to pregnancy and causes up to 40% of premature births. © 2017 Macmillan Publishers Limited,

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: 23746 - Posted: 06.15.2017