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Laura Sanders Busy nerve cells in the brain are hungry and beckon oxygen-rich blood to replenish themselves. But active nerve cells in newborn mouse brains can’t yet make this request, and their silence leaves them hungry, scientists report June 22 in the Journal of Neuroscience. Instead of being a dismal starvation diet, this lean time may actually spur the brain to develop properly. The new results, though, muddy the interpretation of the brain imaging technique called functional MRI when it is used on infants. Most people assume that all busy nerve cells, or neurons, signal nearby blood vessels to replenish themselves. But there were hints from fMRI studies of young children that their brains don’t always follow this rule. “The newborn brain is doing something weird,” says study coauthor Elizabeth Hillman of Columbia University. That weirdness, she suspected, might be explained by an immature communication system in young brains. To find out, she and her colleagues looked for neuron-blood connections in mice as they grew. “What we’re trying to do is create a road map for what we think you actually should see,” Hillman says. When 7-day-old mice were touched on their hind paws, a small group of neurons in the brain responded instantly, firing off messages in a flurry of activity. Despite this action, no fresh blood arrived, the team found. By 13 days, the nerve cell reaction got bigger, spreading across a wider stretch of the brain. Still the blood didn’t come. But by the time the mice reached adulthood, neural activity prompted an influx of blood. The results show that young mouse brains lack the ability to send blood to busy neurons, a skill that influences how the brain operates (SN: 11/14/15, p. 22). © Society for Science & the Public 2000 - 2016.

Related chapters from BP7e: 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: 22348 - Posted: 06.22.2016

Bentley Yoder was born with his brain outside his skull. Doctors said he didn’t have a chance, but he not only survived—he thrived. Now, some seven months later, Bentley has undergone reconstructive surgery to move his brain back into his skull. Bentley’s parents, Sierra and Dustin, both 25, found out something was wrong when they went in for a routine ultrasound at 22 weeks. Still in the womb, he was diagnosed with a rare condition called encephalocele, or cranium bifidum, in which parts of the brain protrude outside of gaps that have formed in the developing skull. The parents were told that their baby likely wouldn’t survive very long after birth, or that if he did he wouldn’t have any brain function; he was simply “incompatible with life.” As Sierra told the Washington Post, “We had no hope whatsoever.” The parents were unwilling to terminate the pregnancy, saying they wanted at least one chance to meet him before saying goodbye. To virtually everyone’s surprise, Bentley came out on his due date, October 31, 2015, kicking and screaming. After the first 36 hours, Sierra and Dustin had to take him home wearing the only onesie they bothered to purchase. Over the course of the next few weeks and months, Bentley continued to march on, save for a staph infection in his lungs. Aside from the large sac containing critical parts of his brain atop his head, Bentley developed normally. He continued to grow, and cried when he was hungry. The doctors were incredulous, and insisted that the growth above his head was just “damaged tissue,” and that “there’s no way it could be functioning,” but Bentley’s behaviors and normal developmental trajectory suggested otherwise.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22347 - Posted: 06.22.2016

By Gretchen Reynolds Physical activity is good for our brains. A wealth of science supports that idea. But precisely how exercise alters and improves the brain remains somewhat mysterious. A new study with mice fills in one piece of that puzzle. It shows that, in rodents at least, strenuous exercise seems to beneficially change how certain genes work inside the brain. Though the study was in mice, and not people, there are encouraging hints that similar things may be going on inside our own skulls. For years, scientists have known that the brains of animals and people who regularly exercise are different than the brains of those who are sedentary. Experiments in animals show that, for instance, exercise induces the creation of many new cells in the hippocampus, which is a part of the brain essential for memory and learning, and also improves the survival of those fragile, newborn neurons. Researchers believe that exercise performs these feats at least in part by goosing the body’s production of a substance called brain-derived neurotropic factor, or B.D.N.F., which is a protein that scientists sometimes refer to as “Miracle-Gro” for the brain. B.D.N.F. helps neurons to grow and remain vigorous and also strengthens the synapses that connect neurons, allowing the brain to function better. Low levels of B.D.N.F. have been associated with cognitive decline in both people and animals. Exercise increases levels of B.D.N.F. in brain tissue. But scientists have not understood just what it is about exercise that prompts the brain to start pumping out additional B.D.N.F. So for the new study, which was published this month in the journal eLIFE, researchers with New York University’s Langone Medical Center and other institutions decided to microscopically examine and reverse engineer the steps that lead to a surge in B.D.N.F. after exercise. They began by gathering healthy mice. Half of the animals were put into cages that contained running wheels. The others were housed without wheels. For a month, all of the animals were allowed to get on with their lives. Those living with wheels ran often, generally covering several miles a day, since mice like to run. The others remained sedentary. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22325 - Posted: 06.15.2016

By Brady Dennis In one city after another, the tests showed startling numbers of children with unsafe blood lead levels: Poughkeepsie and Syracuse and Buffalo. Erie and Reading. Cleveland and Cincinnati. In those cities and others around the country, 14 percent of kids — and in some cases more — have troubling amounts of the toxic metal in their blood, according to new research published Wednesday. The findings underscore how despite long-running public health efforts to reduce lead exposure, many U.S. children still live in environments where they're likely to encounter a substance that can lead to lasting behavioral, mental and physical problems. "We've been making progress for decades, but we have a ways to go," said Harvey Kaufman, senior medical director at Quest Diagnostics and a co-author of the study, which was published in the Journal of Pediatrics. "With blood [lead] levels in kids, there is no safe level." Kaufman and two colleagues at Quest, the nation's largest lab testing provider, examined more than 5.2 million blood tests for infants and children under age 6 that were taken between 2009 and 2015. The results spanned every state and the District of Columbia. The researchers found that while blood lead levels declined nationally overall during that period, roughly 3 percent of children across the country had levels that exceed five micrograms per deciliter — the threshold that the Centers for Disease Control and Prevention considers cause for concern. But in some places and among particular demographics, those figures are much higher.

Related chapters from BP7e: 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: 22322 - Posted: 06.15.2016

By BENEDICT CAREY Jerome S. Bruner, whose theories about perception, child development and learning informed education policy for generations and helped launch the modern study of creative problem solving, known as the cognitive revolution, died on Sunday at his home in Manhattan. He was 100. His death was confirmed by his partner, Eleanor M. Fox. Dr. Bruner was a researcher at Harvard in the 1940s when he became impatient with behaviorism, then a widely held theory, which viewed learning in terms of stimulus and response: the chime of a bell before mealtime and salivation, in Ivan Pavlov’s famous dog experiments. Dr. Bruner believed that behaviorism, rooted in animal experiments, ignored many dimensions of human mental experience. In one 1947 experiment, he found that children from low-income households perceived a coin to be larger than it actually was — their desires apparently shaping not only their thinking but also the physical dimensions of what they saw. In subsequent work, he argued that the mind is not a passive learner — not a stimulus-response machine — but an active one, bringing a full complement of motives, instincts and intentions to shape comprehension, as well as perception. His writings — in particular the book “A Study of Thinking” (1956), written with Jacqueline J. Goodnow and George A. Austin — inspired a generation of psychologists and helped break the hold of behaviorism on the field. To build a more complete theory, he and the experimentalist George A. Miller, a Harvard colleague, founded the Center for Cognitive Studies, which supported investigation into the inner workings of human thought. Much later, this shift in focus from behavior to information processing came to be known as the cognitive revolution. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22300 - Posted: 06.09.2016

James Gorman Fruit flies are far from human, but not as far as you might think. They do many of the same things people do, like seek food, fight and woo mates. And their brains, although tiny and not set up like those of humans or other mammals, do many of the same things that all brains do — make and use memories, integrate information from the senses, and allow the creature to navigate both the physical and the social world. Consequently, scientists who study how all brains work like to use flies because it’s easier for them to do invasive research that isn’t allowed on humans. The technology of neuroscience is sophisticated enough to genetically engineer fly brains, and to then use fluorescent chemicals to indicate which neurons are active. But there are some remaining problems, like how to watch the brain of a fly that is moving around freely. It is one thing to record what is going on in a fly’s brain if the insect’s movement is restricted, but quite another to try to catch the light flash of brain cells from a fly that is walking around. Takeo Katsuki, an assistant project scientist at the Kavli Institute at the University of California, San Diego, is interested in courtship. And, he said, fruit flies simply won’t engage in courtship when they are tethered. So he and Dhruv Grover, another assistant project scientist, and Ralph J. Greenspan, in whose lab they both work, set out to develop a method for recording the brain activity of a walking fly. One challenge was to track the fly as it moved. They solved that problem with three cameras to follow the fly and a laser to activate the fluorescent chemicals in the brain. © 2016 The New York Times Company

Related chapters from BP7e: 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: 22290 - Posted: 06.06.2016

By NICHOLAS ST. FLEUR Nine scientists have won this year’s Kavli Prizes for work that detected the echoes of colliding black holes, revealed how adaptable the nervous system is, and created a technique for sculpting structures on the nanoscale. The announcement was made on Thursday by the Norwegian Academy of Science Letters in Oslo, and was live-streamed to a watching party in New York as a part of the World Science Festival. The three prizes, each worth $1 million and split among the recipients, are awarded in astrophysics, nanoscience and neuroscience every two years. They are named for Fred Kavli, a Norwegian-American inventor, businessman and philanthropist who started the awards in 2008 and died in 2013. Eve Marder of Brandeis University, Michael M. Merzenich of the University of California, San Francisco, and Carla J. Shatz of Stanford won the neuroscience prize. Dr. Marder illuminated the flexibility and stability of the nervous system through her work studying crabs and lobsters and the neurons that control their digestion. Dr. Merzenich was a pioneer in the study of neural plasticity, demonstrating that parts of the adult brain, like those of children, can be reorganized by experience. Dr. Shatz showed that “neurons that fire together wire together,” by investigating how patterns of activity sculpt the synapses in the developing brain. The winners will receive their prizes in September at a ceremony in Oslo. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 1: An Introduction to Brain and Behavior
Link ID: 22279 - Posted: 06.04.2016

By Simon Makin Other species are capable of displaying dazzling feats of intelligence. Crows can solve multistep problems. Apes display numerical skills and empathy. Yet, neither species has the capacity to conduct scientific investigations into other species' cognitive abilities. This type of behavior provides solid evidence that humans are by far the smartest species on the planet. Besides just elevated IQs, however, humans set themselves apart in another way: Their offspring are among the most helpless of any species. A new study, published recently in Proceedings of the National Academy of Sciences (PNAS), draws a link between human smarts and an infant’s dependency, suggesting one thing led to the other in a spiraling evolutionary feedback loop. The study, from psychologists Celeste Kidd and Steven Piantadosi at the University of Rochester, represents a new theory about how humans came to possess such extraordinary smarts. Like a lot of evolutionary theories, this one can be couched in the form of a story—and like a lot of evolutionary stories, this one is contested by some scientists. Kidd and Piantadosi note that, according to a previous theory, early humans faced selection pressures for both large brains and the capacity to walk upright as they moved from forest to grassland. Larger brains require a wider pelvis to give birth whereas being bipedal limits the size of the pelvis. These opposing pressures—biological anthropologists call them the “obstetric dilemma”—could have led to giving birth earlier when infants’ skulls were still small. Thus, newborns arrive more immature and helpless than those of most other species. Kidd and Piantadosi propose that, as a consequence, the cognitive demands of child care increased and created evolutionary pressure to develop higher intelligence. © 2016 Scientific American

Related chapters from BP7e: 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: 22277 - Posted: 06.02.2016

By Roland Pease BBC Radio Science Unit Researchers have invented a DNA "tape recorder" that can trace the family history of every cell in an organism. The technique is being hailed as a breakthrough in understanding how the trillions of complex cells in a body are descended from a single egg. "It has the potential to provide profound insights into how normal, diseased or damaged tissues are constructed and maintained," one UK biologist told the BBC. The work appears in Science journal. The human body has around 40 trillion cells, each with a highly specialised function. Yet each can trace its history back to the same starting point - a fertilised egg. Developmental biology is the business of unravelling how the genetic code unfolds at each cycle of cell division, how the body plan develops, and how tissues become specialised. But much of what it has revealed has depended on inference rather than a complete cell-by-cell history. "I actually started working on this problem as a graduate student in 2000," confessed Jay Shendure, lead researcher on the new scientific paper. "Could we find a way to record these relationships between cells in some compact form we could later read out in adult organisms?" The project failed then because there was no mechanism to record events in a cell's history. That changed with recent developments in so called CRISPR gene editing, a technique that allows researchers to make much more precise alterations to the DNA in living organisms. The molecular tape recorder developed by Prof Shendure's team at the University of Washington in Seattle, US, is a length of DNA inserted into the genome that contains a series of edit points which can be changed throughout an organism's life. © 2016 BBC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22259 - Posted: 05.28.2016

by Bruce Bower For a landmark 1977 paper, psychologist Andrew Meltzoff stuck his tongue out at 2- to 3-week-old babies. Someone had to do it. After watching Meltzoff razz them for 15 seconds, babies often stuck out their own tongues within the next 2½ minutes. Newborns also tended to respond in kind when the young researcher opened his mouth wide, pushed out his lips like a duck and opened and closed the fingers of one hand. Meltzoff, now at the University of Washington in Seattle, and a colleague were the first to report that babies copy adults’ simple physical deeds within weeks of birth. Until then, most scientists assumed that imitation began at around 9 months of age. Newborns don’t care that imitation is the sincerest form of flattery. For them, it may be a key to interacting with (and figuring out) those large, smiley people who come to be known as mommy and daddy. And that’s job number one for tykes hoping to learn how to talk and hang out with a circle of friends. Meltzoff suspected that babies enter the world able to compare their own movements — even those they can feel but not see, such as a projecting tongue — to corresponding adult actions. Meltzoff’s report has inspired dozens of papers on infant imitation. Some have supported his results, some haven’t. A new report, published May 5 in Current Biology, falls in the latter group. The study of 106 Australian babies tracked from 1 to 9 weeks of age concludes that infants don’t imitate anyone. © Society for Science & the Public 2000 - 201

Related chapters from BP7e: 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: 22246 - Posted: 05.25.2016

By PAM BELLUCK BALTIMORE — Leave it to the youngest person in the lab to think of the Big Idea. Xuyu Qian, 23, a third-year graduate student at Johns Hopkins, was chatting in late January with Hongjun Song, a neurologist. Dr. Song was wondering how to test their three-dimensional model of a brain — well, not a brain, exactly, but an “organoid,” essentially a tiny ball of brain cells, grown from stem cells and mimicking early brain development. “We need a disease,” Dr. Song said. Mr. Qian tossed out something he’d seen in the headlines: “Why don’t we check out this Zika virus?” Within a few weeks — a nanosecond compared with typical scientific research time — that suggestion led to one of the most significant findings in efforts to answer a central question: How does the Zika virus cause brain damage, including the abnormally small heads in babies born to infected mothers? The answer could spur discoveries to prevent such devastating neurological problems. And time is of the essence. One year after the virus was first confirmed in Latin America, with the raging crisis likely to reach the United States this summer, no treatment or vaccine exists. “We can’t wait,” said Dr. Song, at the university’s Institute for Cell Engineering, where he and his wife and research partner, Dr. Guo-Li Ming, provided a pipette-and-petri-dish-level tour. “To translate our work for the clinic, to the public, normally it takes years. This is a case where we can make a difference right away.” The laboratory’s initial breakthrough, published in March with researchers at two other universities, showed that the Zika virus attacked and killed so-called neural progenitor cells, which form early in fetal development and generate neurons in the brain. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22203 - Posted: 05.11.2016

By DAN BARRY IDIOT. Imbecile. Cretin. Feebleminded. Moron. Retarded. Offensive now but once quite acceptable, these terms figured in the research for a lengthy article I wrote in 2014 about 32 men who spent decades eviscerating turkeys in a meat-processing plant in Iowa — all for $65 a month, along with food and lodging in an ancient former schoolhouse on a hill. These were men with intellectual disability, which meant they had significant limitations in reasoning, learning and problem solving, as well as in adaptive behavior. But even though “intellectual disability” has been the preferred term for more than a decade, it gave my editors and me pause. We wondered whether readers would instantly understand what the phrase meant. What’s more, advocates and academicians were recommending that I suppress my journalistic instinct to tighten the language. I was told that it was improper to call these men “intellectually disabled,” instead of “men with intellectual disability.” Their disability does not define them; they are human beings with a disability. This linguistic preference is part of society’s long struggle to find the proper terminology for people with intellectual disability, and reflects the discomfort the subject creates among many in the so-called non-disabled world. It speaks to a continuing sense of otherness; to perceptions of what is normal, and not. “It often doesn’t matter what the word is,” said Michael Wehmeyer, the director and senior scientist at the Beach Center on Disability at the University of Kansas. “It’s that people associate that word with what their perceptions of these people are — as broken, or as defective, or as something else.” For many years, the preferred term was, simply, idiot. When Massachusetts established a commission on idiocy in the mid-1840s, it appointed Dr. Samuel G. Howe, an abolitionist and early disability rights advocate, as its chairman. The commission argued for the establishment of schools to help this segment of society, but made clear that it regarded idiocy “as an outward sign of an inward malady.” © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22195 - Posted: 05.09.2016

By Jocelyn Kaiser Gene therapy is living up to its promise of halting a rare, deadly brain disease in young boys. In a new study presented in Washington, D.C., yesterday at the annual meeting of the American Society of Gene and Cell Therapy, all but one of 17 boys with adrenoleukodystrophy (ALD) remained relatively healthy for up to 2 years after having an engineered virus deliver into their cells a gene to replenish a missing protein needed by the brain. The results, which expand on an earlier pilot study, bring this ALD therapy one step closer to the clinic. About one in 21,000 boys are born with ALD, which is caused by a flaw in a gene on the X chromosome that prevents cells from making a protein that the cells need to process certain fats—females have a backup copy of the gene on their second X chromosome. Without that protein, the fats build up and gradually destroy myelin sheaths that protect nerves in the brain. In the cerebral form of ALD, which begins in childhood, patients quickly lose vision and mobility, usually dying by age 12. The disease achieved some degree of fame with the 1992 film Lorenzo’s Oil, inspired by a family’s struggle to prolong their son’s life with a homemade remedy. The only currently approved treatment for ALD is a bone marrow transplant -- white blood cells in the marrow go to the brain and turn into glial cells that produce normal ALD proteins. But bone marrow transplants carry many risks, including immune rejection, and matching donors can’t always be found. As an alternative, in the late 2000s, French researchers treated the bone cells of two boys with a modified virus carrying the ALD gene. They reported in Science in 2009 that this halted progression of the disease. © 2016 American Association for the Advancement of Science

Related chapters from BP7e: 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: 22189 - Posted: 05.07.2016

Mo Costandi This spectacular image – which took the best part of a year to create – shows the fine structure of a nerve terminal at high resolution, revealing, for the very first time, an intricate network of fine filaments that controls the movements of synaptic vesicles. The brain is soft and wet, with the consistency of a lump of jelly. Yet, it is the most complex and highly organized structure that we know of, containing hundreds of billions of neurons and glial cells, and something on the order of one quadrillion synaptic connections, all of which are arranged in a very specific manner. This high degree of specificity extends down to the deepest levels of brain organization. Just beneath the membrane at the nerve terminal, synaptic vesicles store neurotransmitter molecules, and await the arrival of a nervous impulse, whereupon they fuse with the membrane and release their contents into the synaptic cleft, the miniscule gap at the junction between nerve cells, and diffuse across it to bind to receptor protein molecules embedded at the surface of the partner cell. 3D model of a nerve terminal in atomic detail The process of neurotransmitter release is tightly orchestrated. Ready vesicles are ‘docked’ in the ‘active zone’ lying beneath the cell membrane, and are depleted when they fuse with the membrane, only to be replenished from a reservoir of pre-prepared vesicles located further inside the cell. Spent vesicles are quickly pulled back out of the membrane, reformed, refilled with neurotransmitter molecules, and then returned to the reservoir, so that they can be shuttled into the active zone when needed. An individual nerve cell may use up hundreds, or perhaps thousands, of vesicles every second, and so this recycling process occurs continuously to maintain the signalling between nerve cells. © 2016 Guardian News and Media Limited

Related chapters from BP7e: 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: 22067 - Posted: 04.04.2016

By DONALD G. McNEIL Jr The World Health Organization said on Thursday that there is “strong scientific consensus” that Zika virus is a cause of microcephaly, unusually small heads with brain damage in infants, as well as other neurological disorders. Yet a surge in microcephaly has been reported only in Brazil; a small increase was reported in French Polynesia, and a cluster of 32 cases is now under investigation in Colombia. For proof of the connection between infection with the virus and birth defects, scientists are waiting for the results of a large study of 5,000 pregnant women, most of them in Colombia. Women with past Zika infections will be compared with similar women without infections to see if they have more microcephalic children. The epidemic peaked in Colombia in early February, according to the W.H.O. Most of the women in the study are due to give birth in May and June. Virtually all public health agencies already believe the virus is to blame for these birth defects and are giving medical advice based on that assumption. Here are the lines of evidence they cite. As early as last August, hospitals in northeast Brazil realized that something unheard of was happening: Neonatal wards that normally saw one or two microcephalic babies a year were seeing five or more at the same time. Doctors learned from the mothers that many of them had had Zika symptoms months earlier. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22065 - Posted: 04.04.2016

By Daisy Yuhas Something was wrong with Brayson Thibodeaux. At 15 months old, he still was not walking; his parents and grandparents were certain that his development was slower than normal. After pushing doctors for answers they finally got him to a neurologist who recommended a genetic test. Brayson had fragile X syndrome, the leading heritable cause of intellectual disability and of autism. The discovery sent ripples through the extended family, who live outside New Orleans. Brayson’s great-grandmother, Cheryl, recalled having heard of fragile X and discovered a cousin whose grandson had the same condition. She soon learned that many members of her family were confirmed carriers of a genetic condition—the fragile X pre-mutation—that put them at risk of having children with this syndrome. “Fragile X” refers to a mutation that alters the X chromosome in such a way that, viewed under a microscope, it would look like a piece was about to break off. That is because one gene contains multiple repetitions of noncoding DNA—specifically CGG (cytosine, guanine, guanine). The exact number of CGG repetitions is variable, but when it reaches more than 200, it is considered to be the full mutation, which causes the syndrome. People with between 55 and 200 repeats are said to have a partial or pre-mutation, an unstable gene that can expand into the full mutation in future generations. © 2016 Scientific American,

Related chapters from BP7e: 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: 22008 - Posted: 03.19.2016

By Perri Klass, M.D. I got my good sleeper second. My oldest child, my first darling baby, did not reliably sleep through the night till he was well past 2. Since he is now an adult, I can skip right over all the questions of whether we could have trained him to self-soothe and stop calling for us in the night — we tried; we failed; we eventually gave up. The good sleeper was a good sleeper right from the beginning. She followed the timeline in the books, slept longer and longer between feedings, till she was reliably giving us a real night while she was still an infant and she never looked back. Had we matured as parents, become less anxious, more willing to let her learn how to soothe herself? Were our lives calmer? Well, no. In fact, kind of the opposite. We just got dealt two very different babies. I supervise pediatric residents as they learn to provide primary care, to offer guidance to parents as they struggle with all the complexities of baby and toddler sleep, eating, potty training, discipline and tantrums. All of the stuff that shapes your daily life with a small child, and I’m talking about an essentially healthy, normally developing small child. And the hardest thing to teach, especially to people who haven’t yet done any child-rearing, is how different those healthy, normal babies can be, right from the beginning. So we review our sensible pediatric rubrics that deal with these questions, from establishing good sleep patterns to setting limits to encouraging a healthy varied diet. But sometimes it seems that these rubrics work best with the children and families who need them least. Every child is a different assignment — and we can all pay lip service to that cheerfully enough. But the hard thing to believe is how different the assignments can be. Within the range of developmentally normal children, some parents have a much, much harder job than others: more drudge work, less gratification, more public shaming. It sometimes feels like the great undiscussed secret of pediatrics — and of parenting © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21988 - Posted: 03.15.2016

Deborah Orr The psychologist Oliver James has for many years been a part of the cultural landscape, writing best-selling books, making television programmes, contributing articles to newspapers and generally offering his views. As a practicing psychotherapist of many years’ standing, he has good reason to believe that he has important insights to offer. James is particularly exercised by the damage caused by casual emotional abuse – the explosive parent who shouts and swears at their kids, displays resentment against them or tries to coerce them into doing things instead of employing reason. No sensible person disagrees with him on this, and only a harsh critic would deny that James has played a strong and positive part in popularising these simple, important wisdoms. That’s why it’s so very odd that James has chosen now to perpetrate casual emotional abuse on a grand scale. His latest book, Not in Your Genes: The Real Reason Parents Are Like Their Children, expands on an argument he’s been making for years: that there is no scientific basis for belief in the idea that there is any genetic element to any psychological trait. Even illnesses such as schizophrenia and bipolar disorder are completely down to the environment in which you grew up, not the complex interplay between nature and nurture that mainstream science espouses. Even if James had conclusive evidence to back up his absolutist claim – which he does not – I would suggest that such news should be broken gently. © 2016 Guardian News and Media Limited

Related chapters from BP7e: 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: 21983 - Posted: 03.14.2016

By DONALD G. McNEIL Jr. and CATHERINE SAINT LOUIS The Zika virus damages many fetuses carried by infected and symptomatic mothers, regardless of when in pregnancy the infection occurs, according to a small but frightening study released on Friday by Brazilian and American researchers. In a separate report published on Friday, other scientists suggested a mechanism for the damage, showing in laboratory experiments that the virus targets and destroys fetal cells that eventually form the brain’s cortex. The reports are far from conclusive, but the studies help shed light on a mysterious epidemic that has swept across more than two dozen countries in the Western Hemisphere, alarming citizens and unnerving public health officials. In the first study, published in The New England Journal of Medicine, researchers found that 29 percent of women who had ultrasound examinations after testing positive for infection with the Zika virus had fetuses that suffered “grave outcomes.” They included fetal death, tiny heads, shrunken placentas and nerve damage that suggested blindness. “This is going to have a chilling effect,” said Dr. Anthony S. Fauci, the director of the National Institute of Allergy and Infectious Diseases. “Now there’s almost no doubt that Zika is the cause.” The small size of the study, which looked at 88 women at one clinic in Rio de Janeiro, was a limitation, Dr. Fauci added. From such a small sample, it is impossible to be certain how often fetal damage may occur in a much larger population. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21957 - Posted: 03.05.2016

Ewan Birney The Daily Mail recently ran an article about how alcohol abuse could harm future generations, via the (exciting-sounding) mechanism of trans-generational epigenetics. This is an emotive topic, combining a commonplace habit (drinking beer and wine) with a scary outcome (harming your children, grandchildren and future generations) and adding a twist of science for gravitas. It’s not surprising that this research has been handed a megaphone by the mainstream press – but does the science stack up? To start with, the research was carried out in rats, as multi-generational experiments on humans are both grossly unethical and logistically extremely hard. This crucial bit of information is missing from both the Daily Mail headline and the paper’s title. Secondly, the big effects of alcohol consumption were mainly seen on the rats’ children and grandchildren – the effects on their great grandchildren were smaller. That is really important, because if there’s no effect on great grandchildren, it’s probably not due to epigenetics. Drinking large amounts of alcohol (for a rat) whilst pregnant would be expected to have an effect on the children and even the grandchildren. This is because the eggs of female mammals are made early on in foetal development, whilst a daughter is developing in the womb. So if that cell (the egg) also gives rise to a daughter, she will have directly experienced exposures that occurred during her maternal grandmother’s pregnancy. © 2016 Guardian News and Media Limited or its affiliated companies.

Related chapters from BP7e: 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: 21945 - Posted: 03.02.2016