Links for Keyword: Development of the Brain

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Irwin Feinberg, One of the grand strategies nature uses to construct nervous systems is to overproduce neural elements, such as neurons, axons and synapses, and then prune the excess. In fact, this overproduction is so substantial that only about half of the neurons mammalian embryos generate will survive until birth. Why do some neural connections persist, whereas others do not? A common misconception is that neurons that do not make the cut are defective. Although some may indeed be damaged, most simply fail to connect to their chemically defined targets. In a series of brilliant studies performed during the latter half of the 20th century, researchers discovered how pruning works. They found that newborn neurons migrate along chemically defined routes and that when the neurons arrive at their genetically assigned locations, they compete with their “sibling” neurons to connect with predetermined targets. Victorious neurons receive trophic, or nourishing, factors that allow their survival; unsuccessful neurons fade away in a process called apoptosis, or cell death. The timing of cell death is genetically programmed and occurs at different points in the embryonic development of each species. For decades neuroscientists believed that neural pruning ended shortly after birth. But in 1979 the late Peter Huttenlocher, a neurologist at the University of Chicago, demonstrated that this excess production and pruning strategy actually continues for synapses long after birth. Using electron microscopy to analyze carefully selected autopsied human brains, he showed that synapses—the tiny connections between neurons—proliferate after birth, reaching twice their neonatal levels by mid- to late childhood, and then decrease precipitously during adolescence. © 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: 23676 - Posted: 05.30.2017

By Diana Kwon Age as a state of mind is not just the stuff of birthday card clichés. In recent years, scientists have plumbed the molecular depths of the body and surfaced with tell-tale biomarkers of aging, some of which extend to the brain. Now, researchers are harnessing another tool, neuroimaging, to measure the organ’s age, and using that to predict how long a person will live. “People are searching for the tree rings of humans,” James Cole, a research associate at Imperial College London, told The Scientist. Cole and his colleagues recently devised their own technique of predicting the biological age of people’s brains using a combination of machine learning and magnetic resonance imaging (MRI) scans. In a study published last month (April 25) in Molecular Psychiatry, the team reported that this technique was able to predict mortality in humans—people with “older” brains, they found, had greater risk of dying before age 80. To create this marker of brain aging, the researchers first trained a machine-learning algorithm to analyze structural brain scans from a healthy reference sample containing 2,001 individuals between 18 and 90 years old. Then, they used this tool to predict brain age in the Lothian Birth Cohort, a group of 669 adults, all born in 1936. Based on the algorithm’s assessment, individuals who had brains that were “older” than their actual, chronological age also tended to have an increased risk of dying sooner and lower performance on various fitness measures, such as lung function, walking speed, and fluid intelligence. © 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: 23654 - Posted: 05.24.2017

Tina Hesman Saey Face-to-face, a human and a chimpanzee are easy to tell apart. The two species share a common primate ancestor, but over millions of years, their characteristics have morphed into easily distinguishable features. Chimps developed prominent brow ridges, flat noses, low-crowned heads and protruding muzzles. Human noses jut from relatively flat faces under high-domed crowns. Those facial features diverged with the help of genetic parasites, mobile bits of genetic material that insert themselves into their hosts’ DNA. These parasites go by many names, including “jumping genes,” “transposable elements” and “transposons.” Some are relics of former viruses assimilated into a host’s genome, or genetic instruction book. Others are self-perpetuating pieces of genetic material whose origins are shrouded in the mists of time. “Transposable elements have been with us since the beginning of evolution. Bacteria have transposable elements,” says evolutionary biologist Josefa González. She doesn’t think of transposons as foreign DNA. They are parts of our genomes — like genes. “You cannot understand the genome without understanding what transposable elements are doing,” says González, of the Institute of Evolutionary Biology in Barcelona. She studies how jumping genes have influenced fruit fly evolution. Genomes of most organisms are littered with the carcasses of transposons, says Cédric Feschotte, an evolutionary geneticist at the University of Utah in Salt Lake City. Fossils of the DNA parasites build up like the remains of ancient algae that formed the white cliffs of Dover. One strain of maize, the organism in which Nobel laureate Barbara McClintock first discovered transposable elements in the 1940s, is nearly 85 percent transposable elements (SN: 12/19/09, p. 9). Corn is an extreme example, but humans have plenty, too: Transposable elements make up nearly half of the human genome. |© Society for Science & the Public 2000 - 2017

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23627 - Posted: 05.17.2017

Katherine Hobson American Indian and Alaska Native families are much more likely to have an infant die suddenly and unexpectedly, and that risk has remained higher than in other ethnic groups since public health efforts were launched to prevent sudden infant death syndrome in the 1990s. African-American babies also face a higher risk, a study finds. American Indians and Alaska Natives had a rate of 177.6 sudden unexplained infant deaths per 100,000 live births in 2013 (down from 237.5 per 100,000 in 1995) compared with 172.4 for non-Hispanic blacks (down from 203), 84.5 for non-Hispanic whites (down from 93), 49.3 for Hispanics (down from 62.7) and 28.3 for Asians and Pacific Islanders (down from 59.3). The declines were statistically significant only among non-Hispanic blacks, Hispanics and Asians/Pacific Islanders. "There are still significant gaps and disparities between races and ethnicities," says Lori Feldman-Winter, a professor of pediatrics at Cooper University Health Care in Camden, N.J., who wasn't involved with this study but was a co-author of the most recent sleep guidelines from the American Academy of Pediatrics, released in the fall. Overall rates of sudden unexpected infant death, which includes sudden infant death syndrome as well as accidental suffocation or strangulation in bed and other unexplained deaths, declined sharply in the five or so years after a national campaign was launched in 1994 to encourage caregivers to put babies to sleep on their backs. But the rates have not declined since 2000. Researchers at the Centers for Disease Control and Prevention wanted to know whether those changes were uniform across racial and ethnic groups. © 2017 npr

Related chapters from BN8e: Chapter 14: Biological Rhythms, Sleep, and Dreaming; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 10: Biological Rhythms and Sleep; Chapter 13: Memory, Learning, and Development
Link ID: 23616 - Posted: 05.16.2017

by Laura Sanders One of the most pressing and perplexing questions parents have to answer is what to do about screen time for little ones. Even scientists and doctors are stumped. That’s because no one knows how digital media such as smartphones, iPads and other screens affect children. The American Academy of Pediatrics recently put out guidelines, but that advice was based on a frustratingly slim body of scientific evidence, as I’ve covered. Scientists are just scratching the surface of how screen time might influence growing bodies and minds. Two recent studies point out how hard these answers are to get. But the studies also hint that the answers might be important. In the first study, Julia Ma at the University of Toronto and colleagues found that, in children younger than 2, the more time spent with a handheld screen, such as a smartphone or tablet, the more likely the child was to show signs of a speech delay. Ma presented the work May 6 at the 2017 Pediatric Academic Societies Meeting in San Francisco. The team used information gleaned from nearly 900 children’s 18-month checkups. Parents answered a questionnaire about their child’s mobile media use and then filled out a checklist designed to identify heightened risk of speech problems. This checklist is a screening tool that picks up potential signs of trouble; it doesn’t offer a diagnosis of a language delay, points out study coauthor Catherine Birken, a pediatrician at The Hospital for Sick Children in Toronto. Going into the study, the researchers didn’t have expectations about how many of these toddlers were using handheld screens. “We had very little clues, because there is almost no literature on the topic,” Birken says. “There’s just really not a lot there.” |© Society for Science & the Public 2000 - 2017

Related chapters from BN8e: Chapter 14: Biological Rhythms, Sleep, and Dreaming; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 10: Biological Rhythms and Sleep; Chapter 13: Memory, Learning, and Development
Link ID: 23608 - Posted: 05.13.2017

Ian Sample Science editor A landmark project to map the wiring of the human brain from womb to birth has released thousands of images that will help scientists unravel how conditions such as autism, cerebral palsy and attention deficit disorders arise in the brain. The first tranche of images come from 40 newborn babies who were scanned in their sleep to produce stunning high-resolution pictures of early brain anatomy and the intricate neural wiring that ferries some of the earliest signals around the organ. The initial batch of brain scans are intended to give researchers a first chance to analyse the data and provide feedback to the senior scientists at King’s College London, Oxford University and Imperial College London who are leading the Developing Human Connectome Project, which is funded by €15m (£12.5m) from the EU. The images show the intricate neural wiring that ferries some of the earliest signals around the brain. Hundreds of thousands more images will be released in the coming months and years. Most will come from a thousand sleeping babies, but another 500 have had their brains scanned while still in the womb. “The challenge is that you are imaging one person inside another person and both of them move,” said Jo Hajnal, professor of imaging science at King’s College London, who developed new MRI technology for the project. Taking brain scans of sleeping babies is hard enough. At the start of the project in 2013, more than 10% of the scans failed when babies woke up in the middle of the two to three hour procedure. Now the babies are fed and prepared for their scans at their mother’s side before they are carried to the scanner. To cut the odds of the babies waking, scientists tweaked the scanner software to stop it making sudden noises.

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: 23599 - Posted: 05.10.2017

By Simon Makin The past few decades have seen intensive efforts to find the genetic roots of neurological disorders, from schizophrenia to autism. But the genes singled out so far have provided only sketchy clues. Even the most important genetic risk factors identified for autism, for example, may only account for a few percent of all cases. Much frustration stems from the realization that the key mutations elevating disease risk tend to be rare, because they are less likely to be passed on to offspring. More common mutations confer only small risks (although those risks become more significant when calculated across an entire population). There are several other places to look for the missing burden of risk, and one surprising possible source has recently emerged—an idea that overturns a fundamental tenet of biology and has many researchers excited about a completely new avenue of inquiry. Accepted dogma holds that—although every cell in the body contains its own DNA—the genetic instructions in each cell nucleus are identical. But new research has now proved this assumption wrong. There are actually several sources of spontaneous mutation in somatic (nonsex) cells, resulting in every individual containing a multitude of genomes—a situation researchers term somatic mosaicism. “The idea is something that 10 years ago would have been science fiction,” says biochemist James Eberwine of the University of Pennsylvania. “We were taught that every cell has the same DNA, but that's not true.” There are reasons to think somatic mosaicism may be particularly important in the brain, not least because neural genes are very active. © 2017 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 23565 - Posted: 05.04.2017

By Ruth Williams | When the immune system has eliminated the last traces of Zika virus from the blood, low-level infection may continue at certain sites around the body. A study published in Cell today (April 27) reveals that the cerebrospinal fluid (CSF) is one such sanctuary, which, if also true for infected humans, may have implications for long-term neurological health. “Up until now, everyone was focused on the acute [infection]—what happens when a person gets infected initially by a mosquito bite. But what this paper tells us is that maybe, two months down the line, symptoms could manifest from this later stage of virus replication in the central nervous system and other sites,” said microbiologist and immunologist Andres Pekosz of the Johns Hopkins Bloomberg School of Public Health in Baltimore who was not involved in the research. “Right now, we may be missing some of the disease associated with infection because we’re not looking far enough down the path.” Zika virus infection generally causes a short acute illness of fever, fatigue, headache and other mild symptoms, or can be entirely asymptomatic. But, in pregnant women, infection can cause grievous fetal abnormalities, including microcephaly. In rare cases, Zika can also induce Guillain-Barré syndrome and other neurological symptoms in adults. © 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: 23550 - Posted: 04.29.2017

By Olga Mecking When I was a new mother, the parenting books I read encouraged me to treat child-rearing like a science project. I was told to pay particular attention to my baby’s developing brain, which was malleable and awe-inspiring, but also fragile. I thought I was supposed to provide an optimal environment for my children’s brain growth, because didn’t they deserve the very best? And the earlier I started the better, because the stakes were high. If I failed, my children could develop any number of mental disorders. At least, that was my impression after having read nearly every parenting book on the market. I also expected to spontaneously and intuitively know how to care for my babies. But I didn’t have a clue, and articles like these made me feel like a failure. Was it so unnatural for a mother to want time to herself, or to not want to become one with her baby? It seemed that way, but Jan Macvarish, author of the recent book, “Neuroparenting: The Expert Invasion of Family Life,” disagrees. Macvarish is deeply concerned about this ultra-scientific approach to parenting, in part because it reduces everything to the mother-child relationship. “To talk about parenting in this way is untruthful because this isn’t the way that any child is raised,” she says. “There are always other people involved.” And she’s right. I felt that I was solely responsible for my children’s well-being, and that pressure started to get to me. What kind of mother was I if I couldn’t take care of my babies’ developing brains properly? © 1996-2017 The Washington Post

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23547 - Posted: 04.28.2017

Jon Hamilton Tiny, 3-D clusters of human brain cells grown in a petri dish are providing hints about the origins of disorders like autism and epilepsy. An experiment using these cell clusters — which are only about the size of the head of a pin — found that a genetic mutation associated with both autism and epilepsy kept developing cells from migrating normally from one cluster of brain cells to another, researchers report in the journal Nature. "They were sort of left behind," says Dr. Sergiu Pasca, an assistant professor of psychiatry and behavioral sciences at Stanford. And that type of delay could be enough to disrupt the precise timing required for an actual brain to develop normally, he says. The clusters — often called minibrains, organoids or spheroids — are created by transforming skin cells from a person into neural stem cells. These stem cells can then grow into structures like those found in the brain and even form networks of communicating cells. Brain organoids cannot grow beyond a few millimeters in size or perform the functions of a complete brain. But they give scientists a way to study how parts of the brain develop during pregnancy. "One can really understand both a process of normal human brain development, which we frankly don't understand very well, [and] also what goes wrong in the brain of patients affected by diseases," says Paola Arlotta, a professor of stem cell and regenerative biology at Harvard who was not involved in the cell migration study. Arlotta is an author of a second paper in Nature about creating a wide variety of brain cells in brain organoids. © 2017 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 23545 - Posted: 04.27.2017

Laura Sanders Plasma taken from human umbilical cords can rejuvenate old mice’s brains and improve their memories, a new study suggests. The results, published online April 19 in Nature, may ultimately help scientists develop ways to stave off aging. Earlier studies have turned up youthful effects of young mice’s blood on old mice (SN: 12/27/14, p. 21). Human plasma, the new results suggest, confers similar benefits, says study coauthor Joseph Castellano, a neuroscientist at Stanford University. The study also identifies a protein that’s particularly important for the youthful effects, a detail that “adds a nice piece to the puzzle,” Castellano says. Identifying the exact components responsible for rejuvenating effects is important, says geroscientist Matt Kaeberlein of the University of Washington in Seattle. That knowledge will bring scientists closer to understanding how old tissues can be rejuvenated. And having the precise compounds in hand means that scientists might have an easier time translating therapies to people. Kaeberlein cautions that the benefits were in mice, not people. Still, he says, “there is good reason to be optimistic that some of these approaches will have similar effects on health span in people.” Like people, as mice age, brain performance begins to slip. Compared with younger generations, elderly mice perform worse on some tests of learning and memory, taking longer to remember the location of an escape route out of a maze, for instance. Researchers suspect that these deficits come from age-related trouble in the hippocampus, a brain structure important for learning and memory. |© 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: 23517 - Posted: 04.20.2017

Tara García Mathewson You saw the pictures in science class—a profile view of the human brain, sectioned by function. The piece at the very front, right behind where a forehead would be if the brain were actually in someone’s head, is the pre-frontal cortex. It handles problem-solving, goal-setting, and task execution. And it works with the limbic system, which is connected and sits closer to the center of the brain. The limbic system processes emotions and triggers emotional responses, in part because of its storage of long-term memory. When a person lives in poverty, a growing body of research suggests the limbic system is constantly sending fear and stress messages to the prefrontal cortex, which overloads its ability to solve problems, set goals, and complete tasks in the most efficient ways. This happens to everyone at some point, regardless of social class. The overload can be prompted by any number of things, including an overly stressful day at work or a family emergency. People in poverty, however, have the added burden of ever-present stress. They are constantly struggling to make ends meet and often bracing themselves against class bias that adds extra strain or even trauma to their daily lives. And the science is clear—when brain capacity is used up on these worries and fears, there simply isn’t as much bandwidth for other things. Economic Mobility Pathways, or EMPath, has built its whole service-delivery model around this science, which it described in its 2014 report, “Using Brain Science to Design New Pathways Out of Poverty.” The Boston nonprofit started out as Crittenton Women’s Union, a merger of two of the city’s oldest women-serving organizations, both of which focused on improving the economic self-sufficiency of families. It continues that work with a new name and a burgeoning focus on intergenerational mobility. © 2017 by The Atlantic Monthly Group.

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: 23514 - Posted: 04.20.2017

By TIM REQUARTH SAN FRANCISCO — On a cloudy afternoon in the Bayview district, Shaquille, 21, was riding in his sister’s 1991 Acura when another car ran a stop sign, narrowly missing them. Both cars screeched to a halt, and Shaquille and the other driver got out. “I just wanted to talk,” he recalls. But the talk became an argument, and the argument ended when Shaquille sent the other driver to the pavement with a left hook. Later that day, he was arrested and charged with felony assault. He already had a misdemeanor assault conviction — for a fight in a laundromat when he was 19. This time he might land in prison. Instead, Shaquille — who spoke on condition that his full name not be used, lest his record jeopardize his chances of finding a job — wound up in San Francisco’s Young Adult Court, which offered him an alternative. For about a year, he would go to the court weekly to check in with Judge Bruce E. Chan. Court administrators would coordinate employment, housing and education support for him. He would attend weekly therapy sessions and life-skills classes. In return, he would avoid trial and, on successful completion of the program, the felony charge would be reduced to a misdemeanor. This was important, because a felony record would make it nearly impossible for him to get a job. “These are transitional-age youth,” said Carole McKindley-Alvarez, who oversees case management for the court. “They’re supposed to make some kind of screwed-up choices. We all did. That’s how you learn.” © 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: 23502 - Posted: 04.18.2017

By Jef Akst | Previous research has shown that high doses of broad-spectrum antibiotics can affect the behavior of adult animals, and numerous epidemiological studies have begun to link early-life antibiotic use to diverse ailments in humans. A study published last week (April 4) in Nature Communications adds to this growing literature, demonstrating that even low, clinically relevant doses of the classic narrow-spectrum antibiotic penicillin can trigger changes in the gut microbiome, in the blood-brain barrier and brain chemistry, and in the behaviors of mice exposed at a young age. Treating the mice with Lactobacillus rhamnosus bacteria, however, helped protect the mice against the effects of early-life, low-dose penicillin exposure. “There are almost no babies in North America that haven’t received a course of antibiotics in their first year of life,” McMaster University coauthor John Bienenstock, who is also the director of the Brain-Body Institute at St. Joseph’s Healthcare Hamilton, said in a press release. “In this paper, we report that low-dose penicillin taken late in pregnancy and in early life of mice offspring, changes behavior and the balance of microbes in the gut. While these studies have been performed in mice, they point to popular increasing concerns about the long-term effects of antibiotics. Furthermore, our results suggest that a probiotic might be effective in preventing the detrimental effects of the penicillin.” Bienenstock and colleagues gave pregnant female mice low doses of penicillin during their last week of gestation, and continued to treat their pups until they weaned a few weeks after birth. At six weeks old, mice exposed to the antibiotic were less social, slightly less anxious, and more aggressive than unexposed mice, the team reported. In the animals’ brains, the researchers found evidence of a thinned blood-brain barrier, as well as increased production of cytokines and heightened activity of a gene that has been linked to aggressive behavior. © 1986-2017 The Scientist

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: 23474 - Posted: 04.11.2017

Nicola Davis Sitting in a padded car seat, a small black and white bullseye stuck to his cheek, four-month-old Teo Bosten-Lam gazes at a computer. The screen is a mottled grey, like the snow on a old-fashioned television, but in the top right-hand corner is a deep blue circle. Teo has spotted it. He glances at the circle and, as he does so, it morphs into a smiley face and a triumphant jingle fills the darkened room. Buoyed by the reaction, he looks around. Suddenly a black and white spinning disc appears on the screen, issuing a sound that can only be described as “boing”. “Babies can’t resist the black and white swirl things,” says researcher Alice Skelton. “When they look away we play it and it brings them back to the screen.” A PhD student in the baby lab at the University of Sussex, Skelton is attempting to unpick a conundrum that has fascinated parents and scientists alike: when it comes to colour, exactly what can babies can see? It’s a mission that takes technology: Teo’s ability to pick up on colour is being probed with an eye-tracking system. The sticker on his cheek directs the camera to his face, while his corneal reflections and the position of his pupils are automatically detected. “What we are looking to see is, do you have to have a more saturated blue for a baby to see it than you would for a red, for example,” says Skelton. If Teo can see a colour, the novelty will attract his attention, triggering the smiley face and jingle. And this isn’t the only ingenious idea. At the first sound that indicates our participant is becoming fed up with this science lark, the screen flashes to a clip from the 1980s cartoon Dogtanian. Teo, once again, is transfixed.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 7: Vision: From Eye to Brain
Link ID: 23473 - Posted: 04.11.2017

By Tracy Vence Last year, 5 percent of the babies born to nearly 1,000 mothers in the U.S. who showed signs of Zika virus infection during their pregnancies had birth defects, the US Centers for Disease Control and Prevention (CDC) reported this week (April 3). Among babies born to the 250 US mothers with confirmed Zika infection during their pregnancies, just shy of 10 percent had birth defects. The agency’s latest analysis is based on data from the US Zika Pregnancy Registry, which does not include information from Puerto Rico (where CDC has a separate database). During a press briefing, CDC Acting Director Anne Schuchat told reporters that researchers and clinicians have observed a variety of brain-related birth defects in babies with congenital Zika infection, beyond microcephaly. “Some seemingly healthy babies . . . may have developmental problems that become evident months after birth,” she said. “Although we’re still learning about the full range of birth defects that can occur when a women is infected with Zika during pregnancy, we’ve seen that it can cause brain abnormalities, vision problems, hearing problems, and other consequences of brain damage that might require lifelong specialized care.” Schuchat described cases of congenital Zika infection in which babies experienced seizures, reduced motor control, feeding difficulties, missed developmental milestones (like sitting up), or inconsolable crying. “These circumstances are just heartbreaking,” she said. © 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: 23461 - Posted: 04.07.2017

By Eric Boodman, MEDFORD, Mass. — They look like little more than grayish-black grains of couscous floating in water. But they are actually African clawed frogs-to-be, replete with minuscule blobs that will become eyes. “These little beans here are what I do the surgery on,” said Douglas Blackiston, a postdoctoral fellow at Tufts University’s Allen Discovery Center, holding out a Petri dish. On Thursday, Blackiston published the results of a few years’ worth of those microscopic surgeries, and the finding is bizarre: If you transplant an eye onto what will become the tadpole’s tail, that organ — misplaced though it may be — can allow the animal to see. Admittedly, it’s impossible for humans to look through a clawed frog’s eyes, and in this case, Blackiston and the director of his lab, Michael Levin, were mainly testing whether the tadpoles could perceive movement and colored light. But they say their research doesn’t just have implications for scientists’ ability to restore vision; it also sheds light on how to connect implants and grafts to the body’s own wiring. “You implant these organs, but you want them to be functionally integrated with the host nervous system otherwise they aren’t going to work,” said Levin, the lead author of a paper published Thursday in Nature Regenerative Medicine. Do you have to “connect up every neuron,” he wondered, or can you make use of the natural ability of the nervous system to adapt and rewire itself? © 2017 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 7: Vision: From Eye to Brain
Link ID: 23433 - Posted: 03.31.2017

By ALICE CALLAHAN Peruse the infant formula aisle, or check out the options for prenatal nutritional supplements, and you’ll find that nearly all these products boast a “brain nourishing” omega-3 fatty acid called DHA. But despite decades of research, it’s still not clear that DHA in formula boosts brain health in babies, or that mothers need to go out of their way to take DHA supplements. A systematic review of studies published this month by the Cochrane Collaboration concluded there was no clear evidence that formula supplementation with DHA, or docosahexaenoic acid, a nutrient found mainly in fish and fish oil, improves infant brain development. At the same time, it found no harm from adding the nutrient. The findings are consistent with a review of the effects of omega-3 supplements in pregnancy and infancy published by the Agency for Healthcare Research and Quality last fall that found little evidence of benefit. Still, many experts believe there is value in including DHA in formula. “Even if you can’t easily prove it, because it’s hard to prove developmental outcomes, it makes sense to use it,” said Dr. Steven Abrams, a professor of pediatrics at Dell Medical School at the University of Texas at Austin. “It’s probably a good idea to keep it in there, and it’s certainly safe.” During pregnancy and the first few years of life, DHA accumulates in the brain and retina of the eye and plays an important role in neural and vision development. Breast milk contains DHA in varying concentrations, depending on how much is in the mother’s diet, and some DHA can be made in the body from precursor omega-3 fatty acids, although this process is inefficient. © 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: 23428 - Posted: 03.30.2017

Rae Ellen Bichell Exposure to lead as a child can affect an adult decades later, according to a study out Tuesday that suggests a link between early childhood lead exposure and a dip in a person's later cognitive ability and socioeconomic status. Lead in the United States can come from lots of sources: old, peeling paint; contaminated soil; or water that's passed through lead pipes. Before policies were enacted to get rid of lead in gasoline, it could even come from particles in the fumes that leave car tailpipes. "It's toxic to many parts of the body, but in particular in can accumulate in the bloodstream and pass through the blood brain barrier to reach the brain," says the study's first author, Aaron Reuben, a graduate student in clinical psychology at Duke University. Reuben and his colleagues published the results of a long-term study on the lingering effects of lead. Researchers had kept in touch with about 560 people for decades — starting when they were born in Dunedin, New Zealand, in the 1970s, all the way up to the present. As children, the study participants were tested on their cognitive abilities; researchers determined IQ scores based on tests of working memory, pattern recognition, verbal comprehension and ability to solve problems, among other skills. When the kids were 11 years old, researchers tested their blood for lead. (That measurement is thought to be a rough indicator of lead exposure in the few months before the blood draw.) Then, when they turned 38 years old, the cognitive ability of these study participants was tested again. As Reuben and his colleagues write in this week's issue of JAMA, the journal of the American Medical Association, they found a subtle but worrisome pattern in the data. © 2017 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23422 - Posted: 03.29.2017

By Linda Geddes A gentle touch can make all the difference. Premature babies – who miss out on the sensory experiences of late gestation – show different brain responses to gentle touch from babies that stay inside the uterus until term. This could affect later physical and emotional development, but regular skin-to-skin contact from parents and hospital staff seem to counteract it. Infants who are born early experience dramatic events at a time when babies that aren’t born until 40 weeks are still developing in the amniotic fluid. Premature babies are often separated from their parents for long periods, undergo painful procedures like operations and ventilation, and they experience bigger effects of gravity on the skin and muscles. “There is substantial evidence that pain exposure during early life can cause long-term alterations in infant brain development,” says Rebeccah Slater at the University of Oxford. But it has been less clear how gentle touches shape the brains of babies, mainly because the brain’s response to light touch is about a hundredth of that it has to pain, so it’s harder to study. Nathalie Maitre of the Nationwide Children’s Hospital in Columbus, Ohio, and her colleagues have gently stretched soft nets of 128 electrodes over the heads of 125 preterm and full-term babies, shortly before they were discharged from hospital. These were used to record how their brains responded to a gentle puff of air on the skin. © Copyright Reed Business Information Ltd.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 23371 - Posted: 03.17.2017