Links for Keyword: Development of the Brain

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Lizzie Buchen Teenagers can do terrible things. In 1999, Kuntrell Jackson, then 14, was walking with his cousin and a friend in Blytheville, Arkansas, when they decided to rob a local video store. On the way there, his friend, Derrick Shields, revealed that he was carrying a sawn-off shotgun in his coat sleeve. During the robbery, Shields shot a shop worker in the face, killing her. Four years later, 14-year-old Evan Miller and an older friend were getting drunk and stoned with a middle-aged neighbour in a trailer park in Moulton, Alabama. A fight broke out, and Miller and the friend beat the neighbour with a baseball bat. Then they set fire to his home and ran, leaving him to die. Both Miller and Jackson were found guilty of homicide and sentenced to life without parole, meaning that both will spend the rest of their lives in prison. They are not alone. The United States currently has more than 2,500 individuals serving such sentences for crimes they committed as juveniles — that is, before their eighteenth birthdays. It is the only country that officially punishes juveniles in this way. Both Miller and Jackson appealed, arguing that their immaturity at the time of the crime rendered them less culpable for their actions than adults, and that they deserved a less severe punishment. The Supreme Court heard arguments in Miller v. Alabama and Jackson v. Hobbs in March, and is expected to deliver its ruling by this summer. The cases are notable not only because they could abolish life-without-parole sentences for juveniles, but also because neuroscience research may play a part in the decision. © 2012 Nature Publishing Group,

Related chapters from BP6e: 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: 16669 - Posted: 04.19.2012

Brain wiring a no-brainer?

The brain appears to be wired more like the checkerboard streets of New York City than the curvy lanes of Columbia, Md., suggests a new brain imaging study. The most detailed images, to date, reveal a pervasive 3D grid structure with no diagonals, say scientists funded by the National Institutes of Health. “Far from being just a tangle of wires, the brain's connections turn out to be more like ribbon cables — folding 2D sheets of parallel neuronal fibers that cross paths at right angles, like the warp and weft of a fabric,” explained Van Wedeen, M.D., of Massachusetts General Hospital (MGH), A.A. Martinos Center for Biomedical Imaging and the Harvard Medical School. “This grid structure is continuous and consistent at all scales and across humans and other primate species.” Wedeen and colleagues report new evidence of the brain's elegant simplicity March 30, 2012 in the journal Science. The study was funded, in part, by the NIH's National Institute of Mental Health (NIMH), the Human Connectome Project of the NIH Blueprint for Neuroscience Research, and other NIH components. “Getting a high resolution wiring diagram of our brains is a landmark in human neuroanatomy,” said NIMH Director Thomas R. Insel, M.D. “This new technology may reveal individual differences in brain connections that could aid diagnosis and treatment of brain disorders.” Knowledge gained from the study helped shape design specifications for the most powerful brain scanner of its kind, which was installed at MGH's Martinos Center last fall. The new Connectom diffusion magnetic resonance imaging (MRI) scanner can visualize the networks of crisscrossing fibers — by which different parts of the brain communicate with each other — in 10-fold higher detail than conventional scanners, said Wedeen.

Related chapters from BP6e: 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: 16590 - Posted: 03.31.2012

The Connectome: A New Way To Think About What Makes You You

By Maria Popova The nature vs. nurture debate pitted the hard and social sciences against each other for decades, if not centuries, stirred by a central concern with consciousness, what it means to be human, what makes a person, and, perhaps most interestingly to us egocentric beings, what constitutes character and personality. In Connectome: How the Brain's Wiring Makes Us Who We Are, Massachusetts Institute of Technology Professor of Computational Neuroscience Sebastian Seung proposes a new model for understanding the totality of selfhood, one based on the emerging science of connectomics -- a kind of neuroscience of the future that seeks to map and understand the brain much like genomics has mapped the genome. A "connectome" denotes the sum total of connections between the neurons in a nervous system and, like "genome," implies completeness. It's a complex fingerprint of identity, revealing the differences between brains and, inversely, the specificity of our own uniqueness. Seung proposes a simple theory: We are different because our connectomes differ from one another. With that lens, he argues, any kind of personality change -- from educating yourself to developing better habits -- is a matter of rewiring your connectome. That capacity is precisely what makes the connectome intriguing and infinitely promising -- unlike the genome, which is fixed from the moment of conception, the connetome changes throughout life. Seung explains: Neuroscientists have already identified the basic kinds of change. Neurons adjust, or "reweight," their connections by strengthening or weakening them. Neurons reconnect by creating and eliminating synapses, and they rewire by growing and retracting branches. Finally, entirely new neurons are created and existing ones eliminated through regeneration. © 2012 by The Atlantic Monthly Group

A Neuroscientist's Quest to Reverse Engineer the Human Brain

By Gareth Cook MIT scientist Sebastian Seung describes the audacious plan to find the connectome--a map of every single neuron in the brain. Here, he says, is the secret of human identity. What makes us who we are? Where is our personal history recorded, or our hopes? What explains autism or schiziphrenia or remarkable genius? Sebastian Seung argues that it’s all in the connections our neurons make. In his new book, Connectome , he argues that technology has now reached a point where it is conceivable to start mapping at least portions of the connectome. It’s a daunting task, he says, but without it, neuroscience will be stuck. He answered questions from Mind Matters editor Gareth Cook. Cook: You argue in your book that neuroscience has a fundamental problem. What is the problem? Seung: Most people are familiar with the regional approach to neuroscience: divide the brain into regions such as the "left brain" and "frontal lobe," and figure out what each region does. This approach has helped physicians interpret the symptoms of brain injuries, but at the same time has frustrating limitations. How do regions carry out their functions? Why do they malfunction in mental disorders? What happens to regions when we learn? We can never obtain satisfying answers to these questions if we consider regions as the elementary, indivisible units of the brain. An obvious solution is to understand a region by subdividing it into neurons, and figure out how the neurons work together to perform the region's function. This neuronal approach has the potential to answer the big questions above, but so far has not succeeded. In fact, those who study regions sometimes criticize those who study neurons as too focused on minutiae. © 2012 Scientific American

Related chapters from BP6e: Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 14: Attention and Consciousness
Link ID: 16550 - Posted: 03.22.2012

9-Year-Old Boy's Shrinking Brain Disorder Baffles Doctors

By Ferris Jabr Jason Egan does not walk, talk or eat like most nine-year-olds. He gets around in a wheelchair and depends on a feeding tube threaded into his stomach. He makes signs with his hands to communicate and has mustered the word "mom" on occasion. Although he cannot always articulate his feelings, he clearly feels a great deal. He is often seen smiling and laughing, especially when his father pushes him around the block near their home in Victoria, Australia. So far, no one has figured out exactly what is wrong with Egan. His doctors know that the boy's brain has been shrinking since birth, but he has tested negative for all known neurodegenerative disorders. Jason Egan may have a disease that is new to science. At first, Egan's doctors diagnosed him with cerebral palsy—an umbrella term for a group of related movement disorders. Children with cerebral palsy may have difficulty standing, moving, hearing, seeing and speaking. Their muscles are unusually tense and refuse to stretch, and their joints lock in place; some children experience tremors or seizures as well. In many cases, such children's brains were damaged during pregnancy or childbirth, usually in a way that limited oxygen to developing neurons. Symptoms of cerebral palsy may appear as early as three months—difficulty crawling, for instance—and usually make themselves known by age two. One of the defining features of cerebral palsy is that it is nonprogressive, which means that the severity of symptoms remains relatively constant over one's lifetime. Egan's symptoms, however, have changed over time. In 2009, around his sixth birthday, Egan began to lose what little sign language he had and stopped saying "mom." He started shaking and he did not seem to feel pain anymore, even when he injured himself. © 2012 Scientific American,

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 16520 - Posted: 03.15.2012

The Teen Brain on Rage: How It's Different

By Sheila Eldred In the weeks and months following a tragedy like this week's school shooting in Ohio, experts and lawyers and school psychologists and classmates will try to make sense of the actions of the 17-year-old suspect. In all likelihood, though, no one will ever be able to pinpoint a single reason, said pyschologist David Walsh, author of "Why Do They Act That Way? A Survival Guide to the Adolescent Brain for You and Your Teen." "There are usually multiple factors that take a long time to sort out," Walsh said. "It's irrational, so looking for a reason can be somewhat frustrating. There are many kids who probably share that profile who don't do anything remotely like what he did. Science, however, can shed some light on how he and other teenagers think. "Adolescents can make good decisions," insists B. J. Casey, a neuroscientist at Weill Cornell Medical College. "They can make better decisions than you or I. But it is in the heat of the moment that they get into trouble." That's because the reward-sensitive areas of the brain are maturing with the onset of puberty. There's been a long-held view that teens make poor decisions because they don't think through consequences. Since the 1990s, we've known that brains go through extensive development in adolescence. © 2012 Discovery Communications, LLC

Related chapters from BP6e: 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: 16460 - Posted: 03.01.2012

Pollutants long gone, but disease carries on

By Janet Raloff Exposure to certain pollutants early in a rat’s pregnancy can foster disease in her offspring during their adulthood as well as in subsequent generations, a new study shows. A wide range of pollutants elicited such lasting effects, despite future generations never encountering the triggering pollutant. Some chemicals tested led to premature puberty among great-granddaughters, with an increased risk of disease in reproductive tissues. In some tests, the chemicals disrupted ovarian function, something that in humans could lead to infertility or premature menopause. And another chemical exposure caused premature death of sperm-forming cells in the great-grandsons, researchers report online February 28 in PLoS ONE. Rather than altering genes, the tested pollutants altered chemical switches that regulate genes, reports Michael Skinner and his colleagues at Washington State University in Pullman. These epigenetic switches can lock a gene on or off. These master switches for DNA are fairly easy to modify throughout life. Early in development, a fetus erases any epigenetic changes acquired during its parents’ lifetimes, resetting those switches back to healthy, default programming. Because the fetus has a mechanism to erase such changes, a pollutant’s epigenetic effects shouldn’t occur in subsequent generations, says epigeneticist John McCarrey of the University of Texas at San Antonio, who was not involved in the study. That they did emerge in the new study “is pretty heavy in terms of their potential significance,” he says. © Society for Science & the Public 2000 - 2012

Harsh conditions in childhood have long-term effects

By Laura Sanders VANCOUVER — Living in harsh conditions in an orphanage early in life has long-lasting consequences for a child’s social skills, a new study finds. Children who spent their first two years in a Romanian orphanage behaved abnormally in social interactions with other children, even years after leaving the institution. Life in the orphanage was also linked to brain abnormalities, Charles Nelson of Harvard Medical School reported February 17 at the annual meeting of the American Association for the Advancement of Science. “I think this work nails the really important issues in trying to understand the effects of early life experiences,” said psychologist Janet Werker of the University of British Columbia in Vancouver. Since 1999, Nelson and colleagues have followed 136 children who were abandoned at birth and placed in an orphanage in Bucharest, Romania — a Spartan environment where the children spent hours staring at a white wall and followed a highly regimented schedule of activities. The kids received very little attention from caregivers. Nelson and his team arranged for half of these children to move into individual homes for foster care. (A bias against foster care in Romania made the situation unusual.) Called the Bucharest Early Intervention Project, the experiment offered a way to test the importance of a good environment. © Society for Science & the Public 2000 - 2012

Prune bad brain wiring with magnetic pulses

by Wendy Zukerman ZAPPING the brain with a weak magnetic pulse can wipe out unwanted neural connections in mice at least. The discovery could be turned into a treatment for conditions associated with abnormal neural circuitry, such as schizophrenia. In transcranial magnetic stimulation a magnetic coil induces electric currents in the brain that can strengthen or suppress neural connections. This technique has been shown to improve symptoms in people with brain disorders such as autism and depression. Now, Jennifer Rodger from the University of Western Australia in Crawley and colleagues have found that stimulating the brain at intensities lower than would make a neuron fire can remove unwanted neural connections in mice. As children, our brains produce too many connections between cells. As we develop, some connections are pruned away while others are strengthened. Inept pruning has been implicated in schizophrenia. Rodger's team used genetically modified mice with abnormal connections in an area of the brain called the superior colliculus (SC), which is involved in motion detection. In these mice, 90 per cent of the axons in the SC had extended into the wrong areas. These bad connections make it difficult for the rodents to follow moving objects in their line of sight. © Copyright Reed Business Information Ltd.

Jumping Genes in the Brain Ensure That Even Identical Twins Are Different

By Fred H. Gage and Alysson R. Muotri Your brain is special. So is mine. Differences arise at every level of the organ’s astonishingly intricate architecture; the human brain contains 100 billion neurons, which come in thousands of types and collectively form an estimate of more than 100 trillion interconnections. These differences, in turn, lead to variances in the ways we think, learn and behave and in our propensity for mental illness. How does diversity in brain wiring and function arise? Variations in the genes we inherit from our parents can play a role. Yet even identical twins raised by the same parents can differ markedly in their mental functioning, behavioral traits, and risk of mental illness or neurodegenerative disease. In fact, mice bred to be genetically identical that are then handled in exactly the same way in the laboratory display differences in learning ability, fear avoidance and responses to stress even when age, gender and care are held constant. Something more has to be going on. Certainly the experiences we have in life matter as well; they can, for instance, influence the strength of the connections between particular sets of neurons. But researchers are increasingly finding tantalizing indications that other factors are at work—for instance, processes that mutate genes or affect gene behavior early in an embryo’s development or later in life. Such phenomena include alternative splicing, in which a single gene can give rise to two or more different proteins. Proteins carry out most of the operations in cells, and thus which proteins are made in cells will affect the functioning of the tissues those cells compose. Many researchers are also exploring the role of epigenetic changes—DNA modifications that alter gene activity (increasing or decreasing the synthesis of specific proteins) without changing the information in genes. © 2012 Scientific American,

Wonder Dog

By MELISSA FAY GREENE In May 1999, Donnie Kanter Winokur, 43, a writer and multimedia producer, and her husband, Rabbi Harvey Winokur, 49, beheld the son of their dreams, the child infertility denied them. Andrey, a pale dark-eyed 1-year-old in a cotton onesie, held in a standing position by a caregiver, appeared in a short videotape recorded in a Russian orphanage. If the couple liked the little boy, they could begin the legal process of adopting him. They liked the little boy very much. Four months later, the Winokurs flew to Russia from their home in Atlanta to adopt Andrey, whom they renamed Iyal, and to adopt an unrelated little girl two days younger, whom they named Morasha. All four appear in another orphanage video: the beaming new parents on the happiest day of their lives, the toddlers passive in the arms of the strangers cradling and kissing them. In August 1999, the family arrived home to congratulations, gifts and helium balloons. “Sometime after their 3rd birthdays, our wonderful fairy tale of adopting two Russian babies began to show cracks,” said Donnie Winokur, who is now 55. She is pert and trim, with cropped brown hair and a pursed-lips, lemony expression softened by wearying experience. Unlike bright and cheery Morasha, Iyal grew oppositional and explosive. He was a sturdy, big-hearted boy with a wide and open face, shiny black hair in a bowl cut and a winning giggle. But, triggered by the sight of a cartoon image on a plastic cup, or an encounter with Morasha’s Barbie dolls, he threw tantrums that shook the house. He stuffed himself at mealtimes with an inexplicable urgency. In a fast-moving car, he unfastened his seat belt and tried to jump out. He awoke every night in a rage. “I had panic attacks in the night when I heard him coming,” she said. “I assumed everything was my fault, that I was not a good-enough mother.” © 2012 The New York Times Company

Human Brains Wire Up Slowly but Surely

by Jon Cohen As the father-to-son exchange in the old Cat Stevens song advised, "take your time, think a lot, ... think of everything you’ve got." Turns out the mellow ’70s folkie had stumbled upon what may explain a key feature of our brains that sets us apart from our closest relatives: We unhurriedly make synaptic connections through much of our early childhoods, and this plasticity enables us to slowly wire our brains based on our experiences. Given that humans and chimpanzees share 98.8% of the same genes, researchers have long wondered what drives our unique cognitive and social skills. Yes, chimpanzees are smart and cooperative to a degree, but we clearly outshine them when it comes to abstract thinking, self-regulation, assimilation of cultural knowledge, and reasoning abilities. Now a study that looks at postmortem brain samples from humans, chimpanzees, and macaques collected from before birth to up to the end of the life span for each of these species has found a key difference in the expression of genes that control the development and function of synapses, the connections among neurons through which information flows. As researchers describe in a report published online today in Genome Research, they analyzed the expression of some 12,000 genes—part of the so-called transcriptome—from each species. They found 702 genes in the prefrontal cortex (PFC) of humans that had a pattern of expression over time that differed from the two other species. (The PFC plays a central role in social behavior, working toward goals, and reasoning.) By comparison, genes in the chimpanzee PFC at various life stages had only 55 unique expression patterns—12-fold fewer than found in humans. © 2010 American Association for the Advancement of Science.

Related chapters from BP6e: 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: 16333 - Posted: 02.02.2012

Epigenetics: A Turning Point in Our Understanding of Heredity

By Kara Rogers In a study published in late 2011 in Nature, Stanford University geneticist Anne Brunet and colleagues described a series of experiments that caused nematodes raised under the same environmental conditions to experience dramatically different lifespans. Some individuals were exceptionally long-lived, and their descendants, through three generations, also enjoyed long lives. Clearly, the longevity advantage was inherited. And yet, the worms, both short- and long-lived, were genetically identical. This type of finding—an inherited difference that cannot be explained by variations in genes themselves—has become increasingly common, in part because scientists now know that genes are not the only authors of inheritance. There are ghostwriters, too. At first glance, these scribes seem quite ordinary—methyl, acetyl, and phosphoryl groups, clinging to proteins associated with DNA, or sometimes even to DNA itself, looking like freeloaders at best. Their form is far from the elegant tendrils of DNA that make up genes, and they are fleeting, in a sense, erasable, very unlike genes, which have been passed down through generations for millions of years. But they do lurk, and silently, they exert their power, modifying DNA and controlling genes, influencing the chaos of nucleic and amino acids. And it is for this reason that many scientists consider the discovery of these entities in the late 20th century as a turning point in our understanding of heredity, as possibly one of the greatest revolutions in modern biology—the rise of epigenetics. © 2012 Scientific American

Infants Possess Intermingled Senses

By Maria Konnikova What if every visit to the museum was the equivalent of spending time at the philharmonic? For painter Wassily Kandinsky, that was the experience of painting: colors triggered sounds. Now a study from the University of California, San Diego, suggests that we are all born synesthetes like Kandinsky, with senses so joined that stimulating one reliably stimulates another. The work, published in the August issue of Psychological Science, has become the first experimental confirmation of the infant-synesthesia hypothesis—which has existed, unproved, for almost 20 years. Researchers presented infantsand adults with images of repeating shapes (either circles or triangles) on a split-color background: one side was red or blue, and the other side was yellow or green. If the infants had shape-color associations, the scientists hypothesized, the shapes would affect their color preferences. For instance, some infants might look significantly longer at a green background with circles than at the same green background with triangles. Absent synesthesia, no such difference would be visible. The study confirmed this hunch. Infants who were two and three months old showed significant shape-color associations. By eight months the preference was no longer pronounced, and in adults it was gone altogether. © 2012 Scientific American

Related chapters from BP6e: 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: 16259 - Posted: 01.16.2012

Now We Are Six

By NATALIE ANGIER VIEWED superficially, the part of youth that the psychologist Jean Piaget called middle childhood looks tame and uneventful, a quiet patch of road on the otherwise hairpin highway to adulthood. Said to begin around 5 or 6, when toddlerhood has ended and even the most protractedly breast-fed children have been weaned, and to end when the teen years commence, middle childhood certainly lacks the physical flamboyance of the epochs fore and aft: no gotcha cuteness of babydom, no secondary sexual billboards of pubescence. Yet as new findings from neuroscience, evolutionary biology, paleontology and anthropology make clear, middle childhood is anything but a bland placeholder. To the contrary, it is a time of great cognitive creativity and ambition, when the brain has pretty much reached its adult size and can focus on threading together its private intranet service — on forging, organizing, amplifying and annotating the tens of billions of synaptic connections that allow brain cells and brain domains to communicate. Subsidizing the deft frenzy of brain maturation is a distinctive endocrinological event called adrenarche (a-DREN-ar-kee), when the adrenal glands that sit like tricornered hats atop the kidneys begin pumping out powerful hormones known to affect the brain, most notably the androgen dihydroepiandrosterone, or DHEA. Researchers have only begun to understand adrenarche in any detail, but they see it as a signature feature of middle childhood every bit as important as the more familiar gonadal reveille that follows a few years later. © 2011 The New York Times Company

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 16184 - Posted: 12.27.2011

Age of criminal responsibility 'too low', experts say

Advances in neuroscience suggest the age of criminal responsibility - 10 in England, Wales and Northern Ireland - might be too low, according to a study. The Royal Society report considers areas where recent scientific findings could have an impact on the law. At the age of 10 parts of the brain connected with decision-making and judgement are still developing, the study says. But it says there are limits to how the science can be used in court. Professor Nicholas Mackintosh, who chaired the working group that compiled the study, said: "There's now incontrovertible evidence that the brain continues to develop throughout adolescence." He said some regions of the brain - including parts responsible for decision-making and impulse control - are not fully mature "until at least the age of 20". "Now that clearly has some implications for how adolescents behave," he said. The report notes the concern of some neuroscientists that the current age of criminal responsibility in the UK is set too low. In most European countries it is far higher - 18 in Belgium and 16 in Spain. It also suggests that because of differences between individuals a cut-off age may not be justifiable. Professor Mackintosh said it was for policy makers to decide on altering the age of responsibility, but the changing science meant it should at least be reviewed. BBC © 2011

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 15: Language and Our Divided Brain
Link ID: 16147 - Posted: 12.15.2011

Connected Brain Regions Grow Up Together

by Greg Miller Connectivity is a hot topic in neuroscience these days. Instead of trying to figure out what individual brain regions do, researchers are focusing more on how regions work together as a network to enable memory, language, and decision-making. Now, a study of more than 100 children finds that interconnected brain regions develop in concert through childhood and adolescence. The researchers say their work could have implications for understanding various puzzles in neuroscience, such as what goes wrong in autism or why adolescent boys are prone to risky behavior. To look for evidence of coordinated development across brain regions, Armin Raznahan, a child psychiatrist and neuroscientist at the National Institute of Mental Health in Bethesda, Maryland, and his colleagues tapped into a long-running NIMH project that has been collecting magnetic resonance imaging scans of brain anatomy in children at different ages. They analyzed scans from 108 healthy children who'd had at least three scans taken between the ages of 9 and 22. The researchers calculated the thickness of the cerebral cortex, the brain's outermost layer of tissue, which is involved in virtually every aspect of cognition and behavior. In general, the cortex thickens in early childhood and thins in adolescence or adulthood, Raznahan says. He and his colleagues hypothesized that these changes might happen simultaneously in interconnected brain regions. That's exactly what they found. For example, the team will report tomorrow in Neuron, they saw this pattern in the so-called default mode network, which becomes active when people let their minds wander. "These regions are firing together for a lot of one's life," Raznahan says. "What we've shown is that these regions also seem to mature in close synchrony with each other." © 2010 American Association for the Advancement of Science

Steroids boost survival, reduce brain injury for infants born at 23 weeks

Prenatal steroids — given to pregnant women at risk for giving birth prematurely — appear to improve survival and limit brain injury among infants born as early as the 23rd week of pregnancy, according to a study by a National Institutes of Health research network. Current guidelines recommend giving prenatal steroids to women at risk of delivering between the 24th and 34th weeks of pregnancy. "These findings provide strong evidence that prenatal steroids can benefit infants born as early as the 23rd week of pregnancy," said study author Rosemary D. Higgins, M.D., of the NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). The study was conducted by researchers participating in the NICHD Neonatal Research Network and led by Waldemar A. Carlo, director of the Division of Neonatology at the University of Alabama at Birmingham. The findings appear in the Dec. 7 Journal of the American Medical Association. When given to pregnant woman at risk for preterm delivery, steroid hormones help the fetus's lungs to mature. For infants born preterm, increased lung development improves the chances for survival and may decrease the risk of brain injury. Infants born in the 22nd through the 25th week of pregnancy — far earlier than the 40 weeks of a full term pregnancy — are the smallest, most frail category of newborns. Many die soon after birth, despite the best attempts to save them, including the most sophisticated newborn intensive care available. Some survive, and reach adulthood relatively unaffected. The rest will experience some degree of lifelong disability, including minor hearing loss, cerebral palsy, and intellectual disability.

Babies may benefit from moms’ lasting melancholy

By Bruce Bower Infants generally thrive physically and mentally if their mothers’ emotional condition, whether healthy or depressed, remains stable before and after birth, say psychologist Curt Sandman of the University of California, Irvine, and his colleagues. Kids whose mothers stayed depressed from the fourth month of pregnancy on displayed first-year mental and physical development comparable to that of youngsters whose mothers stayed emotionally healthy for the same stretch, Sandman’s team will report in Psychological Science. In contrast, babies’ first-year physical and mental development lagged if their mothers’ emotional state during pregnancy changed after giving birth. That pattern held whether depression during pregnancy resolved after giving birth or depression first appeared after delivering a child. “A human fetus that prepares for inadequate care after birth based on biological messages from a depressed mother will have a survival advantage,” Sandman says. A fetus that gets thrown a caretaking curve upon leaving the womb — whether biologically primed to expect sufficient or deficient treatment — tends to struggle developmentally, at least for the first year, he suggests. Related investigations have found that people whose mothers nearly starved during pregnancy eventually developed higher rates of diabetes and other metabolic disorders if they received enough food after birth, but not if they too got inadequate nutrition. Until now, no one has reported a health advantage for babies exposed to maternal depression before and after birth. © Society for Science & the Public 2000 - 2011

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 16049 - Posted: 11.19.2011

Two feet or four, software is the same

By Nick Bascom Standing fully erect and balancing on only two feet gives humans a strange strut that sets them apart from all other mobile critters. Yet the basic motor commands that direct a human stride may also get other animals moving, a new study suggests. Although legged vertebrates come in many different shapes and sizes and exhibit a wide variety of walking styles, they may all employ a similar nerve system, located in the spine, to coordinate the muscle activity needed for locomotion, neurophysiologist Francesco Lacquaniti of the University of Rome Tor Vergata and colleagues report in the Nov. 18 Science. Networks of spinal nerve cells, called central pattern generators, contain all the necessary information to time the muscles for the step cycle, says neuroscientist Sten Grillner of the Karolinska Institute in Stockholm, who was not involved in the study. The networks still need to be turned on by the brain, but once triggered, the spinal nerves handle locomotion all on their own. A message to start moving gets generated in the spinal cord and travels down the nerve pathway to specialized nerve cells that deliver the message directly to muscle fibers. The central pattern generators are so autonomous that, in some cases, cats can still walk after having their spinal cords severely damaged. It doesn’t work the same in humans, who typically suffer permanent paralysis after significant spinal shock. © Society for Science & the Public 2000 - 2011

Related chapters from BP6e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 16048 - Posted: 11.19.2011

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