Posts tagged brain development
Articles and news from the latest research reports.
Immune System Has Dramatic Impact on Children’s Brain Development
New research from the University of Virginia School of Medicine has revealed the dramatic effect the immune system has on the brain development of young children. The findings suggest new and better ways to prevent developmental impairment in children in developing countries, helping to free them from a cycle of poverty and disease, and to attain their full potential.
U.Va. researchers working in Bangladesh determined that the more days infants suffered fever, the worse they performed on developmental tests at 12 and 24 months. They also found that elevated levels of inflammation-causing proteins in the blood were associated with worse performance, while higher levels of inflammation-fighting proteins were associated with improved performance.
“The problem we sought to address was why millions of young children in low- and middle-income countries are not attaining their full developmental potential,” said lead author Nona Jiang, who performed the research while an undergraduate student in the laboratory of Dr. William Petri Jr. “Early childhood is an absolutely critical time of brain development, and it’s also a time when these children are suffering from recurrent infections. Therefore, we asked whether these infections are contributing to the impaired development we observe in children growing up in adversity.”
Their findings offer a potential explanation for the developmental impairment seen in children living in poverty. They also offer important direction for doctors attempting to combat the problem: By preventing inflammation, physicians may be able to enhance children’s mental ability for a lifetime.
“We are interested in examining factors that predict healthy child development around the world,” said researcher Dr. Rebecca Scharf of U.Va.’s Department of Pediatrics. “By studying which early childhood influences are associated with hindrances to growth and learning, we will know better where to target interventions for the critical period of early childhood.”
In addition, the finding illuminates the complex relationship between the immune system and cognitive development, an increasingly important area of research that U.Va. has helped pioneer.
“This is a very interesting study, showing, probably for the first time, the link between peripheral cytokine levels and improved cognitive development in humans,” said Jonathan Kipnis, a professor of neuroscience and director of U.Va.’s Center for Brain Immunology & Glia. “What is of the most interest and of a great novelty is the fact that [inflammation-fighting cytokines] have positive correlation with cognitive function. My lab published results showing that these IL-4 cytokines are required for proper brain function in mice, and this work from Dr. Petri’s lab completely independently shows similar correlation in humans.
“I hope the scientific community will appreciate how dramatic the effects of the immune system are on the central nervous system and will invest more efforts in studying and better understanding these complex and intriguing interactions between the body’s two major systems.”
(Source: news.virginia.edu)
Family problems experienced in childhood and adolescence affect brain development
New research has revealed that exposure to common family problems during childhood and early adolescence affects brain development, which could lead to mental health issues in later life.
The study led by Dr Nicholas Walsh, lecturer in developmental psychology at the University of East Anglia, used brain imaging technology to scan teenagers aged 17-19. It found that those who experienced mild to moderate family difficulties between birth and 11 years of age had developed a smaller cerebellum, an area of the brain associated with skill learning, stress regulation and sensory-motor control. The researchers also suggest that a smaller cerebellum may be a risk indicator of psychiatric disease later in life, as it is consistently found to be smaller in virtually all psychiatric illnesses.
Previous studies have focused on the effects of severe neglect, abuse and maltreatment in childhood on brain development. However the aim of this research was to determine the impact, in currently healthy teenagers, of exposure to more common but relatively chronic forms of ‘family-focused’ problems. These could include significant arguments or tension between parents, lack of affection or communication between family members, physical or emotional abuse, and events which had a practical impact on daily family life and might have resulted in health, housing or school problems.
Dr Walsh, from UEA’s School of Psychology, said: “These findings are important because exposure to adversities in childhood and adolescence is the biggest risk factor for later psychiatric disease. Also, psychiatric illnesses are a huge public health problem and the biggest cause of disability in the world.
“We show that exposure in childhood and early adolescence to even mild to moderate family difficulties, not just severe forms of abuse, neglect and maltreatment, may affect the developing adolescent brain. We also argue that a smaller cerebellum may be an indicator of mental health issues later on. Reducing exposure to adverse social environments during early life may enhance typical brain development and reduce subsequent mental health risks in adult life.”
The study, which was conducted with the University of Cambridge and the Medical Research Council Cognition and Brain Sciences Unit, Cambridge, is published in the journal NeuroImage: Clinical.
The 58 teenagers who took part in the brain scanning were drawn from a larger study of 1200 young people, whose parents were asked to recall any negative life events their children had experienced between birth and 11 years of age. The interviews took place when the children were aged 14 and of the 58, 27 were classified as having been exposed to childhood adversities. At ages 14 and 17 the teenagers themselves also reported any negative events and difficulties they, their family or closest friends had experienced during the previous 12 months.
A “significant and unexpected” finding was that the participants who reported stressful experiences when aged 14 were subsequently found to have increased volume in more regions of the brain when they were scanned aged 17-19. Dr Walsh said this could mean that mild stress occurring later in development may ‘inoculate’ teenagers, enabling them to cope better with exposure to difficulties in later life, and that it is the severity and timing of the experiences that may be important.
“This study helps us understand the mechanisms in the brain by which exposure to problems in early-life leads to later psychiatric issues,” said Dr Walsh. “It not only advances our understanding of how the general psychosocial environment affects brain development, but also suggests links between specific regions of the brain and individual psychosocial factors. We know that psychiatric risk factors do not occur in isolation but rather cluster together, and using a new technique we show how the general clustering of adversities affects brain development.”
The researchers also found at that those who had experienced family problems were more likely to have had a diagnosed psychiatric illness, have a parent with a mental health disorder and have negative perceptions of their how their family functioned.
Image caption: Stem cells in the cortex of a mouse embryo (cell nuclei: blue). © MPI f. Molecular Cell Biology and Genetics/ D. Stenzel
Brain development - the pivotal role of the stem cell environment
Higher mammals, such as humans, have markedly larger brains than other mammals. Scientists from the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden recently discovered a new mechanism governing brain stem cell proliferation. It serves to boost the production of neurons during development, thus causing the enlargement of the cerebral cortex – the part of the brain that enables us humans to speak, think and dream. The surprising discovery made by the Dresden-based researchers: two components in the stem cell environment – the extracellular matrix and thyroid hormones – work together with a protein molecule found on the stem cell surface, a so-called integrin. This likely explains why iodine deficiency in pregnant women has disastrous consequences for the unborn child, affecting its brain development adversely – without iodine, no thyroid hormones are produced. “Our study highlights this relationship and provides a potential explanation for the condition neurologists refer to as cretinism”, says Wieland Huttner, Director at the Max Planck Institute in Dresden. This neurological disorder severely impairs the mental abilities of a person.
In the course of evolution, certain mammals, notably humans, have developed larger brains than others, and therefore more advanced cognitive abilities. Mice, for example, have brains that are around a thousand times smaller than the human one. In their study, which was conducted in cooperation with the Fritz Lipmann Institute in Jena, the researchers in Dresden wanted to identify factors that determine brain development, and understand how larger brains have evolved.
A cosy bed for brain stem cells
Brain neurons are generated from stem cells called basal progenitors that are able to proliferate in humans, but not in mice. In humans, basal progenitors are surrounded by a special environment, a so-called extracellular matrix (ECM), which is produced by the progenitors themselves. Like a cosy bed, it accommodates the proliferating cells. Mice lack such ECM, which means that they generate fewer neurons and have a smaller brain.
The scientists therefore conducted tests to see whether in mice, basal progenitors start to proliferate if a comparable cell environment is simulated. The result: “We simulated an extracellular matrix for the brain stem cells using a stimulating antibody. This antibody activates an integrin on the cell surface of basal progenitors and thus stimulates their proliferation”, explains Denise Stenzel, who headed the experiments.
Because a requirement of thyroid hormones for proper brain development was previously known, the researchers blocked the production of these hormones in pregnant rats to see if their absence would inhibit basal progenitor proliferation in the embryos. Indeed, fewer progenitors and, consequently, neurons were produced, likely explaining the abnormal brain development in the absence of thyroid hormones. When the action of these hormones on the integrin was blocked, the ECM-simulating antibody alone was no longer able to induce basal progenitor proliferation.
A combination of ECM and thyroid hormones thus appears necessary for basal progenitors to proliferate and produce enough neurons for brain development. Human brain stem cells produce the suitable environment naturally. “That is probably how, in the course of evolution, we humans developed larger brains”, says Wieland Huttner, summing up the study. The research produced another important finding: “We were able to explain the role of iodine in embryonic brain development at the cellular level”, says Denise Stenzel. Iodine is essential for the production of thyroid hormones, and an iodine deficiency in pregnant women is known to have adverse effects on the brain development of the unborn child.
Switching brain development on, and off
The possibility of nerve cell regeneration is a step closer after neuroscientists identified the genetic signals that play a crucial role in normal development - driving stem cells to produce neurons that are correctly positioned and connected neurons within the brain.
Published in Cerebral Cortex, a study led by Dr Julian Heng of the Australian Regenerative Medicine Institute (ARMI) at Monash University, has identified a transcription factor, RP58, which is an important “off switch” for the process of nerve cell formation.
“Known as RP58, this gene switches off Rnd2 expression to control the proper positioning of neurons within the fetal brain - a crucial process,” Dr Heng said.
Absence of RP58 has been linked to a rare brain developmental disorder known as Terminal 1q deletion syndrome, where patients suffer reduced brain growth, experience epileptic seizures and are intellectually disabled.
Dr Heng’s work, on pre-clinical models, builds on previous research in which another transcription factor, Neurog2, operated as the “on-switch” for the crucial process of early brain development whereby stem cells become neurons.
Neurog2 switches on the expression of another gene, Rnd2, to control how new nerve cells of the developing brain find their appropriate location and go on to establish their proper connections. However, too much Rnd2 can impair the path-finding of new neurons, and so the researchers theorised that an “off-switch” controlled the process.
Dr Heng said that the discovery of RP58 was the proof needed to demonstrate that genes such as Rnd2 must be switched on, and then off in order for brain cells to assemble properly.
“Together with a collaborative study we published with our colleagues earlier in the year, this research demonstrates that loss of RP58 impairs the development of new nerve cells in the embryonic mouse brain, including their path-finding,” Dr Heng said.
“Since the early steps of nerve cell production during brain development are comparable between mice and humans, we believe that RP58 carries out similar functions in the foetal human brain as well. This strengthens the notion that disruptions to this gene can cause brain developmental disease.”
Recently, a study led by researchers at Stanford University in the United States provided evidence showing that RP58 (also known as ZFP238) is crucial for the maturation of new human nerve cells.
Dr Heng believes his discoveries could be used in the context of regenerative medicine.
“Ultimately, the goal of our research is to understand the fundamental properties which control the production and maturation of new nerve cells in the brain. Understanding the function of switches like RP58 is crucial to this process,” Dr Heng said.
"In the future, we will use this knowledge to develop novel cell-based therapies to treat neurodegenerative disorders and brain injury.”
Index Detects Early Signs of Deviation from Normal Brain Development
Researchers at Penn Medicine have generated a brain development index from MRI scans that captures the complex patterns of maturation during normal brain development. This index will allow clinicians and researchers for the first time to detect subtle, yet potentially critical early signs of deviation from normal development during late childhood to early adult.
The study, published online in the journal Cerebral Cortex, shows a relationship between cognitive development and physical changes in the developing young brain (aged 8 to 21).
“Our findings suggest that brain imaging via sophisticated MRI scans may be a useful biomarker for the early detection of subtle developmental abnormalities,” said Guray Erus, PhD, a research associate in the department of Radiology at the Perelman School of Medicine at the University of Pennsylvania, and the study’s lead author. “The abnormalities may, in turn, be the first manifestations of subsequent neuropsychiatric problems.”
Among its key findings is the consistency in healthy brain development of young people. The study examined cognitive performance of outliers – adolescents whose brains developed faster or slower than the normal rates. Early maturers performed significantly better than those with delayed brain development in the speed at which they completed certain tasks. The improved speed of performance indicates increased efficiency in neuronal organization and communication. Slower performance in such tests is a precursor to neuropsychiatric disorders, (the research suggests), including adolescent-onset psychosis.
The 14 tests used in the Penn study evaluate a broad range of cognitive functions including abstraction and mental flexibility, attention, working memory, verbal memory, face memory, spatial memory, language reasoning, nonverbal reasoning, spatial processing, emotion identification, and sensorimotor speed.
Penn’s brain development index consolidates a number of complex visual maps derived from sophisticated analysis of MRI scans into a unified developmental template. By looking at an individual’s brain maps in relation to the consolidated findings, researchers can estimate the age of the subject. Subjects whose brain development index was higher than their chronological age had significantly superior cognitive processing speed as measured by the cognitive tests compared to subjects whose brain indices were lower than their actual age.
“This is analogous to producing growth charts used in pediatrics to screen for gross abnormalities of physical development,” said Christos Davatzikos, PhD, professor of Radiology and Electrical and Systems Engineering at Penn and one of the study’s co-senior authors. “We can assess individuals in terms of where they place in relation to the overall trends. While single image maps can be used for an accurate estimation of the age of the subject, the combination of all maps achieves a higher accuracy in age prediction than the accuracy of each map independently.”
Previous studies have outlined normative trajectories of growth for individual brain regions across the lifespan; the Penn study is the first to present a comprehensive index for the entire brain during late childhood, adolescence, and young adulthood — periods when the healthy human brain maturates in a remarkably consistent way, deviations from which possibly signify later neuropsychiatric problems.
The Penn study used a sample of 621 participants in the Philadelphia Neurodevelopmental Cohort, a Grand Opportunity study funded by the National Institute of Mental Health, designed to understand how brain maturation mediates cognitive development and vulnerability to psychiatric illness and how genetics impacts this process.
“All of our young study participants have received a standardized neuropsychiatric evaluation at intake, and all agreed to be contacted for future studies. Some are followed up longitudinally,” said Ruben C. Gur, PhD, director of the Brain Behavior Laboratory at Penn and the study’s other co-senior author. “We can therefore follow those who score low on our index and examine whether interventions such as cognitive remediation can mitigate potential symptoms.”
Color-Coded Cells Reveal Patchwork Patterns of X Chromosome Silencing in Female Brains
Producing brightly speckled red and green snapshots of many different tissues, Johns Hopkins researchers have color-coded cells in female mice to display which of their two X chromosomes has been made inactive, or “silenced.”
(Image caption: Patterns of X chromosome silencing in cells of the cornea, skin, cartilage and inner ear of mice (clockwise). Cells are red or green depending on whether they have inactivated their maternal or paternal X chromosome, respectively. Hao Wu, courtesy of Neuron)
Scientists have long known that the silencing of one X chromosome in females — who have two X chromosomes in every cell — is a normal occurrence whose consequences can be significant, especially if one X chromosome carries a normal copy of a gene and the other X chromosome carries a mutated copy.
By genetically tagging different X chromosomes with genes that code for red or green fluorescent proteins, scientists say they can now peer into different tissue types to analyze genetic diversity within and between individual females at a new level of detail.
Published on Jan. 8 in the journal Neuron, a summary of the research shows wide-ranging variation in patterns of so-called X chromosome inactivation at every level: within tissues, on the left or right sides of a centrally located tissue (like the brain), among different tissue types, between paired organs (like the eyes) and among individuals.
"Calico cats, which are only ever female, have mottled coat colors. They have two different versions of a gene for coat color, which is located on the X chromosome: one version from their mother and the other from their father," explains Jeremy Nathans, M.D., Ph.D., professor of molecular biology and genetics at the Johns Hopkins University and a Howard Hughes Medical Institute investigator. "Their fur is orange or black depending on which X chromosome is silenced in a particular patch of skin cells. X chromosome inactivation actually occurs in all cells in female mammals, including humans, and it affects most of the genes on the X chromosome. Although this phenomenon has been known for over 50 years, it couldn’t be clearly visualized in internal organs and tissues until now."
Nathans adds that early in the development of most mammals, when a female embryo has only about 1,000 cells, each cell makes a “decision” to inactivate one of the two X chromosomes, a process that silences most of the genes on that chromosome. The choice of which X chromosome to inactivate appears to be random, but when those cells divide, their descendants maintain that initial decision.
In the new research, the Johns Hopkins team mated female mice carrying two copies of the gene for green fluorescent protein — one on each of the two X chromosomes — with male mice whose single X chromosome carried the gene for a red fluorescent protein. The female offspring from this mating had cells that glowed red or green based on which X chromosome was silenced. Additionally, the team engineered the mice so that not all of their cells were color-coded, since that would make it hard to distinguish one cell from another. Instead, they designed a system that allowed a single cell type in each mouse, such as heart muscle cells, to be color-coded. Their genetic trick resulted in red and green color maps with distinctive patterns for each cell and tissue type that they examined.
Nathans explains that the patterns are determined by the way each tissue develops. Some tissues are created from a very small number of “founder cells” in the early embryo; others are created from a large number. Statistically, the larger the group of founder cells, the greater the chances are of having a nearly equivalent number of red and green cells. Although the ratio in the founding group is roughly preserved as the tissue grows, the distribution of those cells is determined by how much movement occurs during the development of the tissue. For example, in a tissue like blood, where the cells move a lot, the red and green cells are finely intermingled. By contrast, in skin, where the cells show little movement, each patch of skin consists of the descendants of a single cell, which share the same inactive X chromosome — and therefore the same color — creating a coarse patchwork of red and green.
Normally, the pattern of X chromosome inactivation is not easily visualized. This color-coding technique is likely to be valuable for many studies, Nathans says, especially for research on variations caused by changes in the DNA sequence of the X chromosome, referred to as X-linked variation. X-linked genetic variations, such as hemophilia or color blindness, are relatively common, in part because the X chromosome carries many genes — approximately 1,000, or close to 4 percent of the total.
Males who inherit an X-linked disease usually suffer its effects because they have no second X chromosome to compensate for the mutant version of the gene. Female relatives, on the other hand, are more typically “carriers” of X-linked diseases. They have the ability to pass the disease along to their male progeny, but they do not suffer from it themselves due to the normal copy of the gene on their second X chromosome.
In the tissues of certain carrier females, however, the cells that have silenced the X chromosome with a mutated gene cannot compensate for the defect in the cells that have silenced the X chromosome with the normal gene. Nathans and his team saw such a pattern when they examined the retinas of mice that were carriers for mutations in the Norrie disease gene, which is located on the X chromosome. The Norrie disease gene codes for a protein, Norrin, which controls blood vessel formation in the retina. Women who are carriers for Norrie disease can have defects in their retinas, but some women are more affected than others, and sometimes one eye is more affected than the other eye in the same individual.
The team found that in female mice that were Norrie disease carriers, variation in blood vessel structure corresponded to localized variations in X chromosome inactivation. When the X chromosome carrying the normal copy of the Norrie disease gene was silenced in a group of cells, the blood vessels nearby failed to form properly. In contrast, when the X chromosome carrying the mutated copy of the Norrie disease gene was silenced, the nearby blood vessels developed normally.
“X chromosome inactivation is a fascinating aspect of mammalian biology,” says Nathans. “This new technique for visualizing the pattern of X chromosome inactivation should be particularly useful for looking at the role that this process plays in brain development, including the ways that it contributes to differences between the left and right sides of the female brain, and to differences in brain structure between males and females and among different females, including identical twins.”
Epilepsy drug turns out to help adults acquire perfect pitch and learn language like kids
A team of researchers from across the globe believe they have discovered a means of re-opening “critical periods” in brain development, allowing adults to acquire abilities — such as perfect pitch or fluency in language — that could previously only be acquired early in life.
According to the study in Frontiers in Systems Neuroscience, the mood-stabilizing drug valproate allows the adult brain to absorb new information as effortlessly as it did during critical windows in childhood.
A critical period is “a fixed window of time, usually early in an organism’s lifespan, during which experience has lasting effects on the development of brain function and behavior.” They are, for example, what allows children to enter into language without any formal training in grammar or vocabulary.
The researchers postulated that because such periods close when enzymes “impose ‘brakes’ on neuroplasticity,” a drug that blocks the productions of those enzymes might be able to “reopen critical-period neuroplasticity.”
Brain Chemical Ratios Help Predict Developmental Delays in Preterm Infants
Researchers have identified a potential biomarker for predicting whether a premature infant is at high risk for motor development problems, according to a study published online in the journal Radiology.
"We are living in an era in which survival of premature birth is more common," said Giles S. Kendall, Ph.D., consultant for the neonatal intensive care unit at University College London Hospitals NHS Foundation Trust and honorary senior lecturer of neonatal neuroimaging and neuroprotection at the University College London. "However, these infants continue to be at risk for neurodevelopmental problems."
Patients in the study included 43 infants (24 male) born at less than 32 weeks gestation and admitted to the neonatal intensive care unit (NICU) at the University College of London between 2007 and 2010. Dr. Kendall and his research team performed magnetic resonance imaging (MRI) and MR spectroscopy (MRS) exams on the infants at their approximate expected due dates (or term-equivalent age). MRS measures chemical levels in the brain.
The imaging studies were focused on the white matter of the brain, which is composed of nerve fibers that connect the functional centers of the brain.
"The white matter is especially fragile in the newborn and at risk for injury," Dr. Kendall explained.
One year later, 40 of the 43 infants were evaluated using the Bayley Scales of Infant and Toddler Development, which assess fine motor, gross motor and communication abilities. Of the 40 infants evaluated, 15 (38 percent) had abnormal composite motor scores and four (10 percent) showed cognitive impairment.
Statistical analysis of the MRS results and Bayley Scales scores revealed that the presence of two chemical ratios—increased choline/creatine (Cho/Cr) and decreased N-acetylaspartate/choline (NAA/Cho)—at birth were significantly correlated with developmental delays one year later.
"Low N-acetylaspartate/choline and rising choline/creatine observed during MRS at the baby’s expected due date predicted with 70 percent certainty which babies were at high risk for motor development problems at one year," Dr. Kendall said.
Dr. Kendall said a tool to predict the likelihood of a premature baby having neurodevelopmental problems would be useful in determining which infants should receive intensive interventions and in testing the effectiveness of those therapies.
"Physiotherapy interventions are available but are very expensive, and the vast majority of premature babies don’t need them," Dr. Kendall said. "Our hope is to find a robust biomarker that we can use as an outcome measure so that we don’t have to wait five or six years to see if an intervention has worked."
Dr. Kendall said severe disability associated with premature births has decreased over the past two decades as a result of improved care techniques in the NICU. However, many premature infants today have subtle abnormalities that are difficult to detect with conventional MRI.
"There’s a general shift away from simply ensuring the survival of these infants to how to give them the best quality of life," he said. "Our research is part of an effort to improve the outcomes for prematurely born infants and to identify earlier which babies are at greater risk."
Prenatal Exposure to Alcohol Disrupts Brain Circuitry
Prenatal exposure to alcohol severely disrupts major features of brain development that potentially lead to increased anxiety and poor motor function, conditions typical in humans with Fetal Alcohol Spectrum Disorders (FASD), according to neuroscientists at the University of California, Riverside.
In a groundbreaking study, the UC Riverside team discovered that prenatal exposure to alcohol significantly altered the expression of genes and the development of a network of connections in the neocortex — the part of the brain responsible for high-level thought and cognition, vision, hearing, touch, balance, motor skills, language, and emotion — in a mouse model of FASD. Prenatal exposure caused wrong areas of the brain to be connected with each other, the researchers found.
These findings contradict the recently popular belief that consuming alcohol during pregnancy does no harm.
“If you consume alcohol when you are pregnant you can disrupt the development of your baby’s brain,” said Kelly Huffman, assistant professor of psychology at UC Riverside and lead author of the study that appears in the Nov. 27 issue of The Journal of Neuroscience, the official, peer-reviewed publication of the Society of Neuroscience. Study co-authors are UCR Ph.D. students Hani El Shawa and Charles Abbott.
“This research helps us understand how substances like alcohol impact brain development and change behavior,” Huffman explained. “It also shows how prenatal alcohol exposure generates dramatic change in the brain that leads to changes in behavior. Although this study uses a moderate- to high-dose model, others have shown that even small doses alter development of key receptors in the brain.”
Researchers have long known that ethanol exposure from a mother’s consumption of alcohol impacts brain and cognitive development in the child, but had not previously demonstrated a connection between that exposure and disruption of neural networks that potentially leads to changes in behavior.
Huffman’s team found dramatic changes in intraneocortical connections between the frontal, somatosensory and visual cortex in mice born to mothers who consumed ethanol during pregnancy. The changes were especially severe in the frontal cortex, which regulates motor skill learning, decision-making, planning, judgment, attention, risk-taking, executive function and sociality.
The neocortex region of the mammalian brain is similar in mice and humans, although human processing is more complex. In previous research, Huffman and her team created what amounts to an atlas of the neocortex, identifying the development of regions, gene expression and the cortical circuit over time. That research is foundational to understanding behavioral disorders such as autism and FASD.
Children diagnosed with FASD may have facial deformities and can exhibit cognitive, behavioral and motor deficits from ethanol-related neurobiological damage in early development. Those deficits may include learning disabilities, reduced intelligence, mental retardation and anxiety or depression, Huffman said.
Milder forms of FASD may produce no facial deformities, such as wideset eyes and smooth upper lip, but behavioral issues such as hyperactivity, hyperirritability and attention problems may appear as the child develops, she added.
Based on her earlier research, Huffman said, she expected to find some disruption of intraneocortical circuitry, but thought it would be subtle.
“I was surprised that the result of alcohol exposure was quite dramatic,” she said. “We found elevated levels of anxiety, disengaged behavior, and difficulty with fine motor coordination tasks. These are the kinds of things you see in children with FASD.”
The next phase of her research will examine whether deficits related to prenatal exposure to alcohol continue in subsequent generations.
The bottom line, Huffman said, is that women who are pregnant or who are trying to get pregnant should abstain from drinking alcohol.
“Would you put whiskey in your baby’s bottle? Drinking during pregnancy is not that much different,” she said. “If you ask me if you have three glasses of wine during pregnancy will your child have FASD, I would say probably not. If you ask if there will be changes in the brain, I would say, probably. There is no safe level of drinking during pregnancy.”
Messy children make better learners
Attention, parents: The messier your child gets while playing with food in the high chair, the more he or she is learning.
Researchers at the University of Iowa studied how 16-month-old children learn words for nonsolid objects, from oatmeal to glue. Previous research has shown that toddlers learn more readily about solid objects because they can easily identify them due to their unchanging size and shape. But oozy, gooey, runny stuff? Not so much.
New research shows that changes if you put toddlers in a setting they know well. In those instances, word learning increases, because children at that age are “used to seeing nonsolid things in this context, when they’re eating,” says Larissa Samuelson, associate professor in psychology at the UI who has worked for years on how children learn to associate words with objects. “And, if you expose them to these things when they’re in a highchair, they do better. They’re familiar with the setting and that helps them remember and use what they already know about nonsolids.”
In a paper published in the journal Developmental Science, Samuelson and her team at the UI tested their idea by exposing 16-month-olds to 14 nonsolid objects, mostly food and drinks such as applesauce, pudding, juice, and soup. They presented the items and gave them made-up words, such as “dax” or “kiv.” A minute later, they asked the children to identify the same food in different sizes or shapes. The task required the youngsters to go beyond relying simply on shape and size and to explore what the substances were made of to make the correct identification and word choice.
Not surprisingly, many children gleefully dove into this task by poking, prodding, touching, feeling, eating—and yes, throwing—the nonsolids in order to understand what they were and make the correct association with the hypothetical names. The toddlers who interacted the most with the foods—parents, interpret as you want—were more likely to correctly identify them by their texture and name them, the study determined. For example, imagine you were a 16-month-old gazing at a cup of milk and a cup of glue. How would you tell the difference by simply looking?
“It’s the material that makes many nonsolids,” Samuelson notes, “and how children name them.”
The setting matters, too, it seems. Children in a high chair were more apt to identify and name the food than those in other venues, such as seated at a table, the researchers found.
“It turns out that being in a high chair makes it more likely you’ll get messy, because kids know they can get messy there,” says Samuelson, the senior author on the paper.
The authors say the exercise shows how children’s behavior, environment (or setting), and exploration help them acquire an early vocabulary—learning that is linked to better later cognitive development and functioning.
“It may look like your child is playing in the high chair, throwing things on the ground, and they may be doing that, but they are getting information out of (those actions),” Samuelson contends. “And, it turns out, they can use that information later. That’s what the high chair did. Playing with these foods there actually helped these children in the lab, and they learned the names better.”
“It’s not about words you know, but words you’re going to learn,” Samuelson adds.