Oxytocin spray improves brain function in children with autism

Spacefilling model of oxytocin. Image: Wikipedia.

A single dose of the hormone oxytocin, delivered via nasal spray, has been shown to enhance brain activity while processing social information in children with autism spectrum disorders, Yale School of Medicine researchers report in a new study published in the Dec. 2 issue of Proceedings of the National Academy of Sciences.

"This is the first study to evaluate the impact of oxytocin on brain function in children with autism spectrum disorders," said first author Ilanit Gordon, a Yale Child Study Center postdoctoral fellow, whose colleagues on the study included senior author Kevin Pelphrey, the Harris Professor in the Child Study Center, and director of the Center for Translational Developmental Neuroscience at Yale.

Gordon, Pelphrey, and their colleagues conducted a double-blind, placebo-controlled study of 17 children and adolescents with autism spectrum disorders.

The participants, between the ages of 8 and 16.5, were randomly given either oxytocin spray or a placebo nasal spray during a task involving social judgments.

Oxytocin is naturally occurring hormone produced in the brain and throughout the body.

Kevin Pelphrey

"We found that brain centers associated with reward and emotion recognition responded more during social tasks when children received oxytocin instead of the placebo," said Gordon.

"Oxytocin temporarily normalized brain regions responsible for the social deficits seen in children with autism."

Gordon said oxytocin facilitated social attunement, a process that makes the brain regions involved in social behavior and social cognition activate more for social stimuli (such as faces) and activate less for non-social stimuli (such as cars).

"Our results are particularly important considering the urgent need for treatments to target social dysfunction in autism spectrum disorders," Gordon added.

More information: "Oxytocin enhances brain function in children with autism," by Ilanit Gordon et al. www.pnas.org/cgi/doi/10.1073/pnas.1312857110

Connecting motor control and language

Is it true, as some scientists believe, that to understand words like "spike" (in the volleyball sense) the brain has to "mentally" retrace the sequence of motor commands that accomplish the action?

According to a study just published as a cover story in the December issue of Brain Research and conducted with the participation of scientists from SISSA, the International School for Advanced Studies of Trieste, the high-level motor expertise of subjects (in the case at hand of the volleyball players who responded to instructions to perform volleyball-specific actions) modulates the involvement of the brain motor areas in understanding the actions.

The effect of experience is a novelty that challenges some recent hypotheses, making the theoretical picture more complex.

According to theories of embodied cognition, conceptual representations are construed based on the brain's sensory and motor experience and, when we need to understand or recognise a concept, apparently our brain will subconsciously mime that experience.

In practice, to understand the word "drink" our brain implicitly activates the motor processes involved in drinking, but is that really how it works?

"According to our studies, the involvement of the motor system is not so direct or obvious but depends on several variables: the context, the experience and the feasibility/unfeasibility of the actions", explains Barbara Tomasino.

Tomasino, a former SISSA student now at the IRCCS "E. Medea-La Nostra Famiglia" in San Vito al Tagliamento, is the first author of this study which was conducted together with, amongst others, Raffaella Rumiati, the coordinator of the PhD course in Neuroscience at SISSA.

Tomasino, Rumiati and colleagues used "expert" subjects from the motor point of view, namely professional volleyball players.

"The idea of using expert subjects is interesting because it allows us to see if the degree of mastery of the act has an effect on performance in understanding."

"In fact, supporters of embodied theories state that motor activation is always present and there should be no difference", explains Rumiati, differences which were nonetheless identified.

The subjects (two groups: one of volleyball players and one of non-experts) had to read silently sentences describing acts in the form of commands.

The cue could be an action that was either possible -"go block" – or impossible – "do a forearm dig during a leap" in volleyball.

The sentences could also be positive – "do..." – or negative – "don't do…"–. Even on the basis of a previous behavioural study the research team supposed that the motor system is activated by positive but not by negative orders.

"In the present study we used functional magnetic resonance imaging to observe the activity of the brain during performance of the task."

"In particular, we monitored the activity of the motor areas and the changes in the way these "speak", or rather connect functionally, to the cognitive areas", explains Rumiati.

"One of the interesting things we found is an inhibition of motor activity in expert subjects in response to a positive but impossible command".

By contrast, in non-expert subjects the motor activity had a non-specific character, without the differences observed in experts.

"Overall this indicates that there is a modulating effect of the interaction between the possible/impossible cue and the positive or negative command", comments Tomasino.

"It's as if the volleyball players' experience gave rise to a sort of motor alphabet that affects they way they perform the task", says Rumiati, "an alphabet that is instead absent in non-experts."

"This suggests that the assumption of embodied theories, that is, the constant intervention of the motor system, is not always true but is modulated by contextual factors, such as the subject's experience".

More information: Barbara Tomasino, Marta Maieron, Elisa Guatto, Franco Fabbro, Raffaella Ida Rumiati "How are the motor system activity and functional connectivity between the cognitive and sensorimotor systems modulated by athletic expertise?" Brain Research Volume 1540, 2 December 2013, Pages 21–41 dx.doi.org/10.1016/j.brainres.2013.09.048

Autism and prenatal screening

The internet was ablaze last week with the news that health authorities in Western Australia (WA) have given approval for IVF clinics to 'screen' embryos to reduce the chances of a couple having a child with autism.

The Reproductive Technology Council will now allow certain women undergoing IVF treatment to be selectively implanted with female embryos only.

The rationale for this practice is that autism is more likely to affect males than females (approximately 4 males for every 1 female), and by selecting female embryos, the chances of this child developing autism are reduced.

The West Australian reported that: "only families at high risk of having a child with autism, such as families who already have two boys with severe autism, would be considered for embryo screening".

The reaction to this report was swift and furious, and came from all corners of the globe.

Some were concerned about the science underpinning this approach, and pointed to recent evidence that autism may be under-diagnosed in females, and that the gender imbalance in autism may not be as skewed towards males as we once thought.

These critics argue that the selective implantation of female embryos may not actually reduce the chances of a child developing autism.

Others opted for a more extreme attack on health professionals and families, branding the developments as eugenicist - a scientific discipline that advocates practises that are aimed at improving a population's gene pool.

The connotation of this label is a deeply negative one, and will be forever linked to Nazi regime, who used eugenics as a justification for the genocide of Jews, Gypies, homosexuals and others during World War II.

Prenatal screening for autism
This is an extraordinarily sensitive topic and the arguments on both sides of the debate are impassioned.

The concern about the current state of the science is valid. It is a very blunt technique to 'screen' embryos for autism based on sex alone.

Autism is likely to be caused by dozens of gene sets, perhaps in interaction with the environment. It is also quite possible, perhaps probable, that the genetic causes of autism are quite different between individuals.

There is absolutely a link between an individual's sex and their chances of developing autism, but this is only one factor among a constellation of others – many of which remain unknown to us.

To a certain extent, the concern about the validity of the current science is a moot point. Despite constant hype in the recent years, there is currently no genetic test for autism. Importantly, however, this won't always be the case.

The extraordinary developments in genetic technology in the recent past and the immediate future will undoubtedly lead us to a point, not too far from now, where we have the techniques and information to identify whether a person has autism by their genetic make-up alone.

Science is moving fast and this is a debate that needs to be had.

Pre-implantation genetic diagnosis/screening
And this is where we come to the argument about eugenics. Informed opinions are vital here, and it is important that we understand very clearly the exact technology that has been approved.

Pre-implantation genetic diagnosis/screening (PGD) is an IVF technique that occurs at the embryo stage prior to implantation.

An egg from a woman and a sperm from a man are combined outside of the body (i.e., in a petri dish) to create an embryo (a fertilized egg).

That embryo can then be 'screened' to determine whether its genetic make-up increases risk for a given disorder.

If an individual embryo is found to contain a genetic risk factor for this disorder, then it would not be implanted into the woman's womb.

This technique is used in many countries around the world to identify embryos that contain a gene mutation known to definitively cause a disorder, such as cystic fibrosis, haemophilia A and Huntington's disease.

PGD is not the abortion of a developing baby in the womb. It is the screening of fertilized eggs prior to being implanted in the womb.

Two sides of the debate
Understandably, PGD is a technique that causes concern within certain parts of the autism community. Some autism advocates argue that PGD will eventually be used to select autism out of the gene pool.

This is certainly something I would not want. I have forged dozens of friendships with autistic people and their families, and have seen first-hand the skills, talents, smiles and diversity these individuals bring to the lives of those around them. The world is immeasurably improved by their presence in it.

I also imagine how I would feel if I were a person with autism and I heard a discussion about prenatal screening for 'me'.

I imagine how I would feel if the 'all clear' had been given to screen embryos for short-sightedness or for extraversion, both of which are part of who I am.

Angry, outraged, and certainly more than a little unwanted.
The flip-side of the debate is that autism sometimes associated with significant disability that can affect quality of life.

It is without question that a person's life would be improved if they were free from intellectual disability, if they had the facility to communicate more freely, and if they had the capacity to live independently.

To want a person to live without disability does not diminish in any way our love for people in these circumstances, nor their irreplaceable importance in our lives.

Only a minority of our community know the challenges (and joys) of raising a child with significant disability. It is just plain wrong for people who have never been in this position to judge the wants and desires of those who have.

A debate that needs to be had
The discussion about PGD for autism and other developmental disabilities is an important moment in the intersecting paths of science and society.

It is a debate that requires considerable thought, a debate that needs to remain respectful, and a debate that must include autistic people and their families but the science is coming fast, and so above all, it is a debate that needs to be had.

Credit: Andrew Whitehouse at The Conversation AU

Air pollution and genetics combine to increase risk of autism

Exposure to air pollution appears to increase the risk for autism among people who carry a genetic disposition for the neurodevelopmental disorder, according to newly published research led by scientists at the Keck School of Medicine of the University of Southern California (USC).

"Our research shows that children with both the risk genotype and exposure to high air pollutant levels were at increased risk of autism spectrum disorder compared to those without the risk genotype and lower air pollution exposure," said the study's first author, Heather E. Volk, Ph.D., M.P.H.

Heather Volk is assistant professor of research in preventive medicine and pediatrics at the Keck School of Medicine of USC and principal investigator at The Saban Research Institute of Children's Hospital Los Angeles.

The study, "Autism spectrum disorder: Interaction of air pollution with the MET receptor tyrosine kinase gene," is scheduled to appear in the January 2014 edition of Epidemiology.

Autism spectrum disorder (ASD) is a lifelong neurodevelopmental disability characterized by problems with social interaction, communication and repetitive behaviors.

The Centers for Disease Control and Prevention estimates that one in 88 children in the United States has an ASD.

ASD is highly heritable, suggesting that genetics are an important contributing factor, but many questions about its causes remain. There currently is no cure for the disorder.

"Although gene-environment interactions are widely believed to contribute to autism risk, this is the first demonstration of a specific interaction between a well-established genetic risk factor and an environmental factor that independently contribute to autism risk," said Daniel B. Campbell, Ph.D.

David Campbell is assistant professor of psychiatry and the behavioral sciences at the Keck School of Medicine of USC and the study's senior author.

"The MET gene variant has been associated with autism in multiple studies, controls expression of MET protein in both the brain and the immune system, and predicts altered brain structure and function."

"It will be important to replicate this finding and to determine the mechanisms by which these genetic and environmental factors interact to increase the risk for autism."

Independent studies by Volk and Campbell have previously reported associations between autism and air pollution exposure and between autism and a variant in the MET gene.

The current study suggests that air pollution exposure and the genetic variant interact to augment the risk of ASD.

Campbell and Volk's team studied 408 children between 2 and 5 years of age from the Childhood Autism Risks From Genetics and the Environment Study, a population-based, case-control study of preschool children from California.

Of those, 252 met the criteria for autism or autism spectrum disorder. Air pollution exposure was determined based on the past residences of the children and their mothers, local traffic-related sources, and regional air quality measures. MET genotype was determined through blood sampling.

Campbell and Volk continue to study the interaction of air pollution exposure and the MET genotype in mothers during pregnancy.

Messy children make for better learners

Don't let the mess in the high chair bother you. New research from the University of Iowa shows kids who get messy in the high chair are learning. 

Credit: Tim Schoon, University of Iowa

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, such as shoving stuff in their mouths.

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 behaviour, 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.

Lynn Perry, who helped design the study and analyze the data as part of her doctoral studies at the UI, is the first author on the paper.

Johanna Burdinie, who was an UI undergraduate during the project, is a contributing author.

Genetic discovery could increase understanding of ADHD

Scientists at Trinity College Dublin have discovered that a mutation in a single gene involved in the functioning of the brain's nervous system can lead to hyperactivity symptoms that are characteristic of Attention-Deficit Hyperactivity Disorder (ADHD).

Getting the nervous system wired up properly is a big job. The brain contains billions of different types of nerve cells, which all have to be connected in a very precise fashion.

This circuitry self-assembles as an embryo grows, based on a developmental programme involving the actions of thousands of different genes.

The scientists discovered that a mutation in a single mouse gene, 'Elfn1', can have a big effect.

Their new findings give impetus to discover whether mutations in Elfn1 in humans can give rise to similar symptoms and whether they might play a part in some patients with epilepsy and ADHD.

These two conditions occur together far more often than expected by chance.

In an article just published in the international journal, PLOS ONE, Associate Professor in Genetics at Trinity, Kevin Mitchell, and Research Technical Officer, Dr Jackie Dolan, investigated the importance of the function played by Elfn1 and the protein it produces when expressed.

They did this by experimentally removing it from some mice and comparing the effects against those seen in mice with the normal gene.

Although overall brain anatomy and patterns of connectivity remained normal, there was clear evidence of disturbance in brain function in individuals without Elfn1.

Seizures occurred in some, and these became more common over time and were easily triggered by human interaction.

Secondly, hyperactivity was observed, and this showed an unusual response to the stimulant, amphetamine.

Amphetamine normally causes hyperactivity in animals that have Elfn1 present, as it does in most humans. Here, it reduced the hyperactivity of the mice without the gene.

This is similar to the situation in patients with ADHD, where amphetamine and related drugs have a paradoxical, calming effect.

"These findings clearly show that removal of the Elfn1 gene affects brain circuits with multiple consequences for behaviour," said Dr Dolan.

The seizures likely relate to the function of Elfn1 in dampening the response of the nervous system to strong stimuli in key brain structures called the cortex and hippocampus.

However, the development of ADHD-like hyperactivity focused on a different brain structure, known as the habenula.

This structure is part of a system that integrates information from multiple regions of the brain and regulates the activity of nerve cells that produce mood-regulating chemicals such as dopamine and serotonin.

Professor Mitchell said: "We are at the beginning of this process of figuring out how this gene works and understanding the consequences when it is mutated but, these animals provide a unique model to investigate how subtle changes in brain development can ultimately result in aberrant brain function".

Elfn1 was first discovered by Dr Dolan, Professor Mitchell and colleagues in 2007. The protein it produces when expressed allows communication from one nerve cell to another. In a study published in Science last year, Emily Sylwestrak and Anirvan Ghosh, of the University of California, San Diego, showed that the Elfn1 protein determined what kind of connection was made onto those nerve cells.

More information: dx.plos.org/10.1371/journal.pone.008049

Can Toys help develop Science and Technology (STEM) skills in children?

One of the hot topics on social media this holiday season is finding gifts that can help children, especially girls, develop science- and engineering-related skills.

Beth Holloway, director of the Women in Engineering Program at Purdue University, says toys that help children figure out how to turn their ideas into reality - toys that let them design and build something, for instance - are a great first step in inspiring them to consider a science, technology, engineering and mathematics (STEM) career.

"Toys like that will help children realize that they can make an impact on the world through their ideas," she says.

As for girls in particular, Holloway says they should have a range of toys and experiences.

"Parents need to provide girls with toys that indulge their feminine side but also those that allow them to feel the sense of accomplishment that comes from designing and building something," she says.

"Those accomplishments will encourage them to continue to stretch their imaginations."

Holloway says research shows that girls tend to become interested in what they are confident that they are good at doing.

STEM-inspired toys can help foster that confidence in designing and building while reinforcing their existing interests.

For ideas on STEM-related toys, Holloway suggests the websites www.amightygirl.com/ and www.modernparentsmessykids.com

Fetal Alcohol Syndrome (FASD): 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 neo-cortex—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 behaviour.

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 behaviour.

Huffman's team found dramatic changes in intra-neocortical connections between the frontal, somato-sensory 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.

Research Team first to Map Autism-Risk Genes by Function

Pity the poor autism researcher. Recent studies have linked hundreds of gene mutations scattered throughout the brain to increased autism risk. Where do you start?

UCLA neuroscientists may have an answer. They are the first to map groups of autism-risk genes by function, and to identify where and when these genes normally play major roles in early brain development.

In addition, they discovered disturbances in neural circuits that define key pathways between parts of the cerebral cortex.

The research suggests that these early disruptions are created by mutations in genes during fetal brain development and are not a result of autism itself.

Published in the Nov. 21 edition of Cell, the findings will help scientists understand how genetic changes cause autism on a molecular level and prioritize targets for future studies.

"Identifying gene variants that boost risk is only the first step of unraveling a disease," explained lead author Dr. Daniel Geschwind, the Gordon and Virginia MacDonald Distinguished Professor of Human Genetics, professor of neurology at the David Geffen School of Medicine at UCLA and professor of psychiatry at the Semel Institute for Neuroscience and Human Behaviour.

"We need to figure out where genetic changes appear in the brain, at what stages during development and which biological processes they disrupt. Only then will we understand how mutations cause autism."

Using an online atlas called BrainSpan, the authors charted gene activity in the developing brain before birth.

In particular, they examined what happens during gene expression —when genes copy data from DNA to RNA in order to create proteins.

Geschwind and his colleagues found high activity in risk genes during two processes critical to early brain development.

"We found that gene variants are expressed in the developing brain when cells define their future identities and roles in neural circuits," first author Neelroop Parikshak, a graduate student researcher in Geschwind's lab.

"Therefore, changes in the genes influence the brain's wiring by altering the synapse and shaping how neurons transmit signals to each other."

The mutated genes also interfered with how the brain's layers and halves relate to one another, a phenomenon confirmed by previous imaging studies of the autistic brain.

"We discovered gene-related disruption of circuits that connect the autistic brain's layers and hemispheres to each other," explained Geschwind, who is director of the UCLA Neurogenetics Program and the Center for Autism Research and Treatment and co-director of the Center for Neurobehavioral Genetics at UCLA.

 "Our finding suggests that the mutated genes caused the miswiring; it's not a result of having the disease itself."

The UCLA team also demonstrated that while autism and intellectual disability share similar risk genes, the genes behave uniquely, showing for the first time how the two disorders differ.

"People often lump intellectual disability together with autism, because the disorders' risk genes overlap," said Parikshak.

"We showed that these genes have unique expression patterns in different brain regions at varying times during brain development.

"Genes linked to intellectual disability influence many biological processes in the body," he added. "But genes tied to autism tend to affect specific functions, such as the connections between brain regions that are essential to many human-specific behaviours, like speech and language."

The UCLA study will reap immediate benefits in the near future, when neuroscientists sequence the genomes of several thousand people for genetic mutations linked to autism and intellectual disability.

"We've made our analysis publically available to allow other researchers to expand upon our study and explore the data in detail," said Geschwind.

"We believe this will mark an important step forward in understanding the biology behind autism and other neurodevelopmental disorders."

Researchers explore links between learning disorders in children

New interdisciplinary research from Western University has uncovered fundamental links among three major learning difficulties in some school-age children.

Although many children have specific problems with dyslexia, specific language impairment and dyscalculia, this study is the first to show a significant portion of these children have overlapping deficits.

Importantly, the research team has also devised a 10-minute screening test that could be administered broadly in primary schools to identify children at risk for the different disorders.

The collaborative project includes findings from four researchers at Western's Brain and Mind Institute (BMI) and the Faculty of Health Sciences that independently specialize in the three key developmental disorders.

Dyslexia is a deficit in the development of reading while specific language impairment is a disorder related to poor development of spoken language skills. Dyscalculia is a severe difficulty in making mathematical calculations.

Past research in these disorders has focused on each of these as single impairments, despite the widespread recognition that they commonly overlap.

For a study published in the journal PLOS ONE, Lisa Archibald and Janis Oram Cardy from the Faculty of Health Sciences' School of Communication Sciences and Disorders and Marc Joanisse and Daniel Ansari from BMI collaborated across disciplines and examined – for the first time ever – the co-occurrence of difficulties in reading, spoken language, and mathematical calculations in a large sample of school-age children.

In the study, researchers tested learning profiles of a large sample of school children aged 4 to 10-years old in the region of London, Ontario.

The research team found that although some of the children showed specific deficits in reading, spoken language, or math, a significant number of children exhibited a mixed profile of a reading plus a math deficit, or an even wider-ranging weakness spanning math, reading, and spoken language.

"This is the first time researchers have looked at possible learning difficulties in different areas in a large sample of the same kids," says Archibald, the PLOS One paper's lead author.

"It's an important first step in trying to understand the large variability that is commonly reported for groups with learning disabilities."

The study has also uncovered some essential hints as to why different learning patterns might occur in different children.

For instance, children who showed weaknesses on all three types of abilities also scored very low on a working memory assessment.

NB: Working memory is the ability to hold multiple pieces of information in mind and perform simple operations on them, such as repeating a sequence of digits in the reverse order in which they were presented. 

According to the findings, such children may require a more targeted approach to remediation, due to the complex nature of their difficulties.

Children who have more specific deficits did not show the same difficulty with working memory and would require quite different interventions.

"Educators face significant challenges in identifying learning problems in children. With additional testing, we hope that a new tool that we have developed will someday provide educators with a quick and effective method for identifying which children need extra help, but also a way to develop more individualized remediation programs," says Joanisse.

More information: Original Article: Archibald LMD, Oram Cardy J, Joanisse MF, Ansari D (2013) Language, Reading, and Math Learning Profiles in an Epidemiological Sample of School Age Children. PLoS ONE 8(10): e77463. DOI: 10.1371/journal.pone.0077463