Posts tagged neuroscience
Articles and news from the latest research reports.
Brainpower applied to understanding of neural stem cells
How do humans and other mammals get so brainy? USC researcher Wange Lu and his colleagues shed new light on this question in a paper published in the journal Cell Reports on Oct. 24.
The researchers donned their thinking caps to explain how neural stem and progenitor cells differentiate into neurons and related cells called glia. Neurons transmit information through electrical and chemical signals; glia surround, support and protect neurons in the brain and throughout the nervous system. Glia do everything from holding neurons in place to supplying them with nutrients and oxygen to protect them from pathogens.
By studying the embryo neural stem cells of mice in a petri dish, Lu and his colleagues discovered that a protein called SMEK1 promotes the differentiation of neural stem and progenitor cells. At the same time, SMEK1 keeps these cells in check by suppressing their uncontrolled proliferation.
The researchers also determined that SMEK1 doesn’t act alone: It works in concert with Protein Phosphatase 4 to suppress the activity of PAR3, a third protein that discourages neurogenesis — the birth of new neurons. With PAR3 out of the picture, neural stem cells and progenitors are free to differentiate into new neurons and glia.
“These studies reveal the mechanisms of how the brain keeps the balance of stem cells and neurons when the brain is formed,” said Wange Lu, associate professor of biochemistry and molecular biology at the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC. “If this process goes wrong, it leads to cancer or mental retardation or other neurological diseases.”
Neural stem and progenitor cells offer tremendous promise as a future treatment for neurodegenerative disorders, and understanding their differentiation is the first step toward harnessing the cells’ therapeutic potential. This could offer new hope for patients with Alzheimer’s, Parkinson’s and many other currently incurable diseases.
Child neurologist finds potential route to better treatments for Fragile X, autism
When you experience something, neurons in the brain send chemical signals called neurotransmitters across synapses to receptors on other neurons. How well that process unfolds determines how you comprehend the experience and what behaviors might follow. In people with Fragile X syndrome, a third of whom are eventually diagnosed with Autism Spectrum Disorder, that process is severely hindered, leading to intellectual impairments and abnormal behaviors.
In a study published in the online journal PLoS One, a team of UNC School of Medicine researchers led by pharmacologist C.J. Malanga, MD, PhD, describes a major reason why current medications only moderately alleviate Fragile X symptoms. Using mouse models, Malanga discovered that three specific drugs affect three different kinds of neurotransmitter receptors that all seem to play roles in Fragile X. As a result, current Fragile X drugs have limited benefit because most of them only affect one receptor.
Nearly one million people in the United States have Fragile X Syndrome, which is the result of a single mutated gene called FMR1. In people without Fragile X, the gene produces a protein that helps maintain the proper strength of synaptic communication between neurons. In people with Fragile X, FMR1 doesn’t produce the protein, the synaptic connection weakens, and there’s a decrease in synaptic input, leading to mild to severe learning disabilities and behavioral issues, such as hyperactivity, anxiety, and sensitivity to sensory stimulation, especially touch and noise.
More than two decades ago, researchers discovered that – in people with mental and behavior problems – a receptor called mGluR5 could not properly regulate the effect of the neurotransmitter, glutamate. Since then, pharmaceutical companies have been trying to develop drugs that target glutamate receptors. “It’s been a challenging goal,” Malanga said. “No one so far has made it work very well, and kids with Fragile X have been illustrative of this.”
But there are other receptors that regulate other neurotransmitters in similar ways to mGluR5. And there are drugs already available for human use that act on those receptors. So Malanga’s team checked how those drugs might affect mice in which the Fragile X gene has been knocked out.
By electrically stimulating specific brain circuits, Malanga’s team first learned how the mice perceived reward. The mice learned very quickly that if they press a lever, they get rewarded via a mild electrical stimulation. Then his team provided a drug molecule that acts on the same reward circuitry to see how the drugs affect the response patterns and other behaviors in the mice.
His team studied one drug that blocked dopamine receptors, another drug that blocked mGluR5 receptors, and another drug that blocked mAChR1, or M1, receptors. Three different types of neurotransmitters – dopamine, glutamate, and acetylcholine – act on those receptors. And there were big differences in how sensitive the mice were to each drug.
“Turns out, based on our study and a previous study we did with my UNC colleague Ben Philpot, that Fragile X mice and Angelman Syndrome mice are very different,” Malanga said. “And how the same pharmaceuticals act in these mouse models of Autism Spectrum Disorder is very different.”
Malanga’s finding suggests that not all people with Fragile X share the same biological hurdles. The same is likely true, he said, for people with other autism-related disorders, such as Rett syndrome and Angelman syndrome.
“Fragile X kids likely have very different sensitivities to prescribed drugs than do other kids with different biological causes of autism,” Malanga said.
(Source: news.unchealthcare.org)
A step towards early Alzheimer’s diagnosis
If Alzheimer’s disease is to be treated in the future it requires an early diagnosis, which is not yet possible. Now researchers at higher education institutions such as Linköping University have identified six proteins in spinal fluid that can be used as markers for the illness.
Alzheimer’s causes great suffering and has a one hundred percent fatality rate. The breakdown of brain cells has been in progress for ten years or more by the time symptoms begin to appear. Currently there is no treatment that can stop the process.
(Image: Human neuroblastoma with cell nucleus in blue; beta amyloid as red aggregates within green-tinted lysosomes. Photo: Lotta Agholme.)
Most researchers now agree that one cause of the illness is toxic accumulations – plaques – of the beta amyloid protein. In a healthy brain, the cells are cleansed of such surplus products through lysosomes, the cells’ “waste disposal facilities” (green in the picture).
“In victims of Alzheimer’s, something happens to the lysosomes so that they can’t manage to take care of the surplus of beta amyloid. They fill up with junk that normally is broken down into its component parts and recycled,” says Katarina Kågedal, reader in Experimental Pathology at Linköping University. She led the study that is now being published in Neuromolecular Medicine.
The researchers’ hypothesis was that these changes in the brain’s lysosomal network could be reflected in the spinal fluid, which surrounds the brain’s various parts and drains down into the spinal column. They studied samples of spinal marrow from 20 Alzheimer’s patients and an equal number of healthy control subjects. The screening was aimed at 35 proteins that are associated with the lysosomal network.
“Six of these had clearly increased in the patients; none of them were previously known as markers for Alzheimer’s,” says Kågedal.
Her hope is that the group’s discovery will contribute to early diagnoses of the illness, which is necessary in the first stage in order to be able to begin reliable clinical tests of candidates for drugs. But perhaps the six lysosomal proteins could also be “drug targets” – targets for developing drugs.
“It may be a question of strengthening protection against plaque formation or reactivating the lysosomes so that they manage to break down the plaque,” Kågedal says.
The study was conducted on 20 anonymised, archived spinal marrow samples and the results were confirmed afterwards on an independent range of samples of equal size. All samples were provided by the Laboratory for Clinical Chemistry at Sahlgrenska University Hospital.
(Source: liu.se)
Lower Blood Sugars May Be Good for the Brain
Even for people who don’t have diabetes or high blood sugar, those with higher blood sugar levels are more likely to have memory problems, according to a new study published in the October 23, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.
The study involved 141 people with an average age of 63 who did not have diabetes or pre-diabetes, which is also called impaired glucose tolerance. People who were overweight, drank more than three-and-a-half servings of alcohol per day, and those who had memory and thinking impairment were not included in the study.
The participants’ memory skills were tested, along with their blood glucose, or sugar, levels. Participants also had brain scans to measure the size of the hippocampus area of the brain, which plays an important role in memory.
People with lower blood sugar levels were more likely to have better scores on the memory tests. On a test where participants needed to recall a list of 15 words 30 minutes after hearing them, recalling fewer words was associated with higher blood sugar levels. For example, an increase of about 7 mmol/mol of a long-term marker of glucose control called HbA1c went along with recalling 2 fewer words. People with higher blood sugar levels also had smaller volumes in the hippocampus.
“These results suggest that even for people within the normal range of blood sugar, lowering their blood sugar levels could be a promising strategy for preventing memory problems and cognitive decline as they age,” said study author Agnes Flöel, MD, of Charité University Medicine in Berlin, Germany. “Strategies such as lowering calorie intake and increasing physical activity should be tested.”
Most songbirds learn their songs from an adult model, mostly from the father. However, there are relatively large differences in the accuracy how these songs are copied. Researchers from the Max Planck Institute for Ornithology in Seewiesen now found in juvenile zebra finches a possible mechanism that is responsible for the differences in the intensity of song learning. They provided the nerve growth factor “BDNF” to the song control system in the brain. With this treatment the learning ability in juvenile males could be enhanced in such a way that they were able to copy the songs of the father as good as it had been observed in the best learners in a zebra finch nest.
The improvement of cognitive abilities plays an important role in the therapy of neurological and psychiatric diseases. In this context research focusses more and more on the protein BDNF (Brain Derived Neurotrophic Factor). BDNF is mainly responsible for the preservation, growth and differentiation of nerve cells. Moreover, from experiments in mice it is known that BDNF enhances the ability to solve complex cognitive tasks.
In a learning experiment with zebra finches, researchers from the Max Planck Institute for Ornithology in Seewiesen in collaboration with scientists from the Free University of Amsterdam could now show for the first time in songbirds that BDNF acts as cognitive enhancer. They investigated zebra finch brother pairs that grew up with their genetic parents. In this setup juvenile birds will readily learn the songs from their fathers. However there are differences in the intensity of song learning among siblings of the same age. The worst learners have only a similarity of 20% with their fathers’ songs, whereas the best learners copy almost the entire songs of their fathers.
By now knowing the normal distribution of the learned songs within a zebra finch nest, as a next step the researchers were able to investigate the impact of BDNF on song learning. In one of the two brothers they enhanced the expression of BDNF in the song control system in the brain while the other brother did not get such a treatment. By analysing the songs the researchers found that those sons that received more BDNF had a higher similarity with the song of their fathers compared to normally reared juveniles. Remarkably, the learning efficiency in the BDNF-treated birds was as high as it has been previously observed in the best learners within the nest. This was due to an earlier onset of syllable copying in BDNF-treated birds and these birds also copied more and sang fewer improvised syllables. Therefore it is likely that the presence of BDNF in the song control system could correct possible inaccuracies in the song learning process, state the scientists around Manfred Gahr, who is the senior author of the study.
How and when the auditory system registers complex auditory-visual synchrony
Imagine the brain’s delight when experiencing the sounds of Beethoven’s “Moonlight Sonata” while simultaneously taking in a light show produced by a visualizer.
A new Northwestern University study did much more than that.
To understand how the brain responds to highly complex auditory-visual stimuli like music and moving images, the study tracked parts of the auditory system involved in the perceptual processing of “Moonlight Sonata” while it was synchronized with the light show made by the iTunes Jelly visualizer.
The study shows how and when the auditory system encodes auditory-visual synchrony between complex and changing sounds and images.
Much of related research looks at how the brain processes simple sounds and images. Locating a woodpecker in a tree, for example, is made easier when your brain combines the auditory (pecking) and visual (movement of the bird) streams and judges that they are synchronous. If they are, the brain decides that the two sensory inputs probably came from a single source.
While that research is important, Julia Mossbridge, lead author of the study and research associate in psychology at Northwestern, said it also is critical to expand investigations to highly complex stimuli like music and movies.
“These kinds of things are closer to what the brain actually has to manage to process in every moment of the day,” she said. “Further, it’s important to determine how and when sensory systems choose to combine stimuli across their boundaries.
“If someone’s brain is mis-wired, sensory information could combine when it’s not appropriate,” she said. “For example, when that person is listening to a teacher talk while looking out a window at kids playing, and the auditory and visual streams are integrated instead of separated, this could result in confusion and misunderstanding about which sensory inputs go with what experience.”
It was already known that the left auditory cortex is specialized to process sounds with precise, complex and rapid timing; this gift for auditory timing may be one reason that in most people, the left auditory cortex is used to process speech, for which timing is critical. The results of this study show that this specialization for timing applies not just to sounds, but to the timing of complex and dynamic sounds and images.
Previous research indicates that there are multi-sensory areas in the brain that link sounds and images when they change in similar ways, but much of this research is focused particularly on speech signals (e.g., lips moving as vowels and consonants are heard). Consequently, it hasn’t been clear what areas of the brain process more general auditory-visual synchrony or how this processing differs when sounds and images should not be combined.
“It appears that the brain is exploiting the left auditory cortex’s gift at processing auditory timing, and is using similar mechanisms to encode auditory-visual synchrony, but only in certain situations; seemingly only when combining the sounds and images is appropriate,” Mossbridge said.
New biological links between sleep deprivation and the immune system discovered
Population-level studies have indicated that insufficient sleep increases the risk of cardiovascular diseases and type 2 diabetes. These diseases are known to be linked to inflammatory responses in the body.
University of Helsinki researchers have now shown what kinds of biological mechanisms related to sleep loss affect the immune system and trigger an inflammatory response. They identified the genes which are most susceptible to sleep deprivation and examined whether these genes are involved in the regulation of the immune system. The study was published in the journal PLOS ONE on October 23, 2013.
Conducted at the sleep laboratory of the Finnish Institute of Occupational Health, the study restricted the amount of sleep of a group of healthy young men to four hours per night for five days, imitating the schedule of a normal working week. Blood samples were taken before and after the sleep deprivation test. White blood cells were isolated from the samples, and the expression of all genes at the time of the sampling was examined using microarrays. The results were compared with samples from healthy men of comparable age who had been sleeping eight hours per night for the week.
"We compared the gene expression before and after the sleep deprivation period, and focused on the genes whose behaviour was most strongly altered," explains researcher Vilma Aho. "The expression of many genes and gene pathways related to the functions of the immune system was increased during the sleep deprivation. There was an increase in activity of B cells which are responsible for producing antigens that contribute to the body’s defensive reactions, but also to allergic reactions and asthma. This may explain the previous observations of increased asthmatic symptoms in a state of sleep deprivation."
The amount of certain interleukins, or signalling molecules which promote inflammation, increased, as did the amount of associated receptors such as Toll-like receptors (TLR). On the gene level, this was apparent in the higher-than-normal expression of the TLR4 gene after sleep loss. CRP level was also elevated, indicating inflammation.
The researchers also wanted to examine the impact that long-term sleep deprivation could have on the immune system. For this follow-up study, they used material from the national FINRISKI health survey. Participants in this population study underwent blood tests but also answered questions about their health, for example whether they were getting enough sleep.
The researchers compared participants who believed they were sleeping sufficiently with those who felt that they were not sleeping enough. Some of the gene-level changes observed in the experimental working week sleep restriction study were repeated in the population sample. These results may help explain the connection between shorter sleep and the development of inflammatory diseases, such as cardiovascular disease and diabetes, which has been established in epidemiological studies.
"These results corroborate the idea that sleep does not only impact brain function, but also interacts with our immune system and metabolism. Sleep loss causes changes to the system that regulates our immune defence. Some of these changes appear to be long-term, and may contribute to the development of diseases that have been linked to sleep deprivation in epidemiological research,” Aho states.
Traumatic Brain Injury Research Advances with $18.8M NIH Award
The National Institutes of Health is awarding $18.8 million over five years to support worldwide research on concussion and traumatic brain injury.
The NIH award, part of one of the largest international research collaborations ever coordinated by funding agencies, will be administered through UC San Francisco.
The award supports a team of U.S. researchers at more than 20 institutions throughout the country who are participating in the International Traumatic Brain Injury (InTBIR) Initiative, a collaborative effort of the European Commission, the Canadian Institutes of Health Research (CIHR), the National Institutes of Health (NIH) and the U.S. Department of Defense (DOD).
Although the potential long-term harms due to concussions and blows to the head have gained more attention recently – due in part to media coverage of the experiences of athletes and of soldiers returning from the Middle East – traumatic brain injuries, or TBI, that results from automobile crashes or other common accidents impacts many more people.
Many of those who are affected by TBI are never diagnosed, according to UCSF neurosurgeon Geoffrey Manley, MD, PhD, a principal investigator for the grant who will serve as the U.S. research team’s primary liaison to the NIH, and the chief of neurosurgery at the UCSF-affiliated San Francisco General Hospital, a Level-1 trauma center. SFGH was the first medical center in the nation to achieve certification from the Joint Commission for the treatment of TBI.
The U.S. Centers for Disease Control and Prevention estimates that 2 percent of the U.S. population now lives with TBI-caused disabilities, at an annual cost of about $77 billion.
“Each year in the United States, at least 1.7 million people seek medical attention for TBI,” Manley said. “It is a contributing factor in a third of all injury-related deaths.”
In the work funded by the NIH grant – which also is supported by contributions from the private sector and from the nonprofit One Mind for Research – the researchers aim to refine and improve diagnosis and treatment of TBI, which often has insidious health effects, but which frequently is undiagnosed, misdiagnosed, inadequately understood and undertreated, according to Manley.
New Approach to Lead to Patient-Specific Treatments
“After three decades of failed clinical trials, a new approach is needed,” Manley said. “We expect that our approach will permit researchers to better characterize and stratify patients, will allow meaningful comparisons of treatments and outcomes, and will improve the next generation of clinical trials. The work will advance our understanding of TBI and lead to more effective, patient-specific treatments.”
Since 2009, Manley and Pratik Mukherjee, MD, PhD, a professor of radiology and biomedical imaging at UCSF, have helped lay the groundwork for the continuing TBI research by leading the NIH-funded TRACK-TBI project, through which they and their research collaborators have demonstrated the value of gathering common data across research sites, including a standardized approach to imaging, clinical data, bio-specimens, and tracking outcomes.
Already, TRACK-TBI researchers have made progress toward more useful classification and prognosis of TBI.
Earlier this year, they reported that cases of concussion, or TBI that are classified as “mild” by standard criteria but that show abnormalities on early magnetic resonance imaging (MRI) scans, are much more likely to have worse outcomes three months after the scan in comparison to cases in which scans reveal no abnormalities. Furthermore, the researchers found that elevated blood levels of a protein released during brain injury was associated with the likelihood of an abnormal CT scan.
The new NIH award funds a continuation and expansion of TRACK-TBI. Among the goals is the creation of a widely accessible, comprehensive “TBI information commons” to integrate clinical, imaging, proteomic, genomic and outcome biomarkers from subjects across the age and injury spectra. Another goal is to establish the value of biomarkers that will improve classification of TBI and better optimize selection and assignment of patients for clinical trials.
The researchers also aim to evaluate measures to assess patient outcomes across all phases of recovery and at all levels of TBI severity, to determine which tests, treatments, and services are effective and appropriate – depending on the nature of TBI in particular patients.
In addition to Manley and Mukherjee, principal investigators for the newly funded project include Claudia Robertson, MD, Baylor College of Medicine; Joseph Giacino, PhD, Harvard University; Ramon Diaz-Arrastia, MD, PhD, Uniformed Services University of the Health Sciences; David Okonkwo, MD, PhD, University of Pittsburgh; and Nancy Temkin, PhD, University of Washington. Each of these leading experts has worked in the TBI field for two decades or more.
“The principal investigators bring expertise in neurosurgery, neurology, neuroradiology, critical care medicine, rehabilitation medicine, neuropsychology and biostatistics, all of which are essential and do not reside in any single individual,” Manley said.
International Funding and Collaboration
TRACK-TBI clinical enrollment sites throughout the United States will enroll 3,000 patients across the spectrum of mild to severe brain injuries. Clinical, imaging, proteomic, genomic and clinical outcome databases will be linked into a shared platform that will promote a model for collaboration among scientists within InTBIR and elsewhere.
In addition to the U.S. award, the European Commission, the executive body of the European Union, has awarded €35.2 million to fund the Collaborative European NeuroTrauma Effectiveness-TBI (CENTER-TBI) consortium, also part of the InTBIR. This project will collect data in over 5,000 patients across Europe, where 38 scientific institutes and more than 60 hospitals will participate.
In Canada, CIHR and its national partners also have made a multimillion dollar investment in TBI research, the details of which will be formally announced in the near future.
The InTBIR Scientific Advisory Committee met in Vancouver, British Columbia, on Oct. 17-18, and awardees from all three jurisdictions (EU, USA, Canada) now are aligning efforts to share resources and collaborate on strategies for achieving the InTBIR goals.
![Theatre offers promise for youth with autism
A novel autism intervention program using theatre to teach reciprocal communication skills is improving social deficits in adolescents with the disorder that now affects an estimated one in 88 children, Vanderbilt University researchers released today in the journal Autism Research.
The newly released study assessed the effectiveness of a two-week theatre camp on children with autism spectrum disorder and found significant improvements were made in social perception, social cognition and home living skills by the end of the camp. There were also positive changes in the participants’ physiological stress and reductions in self-reported parental stress.
Called SENSE Theatre, the Social Emotional Neuroscience & Endocrinology (SENSE) program evaluates the social functioning of children with autism and related neurodevelopmental disorders.
Camp participants ages 8 to 17 years join with typically developing peers who are specially trained to serve as models for social interaction and communication, skills that are difficult for children with autism. The camp uses techniques such as role-play and improvisation and culminates in public performances of a play.
“The findings show that treatment can be delivered in an unconventional setting, and children with autism can learn from unconventional ‘interventionists’ – their typically developing peer,” said lead author Blythe Corbett, Ph.D., associate professor of Psychiatry.
Social perception and interaction skills were measured before and after the camp using neuropsychological measures, play with peers and parental reporting. Significant differences were found in face processing, social awareness and social cognition, and duration of interaction with familiar peers increased significantly over the course of the camp.
Additionally, the stress hormone cortisol was measured through saliva samples taken both at home and throughout the camp to compare the stress level of participants at home, at the beginning of the camp and at the end of the camp. Cortisol levels rose on the first day of camp when compared to home values but declined by the end of treatment and during post-treatment play with peers.
“Our findings show that the SENSE Theatre program contributes to improvement in core social deficits when engaging with peers both on and off the stage,” Corbett said. “This research also shows it’s never too late to make a significant difference in the lives of children and youth with autism spectrum disorder, as [this program] targets children who are much older than kids who are participating in early intervention, yet we are still seeing significant gains in the core deficits of autism, and in a rather brief intervention.”
This research was supported by the Martin McCoy-Jesperson Discovery Grant in Positive Psychology and a grant from the National Institute of Mental Health (Grant No. R01 MH085717).
Corbett will continue using theatre techniques to study areas of social functioning among children with autism through a newly awarded grant from the National Institute of Mental Health (Grant No. R34 MH097793). This forthcoming study will explore treatment length and peer familiarity as factors in optimizing and generalizing gains and will enroll more than 30 youth with autism ages 8 to 16 in a 10-week program model beginning January 2014.](http://40.media.tumblr.com/e2806bc80e70035b0238e7cff1782340/tumblr_mv4dx03Ixr1rog5d1o1_500.jpg)
Theatre offers promise for youth with autism
A novel autism intervention program using theatre to teach reciprocal communication skills is improving social deficits in adolescents with the disorder that now affects an estimated one in 88 children, Vanderbilt University researchers released today in the journal Autism Research.
The newly released study assessed the effectiveness of a two-week theatre camp on children with autism spectrum disorder and found significant improvements were made in social perception, social cognition and home living skills by the end of the camp. There were also positive changes in the participants’ physiological stress and reductions in self-reported parental stress.
Called SENSE Theatre, the Social Emotional Neuroscience & Endocrinology (SENSE) program evaluates the social functioning of children with autism and related neurodevelopmental disorders.
Camp participants ages 8 to 17 years join with typically developing peers who are specially trained to serve as models for social interaction and communication, skills that are difficult for children with autism. The camp uses techniques such as role-play and improvisation and culminates in public performances of a play.
“The findings show that treatment can be delivered in an unconventional setting, and children with autism can learn from unconventional ‘interventionists’ – their typically developing peer,” said lead author Blythe Corbett, Ph.D., associate professor of Psychiatry.
Social perception and interaction skills were measured before and after the camp using neuropsychological measures, play with peers and parental reporting. Significant differences were found in face processing, social awareness and social cognition, and duration of interaction with familiar peers increased significantly over the course of the camp.
Additionally, the stress hormone cortisol was measured through saliva samples taken both at home and throughout the camp to compare the stress level of participants at home, at the beginning of the camp and at the end of the camp. Cortisol levels rose on the first day of camp when compared to home values but declined by the end of treatment and during post-treatment play with peers.
“Our findings show that the SENSE Theatre program contributes to improvement in core social deficits when engaging with peers both on and off the stage,” Corbett said. “This research also shows it’s never too late to make a significant difference in the lives of children and youth with autism spectrum disorder, as [this program] targets children who are much older than kids who are participating in early intervention, yet we are still seeing significant gains in the core deficits of autism, and in a rather brief intervention.”
This research was supported by the Martin McCoy-Jesperson Discovery Grant in Positive Psychology and a grant from the National Institute of Mental Health (Grant No. R01 MH085717).
Corbett will continue using theatre techniques to study areas of social functioning among children with autism through a newly awarded grant from the National Institute of Mental Health (Grant No. R34 MH097793). This forthcoming study will explore treatment length and peer familiarity as factors in optimizing and generalizing gains and will enroll more than 30 youth with autism ages 8 to 16 in a 10-week program model beginning January 2014.
Baby’s Innate Number Sense Predicts Future Math Skill
Innate ability to identify quantities previews future mathematics performance
Babies who are good at telling the difference between large and small groups of items even before learning how to count are more likely to do better with numbers in the future, according to new research from the Duke Institute for Brain Sciences.
The use of Arabic numerals to represent different values is a characteristic unique to humans, not seen outside our species. But we aren’t born with this skill. Infants don’t have the words to count to 10. So, scientists have hypothesized that the rudimentary sense of numbers in infants is the foundation for higher-level math understanding.
A new study, appearing online in the Oct. 21 Proceedings of the National Academy of Sciences, suggests that children do, in fact, tap into this innate numerical ability when learning symbolic mathematical systems. The Duke researchers found that the strength of an infant’s inborn number sense can be predictive of the child’s future mathematical abilities.
"When children are acquiring the symbolic system for representing numbers and learning about math in school, they’re tapping into this primitive number sense," said Elizabeth Brannon, Ph.D., a professor of psychology and neuroscience, who led the study. "It’s the conceptual building block upon which mathematical ability is built."
Brannon explained that babies come into the world with a rudimentary understanding referred to as a primitive number sense. When looking at two collections of objects, primitive number sense allows them to identify which set is numerically larger even without verbal counting or using Arabic numerals. For example, a person instinctively knows a group of 15 strawberries is more than six oranges, just by glancing.
Understanding how infants and young children conceptualize and understand number can lead to the development of new mathematics education strategies, said Brannon’s colleague, Duke psychology and neuroscience graduate student Ariel Starr. In particular, this knowledge can be used to design interventions for young children who have trouble learning mathematics symbols and basic methodologies.
To test for primitive number sense, Brannon and Starr analyzed 48 6-month-old infants to see whether they could recognize numerical changes, capitalizing on the interest most babies show in things that change. They placed each baby in front of two screens, one that always showed the same number of dots (e.g., eight), changing in size and position, and another that switched between two different numerical values (e.g., eight and 16 dots). All the arrays of dots changed frequently in size and position. In this task, babies that could tell the difference between the two numerical values (e.g., eight and 16) looked longer at the numerically changing screen.
Brannon and Starr then tested the same children at 3.5 years of age with a non-symbolic number comparison game. The children were shown two different arrays and asked to choose which one had more dots without counting them. In addition, the children took a standardized math test scaled for pre-schoolers, as well as a standardized IQ test. Finally, the researchers gave the children a simple verbal task to identify the largest number word each child could concretely understand.
"We found that infants with higher preference scores for looking at the numerically changing screen had better primitive number sense three years later compared to those infants with lower scores," Starr said. "Likewise, children with higher scores in infancy performed better on standardized math tests."
Brannon said the findings point to a real connection between symbolic math and quantitative abilities that are present in infancy before education takes hold and shapes our mathematical abilities.
"Our study shows that infant number sense is a predictor of symbolic math," Brannon said. "We believe that when children learn the meaning of number words and symbols, they’re likely mapping those meanings onto pre-verbal representations of number that they already have in infancy," she said.
"We can’t measure a baby’s number sense ability at 6 months and know how they’ll do on their SATs," Brannon added. "In fact our infant task only explains a small percentage of the variance in young children"s math performance. But our findings suggest that there is cognitive overlap between primitive number sense and symbolic math. These are fundamental building blocks."
(Source: today.duke.edu)