Posts tagged science
Articles and news from the latest research reports.
Study Links Autistic Behaviors to Enzyme
Fragile X syndrome (FXS) is a genetic disorder that causes obsessive-compulsive and repetitive behaviors, and other behaviors on the autistic spectrum, as well as cognitive deficits. It is the most common inherited cause of mental impairment and the most common cause of autism.
Now biomedical scientists at the University of California, Riverside have published a study that sheds light on the cause of autistic behaviors in FXS. Appearing online today (July 23) in the Journal of Neuroscience, and highlighted also on the cover in this week’s print issue of the journal, the study describes how MMP-9, an enzyme, plays a critical role in the development of autistic behaviors and synapse irregularities, with potential implications for other autistic spectrum disorders.
MMP-9 is produced by brain cells. Inactive, it is secreted into the spaces between cells of the brain, where it awaits activation. Normal brains have quite a bit of inactive MMP-9, and the activation of small amounts has significant effects on the connections between neurons, called synapses. Too much MMP-9 activity causes synapses in the brain to become unstable, leading to functional deficits.
“Our study targets MMP-9 as a potential therapeutic target in Fragile X and shows that genetic deletion of MMP-9 favorably impacts key aspects of FXS-associated anatomical alterations and behaviors in a mouse model of Fragile X,” said Iryna Ethell, a professor of biomedical sciences in the UC Riverside School of Medicine, who co-led the study. “We found that too much MMP-9 activity causes synapses to become unstable, which leads to functional deficits that depend on where in the brain that occurs.”
Ethell explained that mutations in FMR1, a gene, have been known for more than a decade to cause FXS, but until now it has been unclear how these mutations cause unstable synapses and characteristic physical features of this disorder. The new findings expand on earlier work by the research group that showed that an MMP-9 inhibitor, minocycline, can reduce behavioral aspects of FXS, which then led to its use to treat FXS.
To further establish a causative role for MMP-9 in the development of FXS-associated features, including autistic behaviors, the authors generated mice that were missing both FMR1 and MMP-9. They found that while mice with a single FMR1 mutation showed autistic behaviors and macroorchidism (abnormally large testes), mice that also lacked MMP-9 showed no autistic behaviors.
“Our work points directly to MMP-9 over-activation as a cause for synaptic irregularities in FXS, with potential implications for other autistic spectrum disorders and perhaps Alzheimer’s disease,” said Doug Ethell, the head of Molecular Neurobiology at the Western University of Health Sciences, Pomona, Calif., and a coauthor on the study.
The research paper represents many years of bench work and effort by a dedicated team led by the Ethells. The work was primarily done in mice, but human tissue samples were also analyzed, with findings found to be consistent. Specifically, the work involved assessing behaviors, biochemistry, activity and anatomy of synaptic connections in the brain of a mouse model of FXS, as well as the creation of a new mouse line that lacked both the FXS gene and MMP-9.
FXS affects both males and females, with females often having milder symptoms than males. It is estimated that about 1 in 5,000 males are born with the disorder.
The Ethells were joined in the study by UCR’s Harpreet Sidhu (first author of the research paper), Lorraine E. Dansie, and Peter Hickmott. Sidhu and Dansie are neuroscience graduate students; Hickmott is an associate professor of psychology.
Next, the researchers plan to understand how MMP-9 regulates synapse stability inside the neurons. They also plan to find drugs that specifically target MMP-9 without side effects such as new tetracycline derivatives that are potent inhibitors of MMP-9 but lack antibiotic properties.
“Although minocycline was successfully used in clinical trial in FXS, it has some side effects associated with its antibiotic properties, such gastrointestinal irritation,” Iryna Ethell said. “We, therefore, plan to test new non-antibiotic minocycline derivatives. These compounds lack antibiotic activity but still act as non-competitive inhibitors of MMP-9 similar to minocycline.”
Rhymes can inspire reasoning during the third trimester in the womb
Mozart, Beethoven or even Shakespeare — pregnant mothers have been known to expose their babies to many forms of auditory stimulation. But according to researchers at the University of Florida, all a baby really needs is the music of mom’s voice.
Research published in the most recent issue of the journal Infant Behavior and Development shows that babies in utero begin to respond to the rhythm of a nursery rhyme — showing evidence of learning — by 34 weeks of pregnancy and are capable of remembering a set rhyme until just prior to birth. Nursing researcher Charlene Krueger and her team studied pregnant women who recited a rhyme to their babies three times a day for six weeks, beginning at 28 weeks’ gestational age, which is the start of the third trimester of pregnancy.
“The mother’s voice is the predominant source of sensory stimulation in the developing fetus,” said Krueger, an associate professor in the UF College of Nursing. “This research highlights just how sophisticated the third trimester fetus really is and suggests that a mother’s voice is involved in the development of early learning and memory capabilities. This could potentially affect how we approach the care and stimulation of the preterm infant.”
Krueger’s team recruited 32 pregnant women during their 28th week of pregnancy, as determined by fetal ultrasound. The participants were between 18 and 39 years of age, spoke English as a primary language and were pregnant with their first baby. Once recruited, the women were randomly assigned to either an experimental or a control group. The mean age of the women in the group was 25. In addition, 68 percent of the women were white, 28 percent were black and 4 percent were of another race or ethnicity.
From 28 to 34 weeks of pregnancy, all mothers in the study recited a passage or nursery rhyme out loud twice a day and then came in for testing at 28, 32, 33 and 34 weeks’ gestation. To determine whether the fetus could remember the pattern of speech at 34 weeks of age, all mothers were asked to stop speaking the passage. Then the fetuses were tested again at 36 and 38 weeks’ gestational age.
During testing, researchers used a fetal heart monitor, similar to what is used during traditional labor and delivery, to record heart rate and determine any changes. Researchers interpret a small heart rate deceleration in the fetus as an indicator of learning or familiarity with a stimulus.
At testing, the fetuses in the experimental group were played a recording of the same rhyme their mother had been reciting at home but spoken by a female stranger. Those in the control group heard a different rhyme also spoken by a stranger. This was to help determine if the fetus was responding simply to its mother’s voice or to a familiar pattern of speech, which is a more difficult task, Krueger said.
The researchers found that the fetus’ heart rate began to respond to the familiar rhyme recited by a stranger’s voice by 34 weeks of gestational age — once the mother had spoken the rhyme out loud at home for six weeks. They continued to respond with a small cardiac deceleration for as long as four weeks after the mother had stopped saying the rhyme until about 38 weeks. At 38 weeks, there was a statistically significant difference between the two groups in responding to the strangers’ recited rhymes — the experimental group who heard the original rhyme responded with a deeper and more sustained cardiac deceleration, whereas the control group who heard a new rhyme responded with a cardiac acceleration.
Further research is needed to more fully understand how ongoing development affects learning and memory, Krueger said. Her aim is to recognize how this type of research can influence care in preterm infants and their long-term outcomes.
“This study helped us understand more about how early a fetus could learn a passage of speech and whether the passage could be remembered weeks later even without daily exposure to it,” Krueger said. “This could have implications to those preterm infants who are born before 37 weeks of age and the impact an intervention such as their mother’s voice may have on influencing better outcomes in this high-risk population.”
(Source: news.ufl.edu)
Children as young as three recognise ‘cuteness’ in faces of people and animals
Children as young as three are able to recognise the same ‘cute’ infantile facial features in humans and animals which encourage caregiving behaviour in adults, new research has shown.
A study investigating whether youngsters can identify baby-like characteristics – a set of traits known as the ‘baby schema’ – across different species has revealed for the first time that even pre-school children rate puppies, kittens and babies as cuter than their adult counterparts.
The discovery that young children are influenced by the baby schema – a round face, high forehead, big eyes and a small nose and mouth – is a significant step towards understanding why humans are more attracted to infantile features, the study authors believe.
The baby schema has been proven to engender protective, care-giving behaviour and a decreased likelihood of aggression toward infants from adults.
The research was carried out by PhD student Marta Borgi and Professor Kerstin Meints, members of the Evolution and Development Research Group in the School of Psychology at the University of Lincoln, UK.
Marta said: “This study is important for several reasons. We already knew that adults experience this baby schema effect, finding babies with more infantile features cuter.
“Our results provide the first rigorous demonstration that a visual preference for these traits emerges very early during development. Independently of the species viewed, children in our study spent more time looking at images with a higher degree of these baby-like features.
“Interestingly, while participants gave different cuteness scores to dogs, cats and humans, they all found the images of adult dog faces cuter than both adult cats and human faces.”
The researchers carried out two experiments with children aged between three and six years old: one to track eye movements to see which facial areas the children were drawn to, and a second to assess how cute the children rated animals and humans with infantile traits.
Pictures of human adults and babies, dogs, puppies, cats and kittens were digitally manipulated to appear ‘cuter’ by applying baby schema characteristics. The same source images were also made less cute by giving the subjects more adult-like features: a narrow face, low forehead, small eyes, and large nose and mouth – making this study more rigorous than previous work.
The children rated how cute they thought each image was and their eye movements were analysed using specialist eye-tracking software developed by the University of Lincoln.
The research could also lead to improved education in teaching children about safe behaviour with dogs.
Professor Kerstin Meints, Professor in Developmental Psychology at Lincoln’s School of Psychology, supervised the research.
She said: “We have also demonstrated that children are highly attracted to dogs and puppies, and we now need to find out if that attractiveness may override children’s ability to recognise stress signalling in dogs.”
“This study will also lead to further research with an impact on real life, namely whether the ‘cuteness’ of an animal in rescue centres makes them more or less likely to be adopted.”
This research was published in the scientific journal Frontiers in Psychology.
Brain waves show learning to read does not end in 4th grade, contrary to popular theory
Teachers-in-training have long been taught that fourth grade is when students stop learning to read and start reading to learn. But a new Dartmouth study in the journal Developmental Science tested the theory by analyzing brain waves and found that fourth-graders do not experience a change in automatic word processing, a crucial component of the reading shift theory. Instead, some types of word processing become automatic before fourth grade, while others don’t switch until after fifth.
The findings mean that teachers at all levels of elementary school must think of themselves as reading instructors, said the study’s author, Associate Professor of Education Donna Coch.
"Until now, we lacked neurological evidence about the supposed fourth-grade shift," said Coch, also principal investigator for Dartmouth’s Reading Brains Lab. "The theory developed from behavioral evidence, and as a result of it, some teachers in fifth and sixth grade have not thought of themselves as reading instructors. Now we can see from brain waves that students in those grades are still learning to process words automatically; their neurological reading system is not yet adult-like."
Automatic word processing is the brain’s ability to determine whether a group of symbols constitutes a word within milliseconds, without the brain’s owner realizing the process is taking place.
To test how automatic word processing develops, Coch placed electrode caps on the heads of third-, fourth-, and fifth-graders, as well as college students. She had her test subjects view a screen that displayed a mix of real English words (such as “bed”), pseudo-words (such as “bem”), strings of letters (such as “mbe”), and strings of meaningless symbols one at a time. The setup allowed her to see how the subjects’ brains reacted to each kind of stimulus within milliseconds. In other words, she could watch their automatic word processing.
Next, Coch gave the participants a written test, in which they were asked to circle the real words in a list that also contained pseudo-words, strings of letters, and strings of meaningless symbols. This task was designed to test the participants’ conscious word processing, a much slower procedure.
Interestingly, most of the 96 participants got a nearly perfect score on the written test, showing that their conscious brains knew the difference between words and non-words.
However, the electrode cap revealed that only the college students processed meaningless symbols differently than real words. The third-, fourth-, and fifth-graders’ brains reacted to the meaningless symbols the same way they reacted to common English words.
"This tells us that, at least through the fifth grade, even children who read well are letting stimuli into the neural word processing system that more mature readers do not," Coch said. "Their brains are processing strings of meaningless symbols as if they were words, perhaps in case they turn out to be real letters. In contrast, by college, students have learned not to process strings of meaningless symbols as words, saving their brains precious time and energy."
The phenomenon is evidence that young readers do not fully develop automatic word processing skills until after fifth grade, which contradicts the fourth-grade reading shift theory.
The brain waves also showed that the third-, fourth-, and fifth-graders processed real words, psuedowords, and letter strings similarly to college students, suggesting that some automatic word processing begins before the fourth grade, and even before the third grade, also contradicting the reading shift theory.
"There is value to the theory of the fourth grade shift in that it highlights how reading skills and abilities develop at different times," Coch said. "But the neural data suggest that teachers should not expect their fourth-graders, or even their fifth-graders, to be completely automatic, adult-like readers."
Stress tied to change in children’s gene expression related to emotion regulation, physical health
Children who have been abused or neglected early in life are at risk for developing both emotional and physical health problems. In a new study, scientists have found that maltreatment affects the way genes are activated, which has implications for children’s long-term development. Previous studies focused on how a particular child’s individual characteristics and genetics interacted with that child’s experiences in an effort to understand how health problems emerge. In the new study, researchers were able to measure the degree to which genes were turned “on” or “off” through a biochemical process called methylation. This new technique reveals the ways that nurture changes nature—that is, how our social experiences can change the underlying biology of our genes.
The study, from researchers at the University of Wisconsin, Madison, appears in the journal Child Development. Nearly 1 million children in the United States are neglected or abused every year.
The researchers found an association between the kind of parenting children had and a particular gene (called the glucocorticoid receptor gene) that’s responsible for crucial aspects of social functioning and health. Not all genes are active at all times. DNA methylation is one of several biochemical mechanisms that cells use to control whether genes are turned on or off. The researchers examined DNA methylation in the blood of 56 children ages 11 to 14. Half of the children had been physically abused.
They found that compared to the children who hadn’t been maltreated, the maltreated children had increased methylation on several sites of the glucocorticoid receptor gene, also known as NR3C1, echoing the findings of earlier studies of rodents. In this study, the effect occurred on the section of the gene that’s critical for nerve growth factor, which is an important part of healthy brain development.
There were no differences in the genes that the children were born with, the study found; instead, the differences were seen in the extent to which the genes had been turned on or off. “This link between early life stress and changes in genes may uncover how early childhood experiences get under the skin and confer lifelong risk,” notes Seth D. Pollak, professor of psychology and pediatrics at the University of Wisconsin, Madison, who directed the study.
Previous studies have shown that children who have experienced physical abuse, sexual abuse, and neglect are more likely to develop mood, anxiety, and aggressive disorders, as well as to have problems regulating their emotions. These problems, in turn, can disrupt relationships and affect school performance. Maltreated children are also at risk for chronic health problems such as cardiac disease and cancer. The current study helps explain why these childhood experiences can affect health years later.
The gene identified by the researchers affects the hypothalamic-pituitary-adrenal (HPA) axis in rodents. Disruptions of this system in the brain would make it difficult for people to regulate their emotional behavior and stress levels. Circulating through the body in the blood, this gene affects the immune system, leaving individuals less able to fight off germs and more vulnerable to illnesses.
"Our finding that children who were physically maltreated display a specific change to the glucocorticoid receptor gene could explain why abused children have more emotional difficulties as they age," according to Pollak. "They may have fewer glucocorticoid receptors in their brains, which would impair the brain’s stress-response system and result in problems regulating stress."
The findings have implications for designing more effective interventions for children, especially since studies of animals indicate that the effects of poor parenting on gene methylation may be reversible if caregiving improves. The study also adds to what we know about how child maltreatment relates to changes in the body and mind, findings that were summarized recently in an SRCD Social Policy Report by Sara R. Jaffee and Cindy W. Christian.
Researcher shows how stress hormones promote brain’s building of negative memories
When a person experiences a devastating loss or tragic event, why does every detail seem burned into memory whereas a host of positive experiences simply fade away?
It’s a bit more complicated than scientists originally thought, according to a study recently published in the journal Neuroscience by ASU researcher Sabrina Segal.
When people experience a traumatic event, the body releases two major stress hormones: norepinephrine and cortisol. Norepinephrine boosts heart rate and controls the fight-or-flight response, commonly rising when individuals feel threatened or experience highly emotional reactions. It is chemically similar to the hormone epinephrine – better known as adrenaline.
In the brain, norepinephrine in turn functions as a powerful neurotransmitter or chemical messenger that can enhance memory.
Research on cortisol has demonstrated that this hormone can also have a powerful effect on strengthening memories. However, studies in humans up until now have been inconclusive – with cortisol sometimes enhancing memory, while at other times having no effect.
A key factor in whether cortisol has an effect on strengthening certain memories may rely on activation of norepinephrine during learning, a finding previously reported in studies with rats.
In her study, Segal, an assistant research professor at the Institute for Interdisciplinary Salivary Bioscience Research at ASU, and her colleagues at the University of California-Irvine showed that human memory enhancement functions in a similar way.
Conducted in the laboratory of Larry Cahill at U.C. Irvine, Segal’s study included 39 women who viewed 144 images from the International Affective Picture Set. This set is a standardized picture set used by researchers to elicit a range of responses, from neutral to strong emotional reactions, upon view.
Segal and her colleagues gave each of the study’s subjects either a dose of hydrocortisone – to simulate stress – or a placebo just prior to viewing the picture set. Each woman then rated her feelings at the time she was viewing the image, in addition to giving saliva samples before and after. One week later, a surprise recall test was administered.
What Segal’s team found was that “negative experiences are more readily remembered when an event is traumatic enough to release cortisol after the event, and only if norepinephrine is released during or shortly after the event.”
“This study provides a key component to better understanding how traumatic memories may be strengthened in women,” Segal added, “because it suggests that if we can lower norepinephrine levels immediately following a traumatic event, we may be able to prevent this memory enhancing mechanism from occurring, regardless of how much cortisol is released following a traumatic event.”
Further studies are needed to explore to what extent the relationship between these two stress hormones differ depending on whether you are male or female, particularly because women are twice as likely to develop disorders from stress and trauma that affect memory, such as in Posttraumatic Stress Disorder (PTSD). In the meantime, the team’s findings are a first step toward a better understanding of neurobiological mechanisms that underlie traumatic disorders, such as PTSD.
(Image: Wikimedia Commons)
Schizophrenia’s genetic skyline rising
The largest genomic dragnet of any psychiatric disorder to date has unmasked 108 chromosomal sites harboring inherited variations in the genetic code linked to schizophrenia, 83 of which had not been previously reported. By contrast, the “skyline” of such suspect variants associated with the disorder contained only 5 significant peaks in 2011. By combining data from all available schizophrenia genetic samples, researchers supported by the National Institutes of Health powered the search for clues to the molecular basis of the disorder to a new level.
“While the suspect variation identified so far only explains only about 3.5 percent of the risk for schizophrenia, these results warrant exploring whether using such data to calculate an individual’s risk for developing the disorder might someday be useful in screening for preventive interventions,” explained Thomas R. Insel, M.D., director of the NIH’s National Institute of Mental Health, one funder of the study. “Even based on these early predictors, people who score in the top 10 percent of risk may be up to 20-fold more prone to developing schizophrenia.”
The newfound genomic signals are not simply random sites of variation, say the researchers. They converge around pathways underlying the workings of processes involved in the disorder, such as communication between brain cells, learning and memory, cellular ion channels, immune function and a key medication target.
The Schizophrenia Working Group of the Psychiatric Genomic Consortium (PGC) reports on its genome-wide analysis of nearly 37,000 cases and more than 113,000 controls in the journal Nature, July 21, 2014. The NIMH-supported PGC represents more than 500 investigators at more than 80 research institutions in 25 countries.
Prior to the new study, schizophrenia genome-wide studies had identified only about 30 common gene variants associated with the disorder. Sample sizes in these studies were individually too small to detect many of the subtle effects on risk exerted by such widely shared versions of genes. The PGC investigators sought to maximize statistical power by re-analyzing not just published results, but all available raw data, published and unpublished. Their findings of 108 illness-associated genomic locations were winnowed from an initial pool of about 9.5 million variants.
A comparison of the combined study data with findings in an independent sample of cases and controls suggest that considerably more such associations of this type are likely to be uncovered with larger sample sizes, say the researchers.
There was an association confirmed with variation in the gene that codes for a receptor for the brain chemical messenger dopamine, which is known to be the target for antipsychotic medications used to treat schizophrenia. Yet evidence from the study supports the view that most variants associated with schizophrenia appear to exert their effects via the turning on and off of genes rather than through coding for proteins.
The study found a notable overlap between protein-related functions of some linked common variants and rare variants associated with schizophrenia in other studies. These included genes involved in communication between neurons via the chemical messenger glutamate, learning and memory, and the machinery controlling the influx of calcium into cells.
“The overlap strongly suggests that common and rare variant studies are complementary rather than antagonistic, and that mechanistic studies driven by rare genetic variation will be informative for schizophrenia,” say the researchers.
Among the strongest associations detected, as in in previous genome-wide genetic studies, was for variation in tissues involved in immune system function. Although the significance of this connection for the illness process remains a mystery, epidemiologic evidence has long hinted at possible immune system involvement in schizophrenia.
Findings confirm that it’s possible to develop risk profile scores based on schizophrenia-associated variants that may be useful in research – but for now aren’t ready to be used clinically as a predictive test, say the researchers.
They also note that the associated variations detected in the study may not themselves be the source of risk for schizophrenia. Rather, they may be signals indicating the presence of disease-causing variation nearby in a chromosomal region.
Researchers are following up with studies designed to pinpoint the specific sequences and genes that confer risk. The PGC is also typing genes in hundreds of thousands of people worldwide to enlarge the sample size, in hopes of detecting more genetic variation associated with mental disorders. Successful integration of data from several GWAS studies suggests that this approach would likely be transferrable to similar studies of other disorders, say the researchers.
“These results underscore that genetic programming affects the brain in tiny, incremental ways that can increase the risk for developing schizophrenia,” said Thomas Lehner, Ph.D., chief of NIMH’s Genomics Research Branch. “They also validate the strategy of examining both common and rare variation to understand this complex disorder.”
Researchers discover neuroprotective role of immune cell
A type of immune cell widely believed to exacerbate chronic adult brain diseases, such as Alzheimer’s disease and multiple sclerosis (MS), can actually protect the brain from traumatic brain injury (TBI) and may slow the progression of neurodegenerative diseases, according to Cleveland Clinic research published today in the online journal Nature Communications.
The research team, led by Bruce Trapp, PhD, Chair of the Department of Neurosciences at Cleveland Clinic’s Lerner Research Institute, found that microglia can help synchronize brain firing, which protects the brain from TBI and may help alleviate chronic neurological diseases. They provided the most detailed study and visual evidence of the mechanisms involved in that protection.
"Our findings suggest the innate immune system helps protect the brain after injury or during chronic disease, and this role should be further studied," Dr. Trapp said. "We could potentially harness the protective role of microglia to improve prognosis for patients with TBI and delay the progression of Alzheimer’s disease, MS, and stroke. The methods we developed will help us further understand mechanisms of neuroprotection."
Microglias are primary responders to the brain after injury or during illness. While researchers have long believed that activated microglia cause harmful inflammation that destroys healthy brain cells, some speculate a more protective role. Dr. Trapp’s team used an advanced technique called 3D electron microscopy to visualize the activation of microglia and subsequent events in animal models.
They found that when chemically activated, microglia migrate to inhibitory synapses, connections between brain cells that slow the firing of impulses. They dislodge the synapse (called “synaptic stripping”), thereby increasing neuronal firing and leading to a cascade of events that enhance survival of brain cells.
Trapp is internationally known for his work on mechanisms of neurodegeneration and repair in multiple sclerosis. His past research has included investigation of the cause of neurological disability in MS patients, cellular mechanisms of brain repair in neurodegenerative diseases, and the molecular biology of myelination in the central and peripheral nervous systems.
(Source: eurekalert.org)
Brain imaging study examines second-language learning skills
With enough practice, some learners of a second language can process their new language as well as native speakers, research at the University of Kansas shows.
(Credit: bigstockphoto)
Using brain imaging, a trio of KU researchers was able to examine to the millisecond how the brain processes a second language. They then compared their findings with their previous results for native speakers and saw both followed similar patterns.
The research by Robert Fiorentino and Alison Gabriele, both associate professors in the linguistics department, and José Alemán Bañón, a former KU graduate student who is now a postdoctoral researcher at the University of Reading in the United Kingdom, was published this month in the journal Second Language Research.
For years, linguists have debated whether second-language learners would ever resemble native speakers in their ability to process language properties that differ between the first and second language, such as gender agreement, which is a property of Spanish but not English. In Spanish, all nouns are categorized as masculine or feminine, and various elements in the sentence, such as adjectives, need to carry the gender feature of the noun as well.
Some researchers argued that even those who spoke a second language with a high level of accuracy were using a qualitatively different mechanism than native speakers.
“We realized that these different theories proposing that either second-language learners use the same mechanism, or a different mechanism could actually be teased apart by using brain-imaging techniques,” Gabriele said.
The team studied 26 high-level Spanish speakers who hadn’t learned to speak Spanish until after age 11 and grew up with English as the majority language. The speakers used Spanish on a daily basis and had spent an average of a year and a half in a Spanish-speaking country.
They were compared with 24 native speakers, who were raised in Spanish-speaking countries and stayed in their home country until age 17.
To measure language processing as it happens, the team used a method known as electroencephalography (EEG), which uses an array of electrodes placed on the scalp to detect patterns of brain activity with high accuracy in timing.
Once hooked up to the EEG, the test subjects were asked to read sentences, some of which had grammatical errors in either number agreement or gender agreement.
The researchers then compared the results of the second-language learners to native speakers. They found that the highly proficient second-language speakers showed the same patterns of brain activity as native speakers when processing grammatical violations in sentences.
“We show that the learners’ brain activity looks qualitatively similar to that of native speakers, suggesting that they are using the same mechanisms,” Fiorentino said.
The study highlights the brain’s plasticity and its ability to acquire a new complex system even in adulthood.
“A lot of researchers have argued that there is some sort of language learning mechanism that might atrophy over the life span, particularly before puberty. And, we certainly have a lot of evidence that it is difficult to process your second language at nativelike levels and you have to go through quite a bit of effort to find people who can,” Gabriele said. “But I think what this paper shows is that it is possible.”
Gabriele and Fiorentino are working on a second phase of the research, studying how the brain processes a second language at the initial stages of exposure. Their preliminary results suggest that properties that are shared between the first and second language show patterns of brain activity that are very similar in learners and native speakers. This suggests that learners build on the representation for language that is already in place when learning a second language.
(Source: news.ku.edu)
Low Strength Brain Stimulation May Be Effective for Depression
Brain stimulation treatments, like electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS), are often effective for the treatment of depression. Like antidepressant medications, however, they typically have a delayed onset. For example, a patient may receive several weeks of regular ECT treatments before a full response is achieved.
Thus, there is an impetus to develop antidepressant treatments that act to rapidly improve mood.
Low field magnetic stimulation (LFMS) is one such potential new treatment with rapid mood-elevating effects, as reported by researchers at Harvard Medical School and Weill Cornell Medical College.
"LFMS is unlike any current treatment. It uses magnetic fields that are a fraction of the strength but at higher frequency than the electromagnetic fields used in TMS and ECT," explained first author Dr. Michael Rohan.
Indeed, the potential antidepressant properties of LFMS were discovered accidentally, while researchers were conducting an imaging study in healthy volunteers. This led Rohan and his colleagues to conduct a preliminary study in which they identified the imaging parameters that seemed to be causing the antidepressant effect.
They then designed and constructed a portable LFMS device, which delivers a low strength, high frequency, electromagnetic field waveform to the brain. The next step was to test the device in depressed patients, the results of which are published in the current issue of Biological Psychiatry.
A total of 63 currently depressed patients, diagnosed with either major depressive disorder or bipolar disorder, participated in the study and were randomized to receive a single 20-minute treatment of real LFMS or sham LFMS, where the device was on but the electromagnetic fields were inactive. Since neither the patients nor the researchers knew which treatment each person actually received, the true effect of the LFMS could be measured.
An immediate and substantial improvement in mood was observed in the patients who received real LFMS, compared to those who received the sham treatment. There were no reported side effects.
This finding suggests that LFMS may have the potential to provide immediate relief of depressed mood, perhaps even in emergency situations. It also confirms the success of the device’s design.
"The idea that weak electrical stimulation of the brain could produce beneficial effects on depression symptoms is somewhat surprising," said Dr. John Krystal, Editor of Biological Psychiatry. “Yet the data make a compelling case that this safe approach deserves further study.”
Rohan confirmed that additional research is underway to find the best parameters for LFMS use in the clinical treatment of depression. Further research will also be necessary to evaluate the effects of multiple compared to single treatments, and how long the antidepressant effects last following treatment.