Posts tagged science
Articles and news from the latest research reports.
Study uncovers surprising differences in brain activity of alcohol-dependent women
A new Indiana University study that examines the brain activity of alcohol-dependent women compared to women who were not addicted found stark and surprising differences, leading to intriguing questions about brain network functions of addicted women as they make risky decisions about when and what to drink.
The study used functional magnetic resonance imaging, or fMRI, to study differences between patterns of brain network activation in the two groups of women. The findings indicate that the anterior insular region of the brain may be implicated in the process, suggesting a possible new target of treatment for alcohol-dependent women.
"We see that the network dynamics of alcohol-dependent women may be really different from that of healthy controls in a drinking-related task," said Lindsay Arcurio, a graduate student in the Department of Psychological and Brain Sciences. "We have evidence to suggest alcohol-dependent women have trouble switching between networks of the brain."
The research is part of a larger new effort to understand the differences between men and women with respect to alcohol. Arcurio said most of the research on alcohol dependence has been conducted with men or groups of men and women. Yet several factors make looking at women “really important.”
One such factor is that the physiological effects of drinking alcohol, which include liver damage, heart disease or breast cancer, set in much earlier in women than in men. For this reason, the suggested limit on the number of drinks per week that women can safely consume is eight, whereas for men, it is 14. Secondly, binge-drinking in women is on the rise. One in five adolescent girls is binge-drinking three times a month. In women between the ages of 18 and 54, that number is one in eight.
A ‘sledgehammer’ approach to defining differences in brain network activation
Research on decision-making mechanisms in alcohol-dependent individuals typically involves a general risk-taking situation in which money or points are at stake. In this study, participants were placed in the fMRI brain scanner and asked to consider low-risk and high-risk situations specifically related to alcohol — what the researchers describe as “ecological” tasks. Participants were then asked to make decisions regarding control stimuli — food as well as a presumably neutral stimuli, a stapler — to observe whether risky behavior was greater with respect to drinking than with these other items. The same picture cues were used to present high-risk and low-risk scenarios, and these two extremes were as follows:
For the low-risk situation, participants were told: Imagine you are at a bar. You are offered a drink, already paid for, with two shots of alcohol, and you have a safe ride home. For the high-risk, they were told: You are at a bar and are offered a drink already paid for, with six shots of alcohol, but you do not have a safe ride home.
The reason for such an extreme contrast between the two situations, Arcurio said, is that “as one of the first ecological tasks used in the scanner, we wanted to take a sledgehammer approach to really find the differences between cases that are definitely high-risk and those that are definitely low-risk.”
The findings, however, reflect an equally sharp contrast in differences between the brain network activation in alcohol-dependent women versus the controls.
For the control group, high-risk decisions to drink led to the deactivation of regions associated with “approach behavior,” deciding to take the drink in a risky situation. Conversely, women in the control group activate regions associated with the default mode network, a region traditionally thought to involve resting-state behavior or inactive or relaxed mental state, but which some now speculate plays a role in conceptualizing one’s future.
"It gets really interesting," Arcurio said, "comparing this pattern of activation to those in alcohol-dependent women, who behaviorally say they’re more likely to take the high-risk drink compared to the controls. They don’t deactivate anything. In contrast to the controls, alcohol-dependent women activate all three regions in question. They activate regions associated with reward (which release dopamine). They also activate frontal control regions involved in cognitive control and regions associated with the default mode network, involved in resting-state behavior. They are activating everything."
The investigators infer from these findings that alcohol-dependent women have trouble switching between networks. Being unable to activate one region and deactivate another in response to an alcohol-related situation means they are unable to use one strategy over another.
Furthermore, Arcurio said, “a lot of evidence suggests that switching between networks is influenced by the anterior insular and anterior cingulate regions of the brain, and we did find major differences in the insula between the alcohol-dependent women and controls. We’re thinking the issue is pinpointed to that region.”
The researchers are now running analyses to test the hypothesis that the insula helps in this process, which could offer new possibilities for intervention, with both behavioral therapy and medication.
The research is part of a whole research program, both planned and in the works, to further explore the questions about risky decision-making in alcohol-dependent women: studies of adolescent drinking, risky sexual behavior in alcohol-dependent women, the interaction of visual networks with decision-making networks, as well as the way music (or auditory networks) interacts with decision-making mechanisms in alcohol-dependent women. In the latter experiment, college-age participants choose a song that they associate with drinking and one with quiet reflection.
"There’s a lot of Miley Cyrus in the first category," Arcurio said.
(Source: news.indiana.edu)
To answer the seemingly simple question “Have I been here before?” we must use our memories of previous experiences to determine if our current location is familiar or novel. In a new study published in the Journal of Neuroscience researchers from the RIKEN Brain Science Institute have identified a region of the hippocampus, called CA2, which is sensitive to even small changes in a familiar context. The results provide the first clue to the contributions of CA2 to memory and may help shed light on why this area is often found to be abnormal in the schizophrenic brain.
Change comes in many flavors; if we move to a new country, city or house it is easy to recognize the novelty of the environment, but if we come home to find the furniture rearranged or a new piece of art on the wall, this recognition may be much slower. Scientists believe this is because memory formation requires comparing current information with previous experience and the larger the overlap, the more difficult the distinction. It has long been known that the hippocampus is a region of the brain crucial for this type of memory, however the identification of neurons responsible for this comparison has remained elusive.
In this study Marie Wintzer, Roman Boehringer, Denis Polygalov and Thomas McHugh used genetically modified mice and advanced cell imaging techniques to demonstrate that while the entire hippocampus is capable of detecting large changes in context, the small and often overlooked CA2 region is exquisitely sensitive to small changes.
Mice were familiarized with one context and then placed either in a much different context or back in the original with small alterations, such as several new small objects. By detecting the expression of activity induced genes Wintzer and colleagues were able to demonstrate that just a few new objects in the otherwise unchanged context completely altered the pattern of active cells specifically in CA2. Mice that had been genetically engineered to lack this CA2 response explored the new context much less than their normal siblings.
“CA2 has often been overlooked or simply grouped together with its more prominent neighbors, but these data suggest it’s unique and important for recognizing and reacting to changes in our environments” explains Dr. McHugh, the leader of the study.
Compared to rodents, human CA2 is proportionally larger, but still as mysterious. One intriguing finding has been that early in the onset of schizophrenia and bipolar disorder there is a loss of inhibitory neurons specifically in CA2. In addition to the memory problems that accompany these diseases, patients often exhibit a hyper-sensitivity to changes in environment and routine. This study suggests there may be a functional relationship between this sensitivity and CA2 dysfunction, hinting at a new circuit to target in our attempts to understand the function of both the normal and diseased brain.
Molecular biology mystery unravelled
The nature of the machinery responsible for the entry of proteins into cell membranes has been unravelled by scientists, who hope the breakthrough could ultimately be exploited for the design of new anti-bacterial drugs.
Groups of researchers from the University of Bristol and the European Molecular Biology Laboratory (EMBL) used new genetic engineering technologies to reconstruct and isolate the cell’s protein trafficking machinery. Its analysis has shed new light on a process which had previously been a mystery for molecular biologists.
The findings, published this week in the Proceedings of the National Academy of Sciences (PNAS), could also have applications for synthetic biology - an emerging field of science and technology, for the development of novel membrane proteins with useful activities.
Proteins are the building blocks of all life and are essential for the growth of cells and tissue repair. The proteins in the membrane typically help the cell interact with its environment and conserve energy.
Researchers were able to identify the ‘holo-translocon’ as the machinery which inserts proteins into the membrane. It is a large membrane protein complex and is uniquely capable of both protein-secretion and membrane-insertion.
Professor Ian Collinson, from the School of Biochemistry at Bristol University, said: “These findings are important as they address outstanding questions in one of the central pillars of biology, a process essential in every cell in every organism. Having unravelled how this vital holo-translocon works, we’re now in a position to look at its components to see if they can help in the design or screening for new anti-bacterial drugs.”
Why does the brain remember dreams?
Some people recall a dream every morning, whereas others rarely recall one. A team led by Perrine Ruby, an Inserm Research Fellow at the Lyon Neuroscience Research Center (Inserm/CNRS/Université Claude Bernard Lyon 1), has studied the brain activity of these two types of dreamers in order to understand the differences between them. In a study published in the journal Neuropsychopharmacology, the researchers show that the temporo-parietal junction, an information-processing hub in the brain, is more active in high dream recallers. Increased activity in this brain region might facilitate attention orienting toward external stimuli and promote intrasleep wakefulness, thereby facilitating the encoding of dreams in memory.
The reason for dreaming is still a mystery for the researchers who study the difference between “high dream recallers,” who recall dreams regularly, and “low dream recallers,” who recall dreams rarely. In January 2013 (work published in the journal Cerebral Cortex), the team led by Perrine Ruby, Inserm researcher at the Lyon Neuroscience Research Center, made the following two observations: “high dream recallers” have twice as many time of wakefulness during sleep as “low dream recallers” and their brains are more reactive to auditory stimuli during sleep and wakefulness. This increased brain reactivity may promote awakenings during the night, and may thus facilitate memorisation of dreams during brief periods of wakefulness.
In this new study, the research team sought to identify which areas of the brain differentiate high and low dream recallers. They used Positron Emission Tomography (PET) to measure the spontaneous brain activity of 41 volunteers during wakefulness and sleep. The volunteers were classified into 2 groups: 21 “high dream recallers” who recalled dreams 5.2 mornings per week in average, and 20 “low dream recallers,” who reported 2 dreams per month in average. High dream recallers, both while awake and while asleep, showed stronger spontaneous brain activity in the medial prefrontal cortex (mPFC) and in the temporo-parietal junction (TPJ), an area of the brain involved in attention orienting toward external stimuli.
Scientists discover hormone released after exercise can ‘predict’ biological age
Scientists from Aston University have discovered a potential molecular link between Irisin, a recently identified hormone released from muscle after bouts of exercise, and the ageing process.
Irisin, which is naturally present in humans, is capable of reprograming the body’s fat cells to burn energy instead of storing it. This increases the metabolic rate and is thought to have potential anti-obesity effects which in turn could help with conditions such as type-2 diabetes.
The research team led by Dr James Brown have proven a significant link exists between Irisin levels in the blood and a biological marker of ageing called telomere length. Telomeres are small regions found at the end of chromosomes that shorten as cells within the body replicate. Short telomere length has been linked to many age-related diseases including cancer, heart disease and Alzheimer’s disease.
Using a population of healthy, non-obese individuals, the team has shown those individuals who had higher levels of Irisin were found to have longer telomeres. The finding provides a potential molecular link between keeping active and healthy ageing with those having higher Irisin levels more ‘biological young’ than those with lower levels of the hormone.
Dr James Brown from Aston’s Research Centre for Healthy Ageing, said; “Exercise is known to have wide ranging benefits, from cardiovascular protection to weight loss. Recent research has suggested that exercise can protect people from both physical and mental decline with ageing. Our latest findings now provide a potential molecular link between keeping active and a healthy ageing process.”
The Aston Research Centre for Healthy Ageing takes a multidisciplinary approach to successful ageing by asking how technological, therapeutic and psychosocial strategies can be employed to understand and arrest age-related decline and degeneration.
How Well Do Football Helmets Protect Players from Concussions?
A new study finds that football helmets currently used on the field may do little to protect against hits to the side of the head, or rotational force, an often dangerous source of brain injury and encephalopathy. The study released today will be presented at the American Academy of Neurology’s 66th Annual Meeting in Philadelphia, April 26 to May 3, 2014.
"Protection against concussion and complications of brain injury is especially important for young players, including elementary and middle school, high school and college athletes, whose still-developing brains are more susceptible to the lasting effects of trauma," said study co- author Frank Conidi, MD, DO, MS, director of the Florida Center for Headache and Sports Neurology and Assistant Clinical Professor of Neurology at Florida State University College of Medicine in Port Saint Lucie, Fla. Conidi is also the vice chair of the American Academy of Neurology’s Sports Neurology Section.
For the study, researchers modified the standard drop test system, approved by the National Operating Committee on Standards for Athletic Equipment, that tests impacts and helmet safety. The researchers used a crash test dummy head and neck to simulate impact. Sensors were also placed in the dummy’s head to measure linear and rotational responses to repeated 12 mile-per-hour impacts. The scientists conducted 330 tests to measure how well 10 popular football helmet designs protected against traumatic brain injury, including: Adams a2000, Rawlings Quantum, Riddell 360, Riddell Revolution, Riddell Revolution Speed, Riddell VSR4, Schutt Air Advantage, Schutt DNA Pro+, Xenith X1 and Xenith X2.
The study found that football helmets on average reduced the risk of traumatic brain injury by only 20 percent compared to not wearing a helmet. Of the 10 helmet brands tested, the Adams a2000 provided the best protection against concussion and the Schutt Air Advantage the worst. Overall, the Riddell 360 provided the most protection against closed head injury and the Adams a2000 the least, despite rating the best against concussion.
"Alarmingly, those that offered the least protection are among the most popular on the field," said Conidi. "Biomechanics researchers have long understood that rotational forces, not linear forces, are responsible for serious brain damage including concussion, brain injury complications and brain bleeds. Yet generations of football and other sports participants have been under the assumption that their brains are protected by their investment in headwear protection."
The study found that football helmets provided protection from linear impacts, or those leading to bruising and skull fracture. Compared to tests using dummies with no helmets, leading football helmets reduced the risk of skull fracture by 60 to 70 percent and reduced the risk of focal brain tissue bruising by 70 to 80 percent.
The study was supported by BRAINS, Inc., a research and development company based in San Antonio, Fla., focused on biomechanics of traumatic brain injury.
Learning to see better in life and baseball
With a little practice on a computer or iPad—25 minutes a day, 4 days a week, for 2 months—our brains can learn to see better, according to a study of University of California, Riverside baseball players reported in the Cell Press journal Current Biology on February 17. The new evidence also shows that a visual training program can sometimes make the difference between winning and losing.
The study is the first, as far as the researchers know, to show that perceptual learning can produce improvements in vision in normally seeing individuals.
"The demonstration that seven players reached 20/7.5 acuity—the ability to read text at three times the distance of a normal observer—is dramatic and required players to stand forty feet back from the eye chart in order to get a measurement of their vision," says Aaron Seitz of the University of California, Riverside. For reference, 20/20 is considered normal visual acuity.
In the training game, the players’ task was to find and select visual patterns modeled after stimuli to which neurons in the early visual cortex of the brain respond best, Seitz explains. As game play commenced, those patterns were made dimmer and dimmer, exercising the players’ vision as they searched.
"The goal of the program is to train the brain to better respond to the inputs that it gets from the eye," Seitz says. "As with most other aspects of our function, our potential is greater than our normative level of performance. When we go to the gym and exercise, we are able to increase our physical fitness; it’s the same thing with the brain. By exercising our mental processes we can promote our mental fitness."
After the 2 month training period, players reported “seeing the ball much better,” “greater peripheral vision,” “easy to see further,” “able to distinguish lower-contrasting things,” “eyes feel stronger, they don’t get tired as much,” and so on.
The players also showed greater-than-expected improvements in their game. They were less likely to strike out and got more runs. The researchers estimate that those gains in batting statistics may have given the team an additional four or five wins in the 2013 season.
The researchers are now extending their work to include different groups, including members of the Los Angeles and Riverside Police Departments and people with low vision due to cataracts, macular degeneration, or amblyopia. They will also apply the same principles to other aspects of cognition, including memory and attention.
It all comes down to one thing: “Understanding the rules of brain plasticity unlocks great potential for improvement of health and wellbeing,” Seitz says.
Environmentally sensitive cells with a Hulk-like rage
Human exposure to urban air pollution may trigger toxic responses in brain cells and impact neurodegenerative disease pathways
From diesel exhaust to gaseous pollutants and suspended particulate matter, such as dust, smoke and fumes, air pollution from transportation, industry and energy generation has taken a toll on the environment and human health.
While the adverse effects of air pollution on the cardiovascular and respiratory systems have been well documented, little is known about how the associated toxins may impact the brain and the central nervous system. In recent years, experts have reported a marked rise in the prevalence of stroke, autism and cognitive decline in the elderly.
Researchers such as Michelle Block, Ph.D., associate professor in the Department of Anatomy and Neurobiology in the Virginia Commonwealth University School of Medicine, are now on a mission to define the impact of air pollution on the brain and central nervous system.
Through basic science, Block and her team are working to understand the underlying molecular mechanisms in hopes of developing an intervention that can protect human health.
Recent scientific reports suggest air pollution exposure and the activation of a specific group of cells found in the brain being studied in Block’s laboratory may play a role in the increased incidence of central nervous system diseases and neurological conditions. They have observed that these factors may also impact the neurodegenerative disease process.
Last week, Block, presented her team’s significant research findings to peers from across the country during a symposium she co-organized at the 2014 annual meeting of the American Association for the Advancement of Science, held in Chicago, from Feb. 13 to 17.
“Angry” cells, toxic responses
Block’s research examines microglia, a group of resident immune cells found in the brain and spinal cord, which can display a kind of dual personality – one good, and the other bad if agitated.
Under normal conditions, microglia primarily serve as the defenders of the central nervous system. They bring balance to the system. They destroy infectious agents, engulf various unwanted cellular and foreign materials and promote regrowth of damaged neural tissue.
But microglia can be dangerous when they are exceptionally “angry” and are known to leave behind significant bystander damage to neighboring cells. This adverse behavior may lead to the development of any number of neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, or Gulf War Illness.
In some ways, microglia are similar to misunderstood superhero The Incredible Hulk. Despite having a decent-sized heart and extraordinary abilities to help save the day, nobody wants to stir his rage and anger.
Block’s laboratory specializes in understanding the cellular and molecular machinery responsible for essentially fueling microglia “anger” – why they become chronically and excessively activated to drive damage in the brain.
“Our goal is to define how microglia detect and respond to air pollution, reveal when this microglial response may actually be damaging the brain, identify potential markers of ongoing silent neuropathology and ultimately use the mechanistic information we acquire as a tool to halt the induced or augmented neuropathology,” Block said.
In several peer-reviewed, published reports, Block and her colleagues have demonstrated that exposure to a diverse source of urban air pollution can trigger toxic microglial responses and impact neurodegenerative disease pathways.
“Given the prevalence of human exposure to urban air pollution above safety regulations, it is critical to understand the underlying mechanisms through which air pollution affects the brain,” Block said. “We hope to find an opportunity to intervene and protect human central nervous system health.”
According to Block, her team’s work shows that many components of urban air pollution, including the particle components of air pollution, also called particulate matter, and gases, such as ground level ozone, activate microglia.
Some of the problems with this cell type come in when the same molecular tools used by microglia internalize (eat) and clean up toxic stimuli and accidentally trigger the switch to an excessive, angry activation state. The work she presented reveals how air pollution does this, essentially leaving microglia with much more than a mouthful. Her lab has discovered that the MAC1 pattern recognition receptor may be a common mechanism through which microglia detect and ultimately misinterpret different forms of air pollution as an invading pathogen to result in excessive production of reactive oxygen species and consequent damage to neighboring brain cells.
Further, ongoing research in Block’s lab aims to define where damage to the lungs through inhaled toxicants produces injury signals in the circulation that are not only detected by microglia in the brain, but are responsible for shifting microglia to a deleterious phenotype impacting central nervous system health. She refers to this as a “Lung-Brain Axis.”
New blood cells fight brain inflammation
Hyperactivity of our immune system can cause a state of chronic inflammation. If chronic, the inflammation will affect our body and result in disease. In the devastating disease multiple sclerosis, hyperactivity of immune cells called T-cells induce chronic inflammation and degeneration of the brain. Researchers at BRIC, the University of Copenhagen, have identified a new type of regulatory blood cells that can combat such hyperactive T-cells in blood from patients with multiple sclerosis. By stimulating the regulatory blood cells, the researchers significantly decreased the level of brain inflammation and disease in a biological model. The results are published in the journal Nature Medicine.
Molecule activate anti-inflammatory blood cells
The new blood cells belong to the group of our white blood cells called lymphocytes. The cells express a molecule called FoxA1 that the researchers found is responsible for the cells’ development and suppressive functions.
"We knew that some unidentified blood cells were able to inhibit multiple sclerosis-like disease in mice and through gene analysis we found out, that these cells are a subset of our lymphocytes expressing the gene FoxA1. Importantly, when inserting FoxA1 into normal lymphocytes with gene therapy, we could change them to actively regulate inflammation and inhibit multiple sclerosis", explains associated professor Yawei Liu leading the experimental studies.
Image caption: Tissue sections from an untreated diseased brain and a FoxA1-treated brain from the researchers biological model. (Photo: Yawei Liu)
Activating own blood cells for treatment of disease
FoxA1 expressing lymphocytes were not known until now, and this is the first documentation of their importance in controlling multiple sclerosis. The number of people living with this devastating disease around the world has increased by 10 percent in the past five years to 2.3 million. It affects women twice more than men and no curing treatment exists. The research group headed by professor Shohreh Issazadeh-Navikas from BRIC examined blood of patients with multiple sclerosis, before and after two years of treatment with the drug interferon-beta. They found that patients who benefit from the treatment increase the number of this new blood cell type, which fight disease.
Image caption: FoxA1-lymphocytes. (Photo: Yawei Liu)
“From a therapeutic viewpoint, our findings are really interesting and we hope that they can help finding new treatment options for patients not benefiting from existing drugs, especially more chronic and progressive multiple sclerosis patients. In our model, we could activate lymphocytes by chemical stimulation and gene therapy, and we are curios whether this can be a new treatment strategy”, says professor Shohreh Issazadeh-Navikas.
And this is exactly what the research group will focus on at next stage of their research. They have already started to test whether the new FoxA1-lymphocytes can prevent degradation of the nerve cell’s myelin layer and brain degeneration in a model of progressive multiple sclerosis. Besides multiple sclerosis, knowledge on how to prevent chronic inflammation will also be valuable for other autoimmune diseases like type 1 diabetes, inflammatory bowel disease and rheumatoid arthritis, where inflammation is a major cause of the disease.
(Source: news.ku.dk)
Gender and genes play an important role in delayed language development
Boys are at greater risk for delayed language development than girls, according to a new study using data from the Norwegian Mother and Child Cohort Study. The researchers also found that reading and writing difficulties in the family gave an increased risk.
“We show for the first time that reading and writing difficulties in the family can be the main reason why a child has a speech delay that first begins between three to five years of age,” says Eivind Ystrøm, senior researcher at the Norwegian Institute of Public Health.
Ystrøm was supervisor of Imac Maria Zambrana, a former PhD student at the Norwegian Institute of Public Health who conducted the research in this study as part of her doctoral research.
The researchers used data from questionnaires completed by the mothers who are participating in the Norwegian Mother and Child Cohort Study (MoBa). The study included more than 10,000 children from week 17 of pregnancy up to five years of age.
“MoBa is a large study with a normal cross-section of the population. It gives us a unique opportunity to examine changes over time, the scope and any risk factors for delayed language development,” says Ystrøm.
Mostly boys
The researchers classified the language difficulties at three and five years of age in three groups: persistent delayed language development (present at both times), transient delayed language development (only present at three years) and delayed language development first identified at five years old.
Boys are in the majority for the groups with persistent and transient language difficulties. Ystrøm explains that boys are biologically at greater risk for developmental disorders in utero than girls. British scientists have measured the male sex hormone (testosterone) in amniotic fluid and they found that the levels were related to the development of both autism and language disorders. Ystrøm points out that boys are generally a little later in language development than girls, but that most catch up during the first year. Therefore, many boys could be at risk of persistent language impairment and increasingly have transient language difficulties that disappear before school age.
The researchers found that gender was irrelevant for the third group who have language difficulties that begin sometime between three and five years of age.
Hereditary factors
We have good knowledge about normal language development in children. Many genes are important for language development and research suggests that different genes are involved in different types of language difficulty.
“Reading and writing difficulties in the family are the predominant risk factors for late-onset language difficulties. We see no language problems when the child is between 18 months and three years old. They are latent” says Ystrøm.
The researchers believe that both specific genes and factors in the child’s external environment can lead to delays in language development at three to five years of age.
What can we do?
Ystrøm believes that children with delayed language development must be identified as early as possible. Parents, health care workers and child care staff should be aware of the language development of children and encourage an enabling language environment, in some cases with specially adapted measures. In particular, they must be aware of children who have sustained disabilities, or who have had normal language development up to three years and then unexpectedly began to have difficulties.
“Professionals and caregivers must be vigilant. It is difficult to detect language difficulties when language becomes more complex in older children. They must be trained so that they are confident in how to spot language difficulties and how to encourage a child’s language. We need more research into the needs of children with different trajectories”, says Ystrøm.
Parents who are concerned about their child’s language development should consult their doctor. They should also raise the issue at the regular check-ups at the health clinic when the child is between two and four years old.
“The checks must take place at the appropriate time. It is important that they are not delayed or not implemented at all,” says Ystrøm.
A few years ago, a survey by the Health and Welfare Department in Oslo showed that few of the health centres in Oslo met the required 14 consultations for each child from birth to school stipulated by the Norwegian Directorate of Health.
Further research
In addition to researchers at the Norwegian Institute of Public Health, researchers at the University of Oslo and the University of Melbourne in Australia participated in this study. The work is funded by the Extra Foundation for Health and Rehabilitation.
“We hope to continue this research and specifically look at the relationship between gender and language. We need more research into the needs of children with various types of language delay”, says Eivind Ystrøm.
Reference
Zambrana, IM, Pons, F., Eadie, P. and Ystrom, E. (2013). Trajectories of language delay from age 3 to 5: persistence, recovery and late onset. International Journal of Language & Communication
(Source: fhi.no)