Neuroscience
Month
September 5, 2012 by Michael C. Purdy
Sleep disruptions may be among the earliest indicators of Alzheimer’s disease, scientists at Washington University School of Medicine in St. Louis report Sept. 5 in Science Translational Medicine.
Working in a mouse model, the researchers found that when the first signs of Alzheimer’s plaques appear in the brain, the normal sleep-wake cycle is significantly disrupted.
“If sleep abnormalities begin this early in the course of human Alzheimer’s disease, those changes could provide us with an easily detectable sign of pathology,” says senior author David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of Washington University’s Department of Neurology. “As we start to treat Alzheimer’s patients before the onset of dementia, the presence or absence of sleep problems may be a rapid indicator of whether the new treatments are succeeding.”
Holtzman’s laboratory was among the first to link sleep problems and Alzheimer’s through studies of sleep in mice genetically altered to develop Alzheimer’s plaques as they age. In a study published in 2009, he showed that brain levels of a primary ingredient of the plaques naturally rise when healthy young mice are awake and drop after they go to sleep. Depriving the mice of sleep disrupted this cycle and accelerated the development of brain plaques.
A similar rising and falling of the plaque component, a protein called amyloid beta, was later detected in the cerebrospinal fluid of healthy humans studied by co-author Randall Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology at Washington University.
The new research, led by Jee Hoon Roh, MD, PhD, a neurologist and postdoctoral fellow in Holtzman’s laboratory, shows that when the first indicators of brain plaques appear, the natural fluctuations in amyloid beta levels stop in both mice and humans.
“We suspect that the plaques are pulling in amyloid beta, removing it from the processes that would normally clear it from the brain,” Holtzman says.
Mice are nocturnal animals and normally sleep for 40 minutes during every hour of daylight, but when Alzheimer’s plaques began forming in their brains, their average sleep times dropped to 30 minutes per hour.
To confirm that amyloid beta was directly linked to the changes in sleep, researchers gave a vaccine against amyloid beta to a new group of mice with the same genetic modifications. As these mice grew older, they did not develop brain plaques. Their sleeping patterns remained normal and amyloid beta levels in the brain continued to rise and fall regularly.
Scientists now are evaluating whether sleep problems occur in patients who have markers of Alzheimer’s disease, such as plaques in the brain, but have not yet developed memory or other cognitive problems.
“If these sleep problems exist, we don’t yet know exactly what form they take—reduced sleep overall or trouble staying asleep or something else entirely,” Holtzman says. “But we’re working to find out.”
A North Carolina State University researcher has created a roadmap to areas of the brain associated with affective aggression in mice. This roadmap may be the first step toward finding therapies for humans suffering from affective aggression disorders that lead to impulsive violent acts.
Affective aggression differs from defensive aggression or premeditated aggression used by predators, in that the role of affective aggression isn’t clear and could be considered maladaptive. NC State neurobiologist Dr. Troy Ghashghaei was interested in finding the areas of the brain engaged with this type of aggressive behavior. Using mice that had been specially bred for affective aggression by his research associate Dr. Derrick L Nehrenberg, Ghashghaei and former undergraduate student Atif Sheikh were able to locate the regions in the mouse brain that switched on and those that were off when the mice displayed affective aggression.
“The brain works by using clusters of neurons that cross communicate at extremely rapid rates, much like a computer,” Ghashghaei explains. “One region will process a stimulus, and then that region sends messages to other clusters within the brain, like circuits within a computer. We looked at how the switches flipped in the brains of aggressive mice, and compared that with the brains of completely nonaggressive mice in the same setting, to see how the two processed the situation differently.”
They found that affectively aggressive mice demonstrated a large difference in the way their “executive centers” operated when the mice encountered another mouse. “Sensory inputs come in and are sent to the executive center, the part of the brain that decides how to respond to the input,” Ghashghaei says. “In the meantime, the information about the response you made gets processed back with either a pleasant or unpleasant association.”
According to Ghashghaei, the affectively aggressive mice could react violently because their brains are hardwiredto respond to certain situations aggressively without assessing whether their response to the situation is appropriate or without regard to the behavior’s consequences. In addition, affectively aggressive mice may be forming pleasant associations with their violent displays, which would reinforce their aggressive tendencies.
“We cannot say which of the two possibilities underlie the persistent aggressive displays by our mice,” Ghashghaei says, “but we can see that the patterns of neuronal activity are very different in the executive centers of these mice. Additionally, there are differences in the neuronal clusters involved with creating pleasant or unpleasant associations to the stimulus or their response. That gives us a few starting spots to begin identifying the mechanisms that underlie these profound behavioral differences.”
The regions of the brain that were involved in affective aggression in the mice are similar across all mammalian species. Ghashghaei hopes that his findings in mice will be useful to researchers studying violent behavior in humans, as well as aggression in other animals.
“With the brain, just knowing where to start looking is huge,” Ghashghaei says. “Once you have a few targets, you can tease out the possibilities and get to the heart of the problem. We are confident that manipulation of some of the identified targets in our study will disrupt displays of affective aggression in our mouse model.”
A new University of Wisconsin-Madison imaging study shows the brains of people with generalized anxiety disorder (GAD) have weaker connections between a brain structure that controls emotional response and the amygdala, which suggests the brain’s “panic button” may stay on due to lack of regulation.
Anxiety disorders are the most common class of mental disorders and GAD, which is characterized by excessive, uncontrollable worry, affects nearly 6 percent of the population.
Lead author Dr. Jack Nitschke, associate professor of psychiatry in the UW School of Medicine and Public Health, says the findings support the theory that reduced communications between parts of the brain explains the intense anxiety felt by people with GAD.
In this case, two types of scans showed the amygdala, which alerts us to threat in our surroundings and initiates the “fight-or-flight” response, seems to have weaker “white matter” connections to the prefrontal and anterior cingulate cortex (ACC), the center of emotional regulation.
The researchers did two types of imaging - diffusion tensor imaging (DTI) and functional magnetic resonance (fMRI) - on the brains of 49 GAD patients and 39 healthy volunteers. Compared with the healthy volunteers, the imaging showed the brains of people with GAD had reduced connections between the prefrontal and anterior cingulate cortex and the amygdala via the uncinate fasciculus, a primary “white matter” tract that connects these brain regions. This reduced connectivity was not found in other white matter tracts elsewhere in their brains.
"We know that in the brain, if you use a circuit you build it up, the way you build muscle by exercise,” says Nitschke, a clinical psychologist who treats patients with anxiety disorders and does research at the UW-Madison’s Waisman Center.
Nitschke says that researchers wonder if this weak connection results in the intense anticipatory anxiety and worry that is the hallmark of GAD, because the ACC is unable to tell the amygdala to “chill out.” It also suggests that behavioral therapy that teaches patients to consciously exercise this emotional regulation works to reduce anxiety by strengthening the connection.
"It’s possible that this is exactly what we’re doing when we teach patients to regulate their reactions to the negative events that come up in everyone’s lives,” Nitschke says. "We can help build people’s tolerance to uncontrollable future events by teaching them to regulate their emotions to the uncertainty that surrounds those events.
03 September 2012 by Andy Coghlan
For the first time, people with broken spines have recovered feeling in previously paralysed areas after receiving injections of neural stem cells.
(Image: Medical Images/Getty Images)
Three people with paralysis received injections of 20 million neural stem cells directly into the injured region of their spinal cord. The cells, acquired from donated fetal brain tissue, were injected between four and eight months after the injuries happened. The patients also received a temporary course of immunosuppressive drugs to limit rejection of the cells.
None of the three felt any sensation below their nipples before the treatment. Six months after therapy, two of them had sensations of touch and heat between their chest and belly button. The third patient has not seen any change.
"The fact we’ve seen responses to light touch, heat and electrical impulses so far down in two of the patients is very unexpected," says Stephen Huhn of StemCells, the company in Newark, California, developing and testing the treatment. "They’re really close to normal in those areas now in their sensitivity," he adds.
"We are very intrigued to see that patients have gained considerable sensory function," says Armin Curt of Balgrist University Hospital in Zurich, Switzerland, where the patients were treated, and principal investigator in the trial.
The data are preliminary, but “these sensory changes suggest that the cells may be positively impacting recovery”, says Curt, who presented the results today in London at the annual meeting of the International Spinal Cord Society.
3-Sep-2012
Researchers at Emory University have found that a medication that inhibits inflammation may offer new hope for people with difficult-to-treat depression. The study was published Sept. 3 in the online version of Archives of General Psychiatry.
"Inflammation is the body’s natural response to infection or wounding, says Andrew H. Miller, MD, senior author for the study and professor of Psychiatry and Behavioral Sciences at Emory University School of Medicine. "However when prolonged or excessive, inflammation can damage many parts of the body, including the brain."
Prior studies have suggested that depressed people with evidence of high inflammation are less likely to respond to traditional treatments for the disorder, including anti-depressant medications and psychotherapy. This study was designed to see whether blocking inflammation would be a useful treatment for either a wide range of people with difficult-to-treat depression or only those with high levels of inflammation.
The study employed infliximab, one of the new biologic drugs used to treat autoimmune and inflammatory diseases such as rheumatoid arthritis and inflammatory bowel disease. A biologic drug copies the effects of substances naturally made by the body’s immune system. In this case, the drug was an antibody that blocks tumor necrosis factor (TNF), a key molecule in inflammation that has been shown to be elevated in some depressed individuals.
Study participants all had major depression and were moderately resistant to conventional antidepressant treatment. Each participant was assigned either to infliximab or to a non-active placebo treatment.
When investigators looked at the results for the group as a whole, no significant differences were found in the improvement of depression symptoms between the drug and placebo groups. However, when the subjects with high inflammation were examined separately, they exhibited a much better response to infliximab than to placebo.
Inflammation in this study was measured using a simple blood test that is readily available in most clinics and hospitals and measures C-reactive protein or CRP. The higher the CRP, the higher the inflammation, and the higher the likelihood of responding to the drug.
"The prediction of an antidepressant response using a simple blood test is one of the holy grails in psychiatry," says Miller. "This is especially important because the blood test not only measured what we think is at the root cause of depression in these patients, but also is the target of the drug."
"This is the first successful application of a biologic therapy to depression," adds Charles L. Raison, MD, first author of the study. "The study opens the door to a host of new approaches that target the immune system to treat psychiatric diseases." Raison, formerly at Emory, is now associate professor in the Department of Psychiatry at the University of Arizona College of Medicine – Tucson.
September 3, 2012
People whose blood sugar is on the high end of the normal range may be at greater risk of brain shrinkage that occurs with aging and diseases such as dementia, according to new research published in the September 4, 2012, print issue of Neurology, the medical journal of the American Academy of Neurology.
"Numerous studies have shown a link between type 2 diabetes and brain shrinkage and dementia, but we haven’t known much about whether people with blood sugar on the high end of normal experience these same effects," said study author Nicolas Cherbuin, PhD, with Australian National University in Canberra.
The study involved 249 people age 60 to 64 who had blood sugar in the normal range as defined by the World Health Organization. The participants had brain scans at the start of the study and again an average of four years later.
Those with higher fasting blood sugar levels within the normal range and below 6.1 mmol/l (or 110 mg/dL) were more likely to have a loss of brain volume in the areas of the hippocampus and the amygdala, areas that are involved in memory and cognitive skills, than those with lower blood sugar levels. A fasting blood sugar level of 10.0 mmol/l (180 mg/dL) or higher was defined as diabetes and a level of 6.1 mmol/l (110 mg/dL) was considered impaired, or prediabetes.
After controlling for age, high blood pressure, smoking, alcohol use and other factors, the researchers found that blood sugar on the high end of normal accounted for six to 10 percent of the brain shrinkage.
"These findings suggest that even for people who do not have diabetes, blood sugar levels could have an impact on brain health," Cherbuin said. "More research is needed, but these findings may lead us to re-evaluate the concept of normal blood sugar levels and the definition of diabetes."
Source: medicalxpress.com
ScienceDaily (Sep. 3, 2012) — A new study by researchers at NYU School of Medicine reveals for the first time that metabolic syndrome (MetS) is associated with cognitive and brain impairments in adolescents and calls for pediatricians to take this into account when considering the early treatment of childhood obesity.
The study, funded by the National Institutes of Health under award number DK083537, and in part by award number 1ULIRR029892, from the National Center for Research Resources, appears online September 3 in Pediatrics.
As childhood obesity has increased in the U.S., so has the prevalence of metabolic syndrome — a constellation of three or more of five defined health problems, including abdominal obesity, low HDL (good cholesterol), high triglycerides, high blood pressure and pre-diabetic insulin resistance. Lead investigator Antonio Convit, MD, professor of psychiatry and medicine at NYU School of Medicine and a member of the Nathan Kline Research Institute, and colleagues have shown previously that metabolic syndrome has been linked to neurocognitive impairments in adults, but this association was generally thought to be a long-term effect of poor metabolism. Now, the research team has revealed even worse brain impairments in adolescents with metabolic syndrome, a group absent of clinically-manifest vascular disease and likely shorter duration of poor metabolism.
"The prevalence of MetS parallels the rise in childhood obesity," Dr. Convit said. "There are huge numbers of people out there who have problems with their weight. If those problems persist long enough, they will lead to the development of MetS and diabetes. As yet, there has been very little information available about what happens to the brain in the setting of obesity and MetS and before diabetes onset in children."
Electrodes inside the skull can temporarily mimic brain disease – and so allow us to find out more about the way we work
Second thoughts: electrodes are inserted into a patient’s brain. Photograph: University of Utah Department of Neurosurgery
The first person to electrically stimulate the brain of a living human during surgery was the 19th-century British neurosurgeon Sir Victor Horsley. The operation was to treat a deformation called an encephalocele, where the bones of the skull do not close properly in the womb, causing the brain to protrude from the head. Horsely applied a weak electrical current to the surgically exposed brain tissue, making the patient’s eyes swivel to the side, which told the surgeon that the out-of-place area was the top of the midbrain – normally a deeply embedded neural structure essential for directing vision.
The technique was later picked up to treat epilepsy as it became clear that removing the part of the brain that triggered seizures could be an effective treatment, even if identifying it could be tricky. Small, clearly identified points of damage or localised tumours could often trigger seizures but sometimes the errant waves of epileptic activity would start far away from the original point of visible injury. Horsley used the electrical stimulation technique while patients were awake to find the sensitive area and remove it. Not bad for 1886.
Although initially invented for medical reasons, this surgical technique began to throw up some curious scientific data. In the 1930s the Canadian neurosurgeon Wilder Penfield asked patients undergoing epilepsy surgery if he could perform brief experiments while they were being operated on. He found that stimulating parts of the brain could cause a range of reactions from tingling to weeping to a “desire to move” – providing crucial evidence that activity in specific brain areas could trigger surprisingly complex behaviours.
People with epilepsy have remained an important part of our quest to understand ourselves as they have regularly volunteered to take part in neuroscience experiments while undergoing open-brain operations. Even though these experiments are a relatively brief pause in the procedure, they still require people to offer some of their time while their skull has been opened and their brain exposed, and we know much more about the brain thanks to their generosity.
As surgical techniques have moved on, so has the science. The starting points of some seizures are not easily located in the relatively short period available during surgery. To compensate for this, neurosurgeons have taken to implanting electrodes in the brains of people with epilepsy before the skull is replaced and the skin sewn up, which allows the medical team to record brain activity as the patients go about their daily life. One form of this “in brain” recording, known as electrocorticography, involves surgically inserting a grid of electrodes over the surface of the brain.
This has allowed neuroscientists to measure the brain at work in the real world via cables that go from the brain into a small digital recorder. A study published last year in the Journal of Neurosurgery mapped the main language areas of the cortex, the brain’s outer layer, using an implanted electrode grid and a simple word task that took an average of just 47 seconds. More than 100 other studies have used this technique with similarly impressive results.
One innovation is particularly mind-boggling. After years of using implanted electrode grids to read from the brain, neuroscientists have begun to use the electrodes to write to it – in other words, to alter the function of the brain through the same electrodes that record its activity. “By having a grid of electrodes in place,” says Matthew Lambon Ralph, professor of cognitive neuroscience at Manchester University, “it is possible to probe many different regions rather than just one.”
The precision is such that the Lambon Ralph team and a team at Kyoto University Medical School, led by Riki Matsumoto, have used an implanted grid to temporarily simulate characteristics of a brain disease called semantic dementia. Like Alzheimer’s, semantic dementia is a degenerative disorder, but one in which brain cells that specifically support our understanding of meaning rapidly decline. Studies of patients with semantic dementia have taught us a great deal about how memory is organised in the brain but the disorder is swift and unpredictable, and a method that can mimic the effects while recording directly from the cortex is a powerful tool.
The technique is safe and reversible, as we know from a simple version that is often done pre-neurosurgery to ensure that no tissue that supports key mental functions is removed during the operation. Using it as a way of briefly simulating more complex cognitive difficulties is an exciting development. “Stimulation is injected in one part of a grid and the evoked response across other grids is measured. It’s a direct measure of functional connectivity,” explains Lambon Ralph, highlighting how these sorts of studies can allow the brain’s function, in terms of thinking skills, to be closely linked to its physical connections.
The research was presented at the British Neuropsychological Society spring conference by UK-based team member Taiji Ueno. The main findings are still being prepared for peer review but the use of implant grids in neuroscience research is sure to become more common as the surgical procedure becomes more widely used.
These procedures are only done for medical reasons, and researchers get no say about how and on whom they are performed. But, as ever, patients have been generous with their time. From 1886 until now, these exciting discoveries have been made possible by people on the operating table.
Picower Institute for Learning and Memory Neuroscientist Matt Wilson has shown not only that animals dream, but that they dream about what they experience. In a lab rat’s world, that means navigating mazes. In Wilson’s latest study, slated to appear Sept. 2 in Nature Neuroscience, researchers manipulated the content of rodent dreams by replaying an audio cue that accompanied that day’s maze.
Matthew Wilson, the Sherman Fairchild Professor of Neuroscience and a member of the Picower Institute for Learning and Memory at MIT. Photo: Patrick Gillooly
In a study — led by Daniel Bendor, Picower Institute postdoctoral fellow, and Wilson, the Associate Department Head for Education and Sherman Fairchild Professor of Neuroscience in MIT’s Department of Brain and Cognitive Sciences — rats were trained to run a maze using audio cues: one sound directed the animal to run to the right end of the track for a reward and a different sound meant the reward could be found on the left.
As the animals slept, researchers recorded the activity of specific neurons within their brains that allowed them to see, as in previous experiments, that the animals’ dreams were a replay of the maze-running task they had learned while awake. Except this time, when the researchers played the audio cues into the cages of the slumbering rodents, the rats were more likely to dream about the section of the maze previously associated with the audio cue.
“Our most recent experiments demonstrate the ability to bias the content of reactivated memory during sleep to specific past experiences. This could be thought of as a simple form of dream engineering and opens up the possibility of more extensive control of memory processing during sleep to enhance selected memories and to block or modify unwanted memories,” the researchers wrote.
Wilson’s lab, which aims to establish the role of sleep in memory and cognition, hopes the knowledge will lead to new approaches to learning and behavioral therapy through manipulation of brain systems during sleep.
Source: MIT
ScienceDaily (Sep. 1, 2012) — Flying high, or down in the dumps — individuals suffering from bipolar disorder alternate between depressive and manic episodes. Researchers from the University of Bonn and the Central Institute of Mental Health in Mannheim have now discovered, based on patient data and animal models, how the NCAN gene results in the manic symptoms of bipolar disorder.
(Credit: © Bastos / Fotolia)
The results have been published in the current issue of The American Journal of Psychiatry.
Individuals with bipolar disorder are on an emotional roller coaster. During depressive phases, they suffer from depression, diminished drive and often, also from suicidal thoughts. The manic episodes, however, are characterized by restlessness, euphoria, and delusions of grandeur. The genesis of this disease probably has both hereditary components as well as psychosocial environmental factors.
The NCAN gene plays a major part in how manias manifest
"It has been known that the NCAN gene plays an essential part in bipolar disorder," reports Prof. Dr. Markus M. Nöthen, Director of the Institute of Human Genetics at the University of Bonn. "But until now, the functional connection has not been clear." In a large-scale study, researchers led by the University of Bonn and the Central Institute of Mental Health in Mannheim have now shown how the NCAN gene contributes to the genesis of mania. To do so, they evaluated the genetic data and the related descriptions of symptoms from 1218 patients with differing ratios between the manic and depressive components of bipolar disorder.
Comprehensive data from patients and animal models
Using the patients’ detailed clinical data, the researchers tested statistically which of the symptoms are especially closely related to the NCAN gene. “Here it became obvious that the NCAN gene is very closely and quite specifically correlated with the manic symptoms,” says Prof. Dr. Marcella Rietschel from the Central Institute of Mental Health in Mannheim. According to the data the gene is, however, not responsible for the depressive episodes in bipolar disorder.
Manic mice drank from sugar solution with abandon
A team working with Prof. Dr. Andreas Zimmer, Director of the Institute of Molecular Psychiatry at the University of Bonn, examined the molecular causes effected by the NCAN gene. The researchers studied mice in which the gene had been “knocked out.” “It was shown that these animals had no depressive component in their behaviors, only manic ones,” says Prof. Zimmer. These knockout mice were, e.g., considerably more active than the control group and showed a higher level of risk-taking behavior. In addition, they tended to exhibit increased reward-seeking behavior, which manifested itself by their unrestrained drinking from a sugar solution offered by the researchers.
Lithium therapy also effective against hyperactivity in mice
Finally, the researchers gave the manic knockout mice lithium — a standard therapy for humans. “The lithium dosage completely stopped the animals’ hyperactive behavior,” reports Prof. Zimmer. So the results also matched for lithium; the responses of humans and mice regarding the NCAN gene were practically identical. It has been known from prior studies that knocking out the NCAN gene results in a developmental disorder in the brain due to the fact that the production of the neurocan protein is stopped. “As a consequence of this molecular defect, the individuals affected apparently develop manic symptoms later,” says Prof. Zimmer.
Opportunity for new therapies
Now the scientists want to perform further studies of the molecular connections of this disorder — also with a view towards new therapies. “We were quite surprised to see how closely the findings for mice and the patients correlated,” says Prof. Nöthen. “This level of significance is very rare.” With a view towards mania, the agreement between the findings opens up the opportunity to do further molecular studies on the mouse model, whose results will very likely also be applicable to humans. “This is a great prerequisite for advancing the development of new drugs for mania therapy,” believes Prof. Rietschel.
Source: Science Daily
Brain in a Dish Tony Latham/Getty Images
Scientists have isolated the brains of dogs, cats and monkeys and kept them alive for short periods in one way or another. But the most successful “whole-brain preparation” of a mammal was developed in the mid-1980s. A neuroscientist at NYU Langone Medical Center named Rodolfo Llinás came up with a way to keep the brain of a young guinea pig alive in a fluid-filled tank for the length of a standard workday.
To begin with, Llinás and his colleagues anesthetized the animal, opened up its chest, and cooled its brain by injecting cold saline into the ascending aorta. After extracting the brain from the skull, the researchers tied it to the bottom of the tank with some thread and surrounded it with glass beads, so it wouldn’t slide around. They kept the brain alive by injecting a solution of sugar, electrolytes and dissolved oxygen (among other ingredients) directly into one of its vertebral arteries. Guinea pigs turned out to be a good animal for this preparation because their vertebral arteries are accessible and because their brains are small enough to handle—but not too small for fine dissection.
Llinás’s preparation allows for the brain to be poked with electrodes, injected with drugs, or otherwise studied from any angle with all its circuitry intact. But there are only a handful of labs that still use this approach; many physiologists do experiments with whole, living animals or slices of brain tissue kept alive in a dish instead. “The preparation is difficult and expensive to maintain as a model system for brain study,” says University of Alberta neuroscientist Clayton Dickson, who learned the method in Italy but has since abandoned it. “It requires a dedicated, continuous and persistent research team to keep it going.”
Source: PopSci
The best way to learn is to teach. Now a classroom robot that helps Japanese children learn English has put that old maxim to the test.
(Image: Sinopix/Rex Features)
Shizuko Matsuzoe and Fumihide Tanaka at the University of Tsukuba, Japan, set up an experiment to find out how different levels of competence in a robot teacher affected children’s success in learning English words for shapes.
They observed how 19 children aged between 4 and 8 interacted with a humanoid Nao robot in a learning game in which each child had to draw the shape that corresponded to an English word such as ‘circle’, ‘square’, ‘crescent’, or ‘heart’.
The researchers operated the robot from a room next to the classroom so that it appeared weak and feeble, and the children were encouraged to take on the role of carers. The robot could then either act as an instructor, drawing the correct shape for the child, or make mistakes and act as if it didn’t know the answer.
When the robot got a shape wrong, the child could teach the robot how to draw it correctly by guiding its hand. The robot then either “learned” the English word for that shape or continued to make mistakes.
Robot learner aids learningMatsuzoe and Tanaka found that the children did best when the robot appeared to learn from them. This also made the children more likely to want to continue learning with the robot. The researchers will present their results at Ro-Man - an international symposium on robot and human interactive communication - in September.
"Anything that gets a person more actively engaged and motivated is going to be beneficial to the learning process," says Andrea Thomaz , director of the Socially Intelligent Machines lab at the Georgia Institute of Technology in Atlanta. "So needing to teach the robot is a great way of doing that."
The idea of students learning by teaching also agrees with a lot of research in human social learning, she says. The process of teaching a robot is akin to what happens in peer-to-peer learning, where students teach each other or work in groups to learn concepts – common activities in most classrooms.
Source: NewScientist
Ignacio Arganda, a young researcher from San Sebastián de los Reyes (Madrid) working for the Massachusetts Institute of Technology (MIT) is one of the driving forces behind Fiji, an open source platform that allows for application sharing as a way of improving biomedical-image processing. Arganda explains to SINC that Fiji, which has enjoyed the voluntary collaboration of some 20 developers from all over the world, has become a de facto standard that assists laboratories and microscope companies in their development of more precise products.
Ignacio Arganda is a postdoctoral researcher at the Laboratory of Computational Neuroscience of the Massachusetts Institute of Technology (MIT). Along with a group of researchers he implemented Fiji, a platform that allows for applications to be shared in order to improve and advance in the processing and analysis of biomedical imaging. “All of this in open source,” outlines Arganda.
The platform was built from a previous one, ImageJ, which was well known in the industry at the time. ImageJ was not an open source platform but it was publicly accessible. According to Arganda, it had the advantage that any person working in medical imaging could easily create small software applications to resolve their particular problems and then incorporate it into the platform by means of a plug-in (an application which is linked to another providing a new or specific function).
Nonetheless, the researcher adds that this platform became too chaotic with applications of all kinds, some of which were not related to biomedical-imaging. It also began being used to handle astronomical images, in video tracking, etc. “There was a significant lack of control and structure,” he says.
Therefore, “in a spontaneous manner and without any help” this group of researchers decided to create the new open source platform that could put order to that already in place, reusing what was of interest and useful in their work.
"We created a webpage organised like Wikipedia where people could contribute and use their knowledge to help others. To our surprise, it became very popular," he ensures. According to Ignacio Aranda, Fiji currently has 127,000 unique visits (20,000 each month).
Mathematical models developed by scientists at the University of Bristol are providing new insights into why the placebo effect exists and when it should occur. Their research is published in the journal of Evolution and Human Behaviour.
A placebo – such as a sugar pill – is a treatment which is not effective through its direct action on the body but works because of its effect on the patient’s beliefs. But if individuals are capable of recovering without external aid, why do they rely on an external cue? In other words, why have individuals not evolved the ability to get better immediately on their own?
Members of the Modelling Animal Decisions group in the University of Bristol’s School of Biological Sciences built mathematical models of the placebo effect which examine the trade-off between the costs and benefits of an immune response when faced with a health problem.
The work is based on an idea proposed by the theoretical psychologist Professor Nicholas Humphrey. He proposed that, as it can be beneficial to hold the immune system back from full operation due to uncertainties about the state of the world (such as the possibility of starvation), cues which indicate a change can therefore lead to an altered level of immune response.
The models take this argument even further and demonstrate that the placebo effect is modulated by the patient’s expectations. Previous studies measuring brain activity using functional magnetic resonance imaging (fMRI) provide experimental evidence which support the models, by showing correlations between the placebo effect and regions of the brain associated with expectation.
The models show why changes to the perceived cost of getting well, the value of being well or external environmental factors can induce the placebo effect.
Dr Pete Trimmer, lead author of the work, said: “The placebo effect comes down to expectations about when to take action. Waiting for a useless pill before taking action is not optimal. But the general responsiveness to cues is adaptive, so it is logical for evolved organisms to display the placebo effect.”
The models indicate that under stress it can be better for the immune system to work less effectively. However, the most important finding of the research is that the particular type of belief in the treatment can lead to positive or negative effects. The belief that a treatment will cure, without any need for the immune system to do anything, could have deleterious effects on the patient’s health.
Now that a theoretical approach has laid the foundations of understanding the placebo effect, future empirical work may provide insights as to how the placebo effect can be invoked and controlled in a clinical environment. The Bristol study clearly shows that the focus of future placebo studies should be shifted to the type of belief patients have about their treatment rather than just whether a treatment is helpful or harmful. A better understanding of the placebo effect may change the code of practice for health practitioners and save human lives.
Source: University of Bristol
Researchers at the University of Southern California have devised a method for detecting certain neurological disorders through the study of eye movements.
In a study published today in the Journal of Neurology, researchers claim that because Attention Deficit Hyperactivity Disorder (ADHD), Fetal Alcohol Spectrum Disorder (FASD) and Parkinson’s Disease (PD) each involve ocular control and attention dysfunctions, they can be easily identified through an evaluation of how patients move their eyes while they watch television.
“Natural attention and eye movement behavior – like a drop of saliva – contains a biometric signature of an individual and her/his state of brain function or dysfunction,” the article states. “Such individual signatures, and especially potential biomarkers of particular neurological disorders which they may contain, however, have not yet been successfully decoded.”
Typical methods of detection—clinical evaluation, structured behavioral tasks and neuroimaging—are costly, labor-intensive and limited by a patient’s ability to understand and comply with instructions. To solve this problem, doctoral student Po-He Tseng and Professor Laurent Itti of the Department of Computer Science at the USC Viterbi School of Engineering, along with collaborators at Queen’s University in Canada, have devised a new screening method.
Participants in the study were simply instructed to “watch and enjoy” television clips for 20 minutes while their eye movements were recorded. Eye-tracking data was then combined with normative eye-tracking data and a computational model of visual attention to extract 224 quantitative features, allowing the team to use new machine learning techniques to identify critical features that differentiated patients from control subjects.
With eye movement data from 108 subjects, the team was able to identify older adults with Parkinson’s Disease with 89.6% accuracy, and children with either ADHD or FASD with 77.3% accuracy.
Providing new insights into which aspects of attention and gaze control are affected by specific disorders, the team’s method provides considerable promise as an easily-deployed, low-cost, high-throughput screening tool, especially for young children and elderly populations who may be less compliant to traditional tests.
“For the first time, we can actually decode a person’s neurological state from their everyday behavior, without having to subject them to difficult or time-consuming tests,” Itti said.