Posts tagged neuroscience
Articles and news from the latest research reports.
Advance in tuberous sclerosis brain science
By manipulating the timing of disease-causing mutations in the brains of developing mice, Brown University researchers have found that early genetic deletions in the thalamus may play an important role in course and severity of the developmental disease tuberous sclerosis complex. Findings appear in the journal Neuron.
Doctors often diagnose tuberous sclerosis complex (TSC) based on the abnormal growths the genetic disease causes in organs around the body. Those overt anatomical structures, however, belie the microscopic and mysterious neurological differences behind the disease’s troublesome behavioral symptoms: autism, intellectual disabilities, and seizures. In a new study in mice, Brown University researchers highlight a role for a brain region called the thalamus and show that the timing of gene mutation during thalamus development makes a huge difference in the severity of the disease.
TSC can arise in humans and mice alike when both alleles (the one from mom and the one from dad) of the TSC1 gene are deleted. One bad gene is often inherited and the other accumulates a mutation some time during embryonic development. This happens to one in 6,000 people.
“We don’t know when during development the mutations are occurring in the patients,” said Elizabeth Normand, a Brown neuroscience graduate student and lead author of the paper in the journal Neuron. “That’s why we chose to look at the timing. It can give us some insight into the role of genes during embryonic development.”
Normand and adviser Mark Zervas, assistant professor of biology, not only wanted to assess the timing but also to probe the role the thalamus might have in contributing to the neurological symptoms of the disease. To do both, their team genetically engineered a clever mouse model in which they could, with a dose of the drug tamoxifen, delete both alleles exclusively in thalamus neurons at the developmental stage of their choosing.
Their interest in the thalamus comes from its role in forging strong but intricate links to the cortex, which is where most other TSC researchers have focused. As for timing, they tested the effect of controlling allele deletions on day 12 of gestation in some mice and day 18 (just before birth) in others. Still other mice were left healthy as experimental controls.
Significant symptoms
Overall, the researchers found they could indeed generate TSC-like behavioral symptoms in the mice, such as seizures, by deleting TSC1 alleles in developing cells of the thalamus. They also found that the timing of the deletion mattered tremendously to the extent of the disease in the brain, the degree of abnormality, and the severity of TSC-like symptoms.
The mice whose alleles were deleted on embryonic day 12 fared much worse behaviorally than the mice whose alleles were deleted on embryonic day 18.
At two months of age, the mice with the embryonic day 12 deletion exhibited excessive self-grooming to the point where they experienced lesions. Among those mice, 10 of 11 experienced seizures at an average rate of more than three per hour.
The mice with the embryonic day 18 deletion, on the other hand, fared better without any over-grooming. By eight months of age, however, four of 17 of the mice did exhibit rare seizures.
These behavioral differences traced to differences in the the way the mice’s brains became wired. A comparison of brain tissue from adult mice — some of which had the early TSC1 deletions and some of which didn’t — revealed differences in the connections between the thalamus and the cortex and in the electrical and physical properties of thalamus cells.
“We’re building off the core idea of the thalamus playing an important role in brain function and showing that if you disrupt the way that the thalamic neurons develop that you can get some of these behavioral consequences such as overgrooming or seizures,” said Zervas, who is affiliated with the Brown Institute for Brain Science.
The extent of mutant neurons was much more severe in the mice with the embryonic day 12 versus day 18 mutations. In embryonic day 12 deleted mice, for example, the deletion disrupted the growth-regulating “mTOR” pathway in 70 percent of neurons versus only 29 percent of neurons in the embryonic day 18 deleted mice. The disruptions occurred in more areas of the thalamus in embryonic day 12 than in day 18 mice as well. The overactivity of mTOR in TSC is what produces the unusual growths around the body, though these new findings indicate additional roles for the mTOR pathway in brain development and function, Zervas said.
In future work, the team plans to study the effects of deleting the TSC1 allele at other days during development as well as to understand whether there is a threshold of mutant neurons with mTOR disruption at which TSC-like symptoms begin to emerge.
Researchers discover a missing link in signals contributing to neurodegeneration
In many neurodegenerative diseases the neurons of the brain are over-stimulated and this leads to their destruction. After many failed attempts and much scepticism this process was finally shown last year to be a possible basis for treatment in some patients with stroke. But very few targets for drugs to block this process are known.
In a new highly detailed study, researchers have discovered a previously missing link between over-stimulation and destruction of brain tissue, and shown that this might be a target for future drugs. This research, led by the A. I. Virtanen Institute at the University of Eastern Finland in collaboration with scientists from Lausanne University Hospital, University of Lausanne and the company Xigen Pharma AG, was published in the Journal of Neuroscience. Research was funded mainly by the Academy of Finland.
What is this missing link? We have known for years that over-stimulated neurons produce nitric oxide molecules. Although this can activate a signal for destruction of cells, the small amount of nitric oxide produced cannot alone explain the damage to the brain. The team now show that a protein called NOS1AP links the nitric oxide that is produced to the damage that results. NOS1AP binds an initiator of cell destruction called MKK3 and also moves within the cell to the source of nitric oxide when cells are over-activated. The location of these proteins in cells causes them to convert the over-stimulation signal into a cell destruction response. The team designed a chemical that prevents NOS1AP from binding the source of nitric oxide. This reduces the cell destruction response in cells of the brain and as a result it limits brain lesions in rodents.
Other funders are the European Union and the University of Eastern Finland. Researchers used the recently developed high-throughput imaging facilities at the A. I. Virtanen Institute. The researchers hope that continuation of their work could lead to improved treatments for diseases such as stroke, epilepsy and chronic conditions like Alzheimer’s disease. As NOS1AP is associated with schizophrenia, diabetes and sudden cardiac death, future research in this area may assist the treatment of a wider range of diseases.
(Source: aka.fi)
Scientists show how nerve wiring self-destructs
Many medical issues affect nerves, from injuries in car accidents and side effects of chemotherapy to glaucoma and multiple sclerosis. The common theme in these scenarios is destruction of nerve axons, the long wires that transmit signals to other parts of the body, allowing movement, sight and sense of touch, among other vital functions.
Now, researchers at Washington University School of Medicine in St. Louis have found a way the body can remove injured axons, identifying a potential target for new drugs that could prevent the inappropriate loss of axons and maintain nerve function.
“Treating axonal degeneration could potentially help a lot of patients because there are so many diseases and conditions where axons are inappropriately lost,” says Aaron DiAntonio, MD, PhD, professor of developmental biology. “While this would not be a cure for any of them, the hope is that we could slow the progression of a whole range of diseases by keeping axons healthy.”
DiAntonio is senior author of the study that appears online May 9 in the journal Cell Reports.
While axonal degeneration appears to be a major culprit in diseases like multiple sclerosis, it also paradoxically plays an important role in properly wiring the nervous systems of developing embryos.
“When an embryo is building its nervous system, there can be inappropriate or excessive axonal sprouts, or axons that are only needed at one time in development and not later,” DiAntonio says. “These axons degenerate, and that’s very important for wiring the nervous system. And in adult organisms, it might be useful to have a clean and quick way to remove a damaged axon from a healthy nerve, instead of letting it decay and potentially damage its neighboring axons.”
DiAntonio compares the process to programmed cell death, or apoptosis, which is also important in embryonic development. Apoptosis culls unnecessary or damaged cells from the body. If cell death programs become overactive, they can kill healthy cells that should remain. And if apoptosis fails to destroy damaged cells in adults, it can lead to cancer.
The new discovery also underscores the relatively recent understanding that loss of axons is not a passive decay process resulting from injury. Just as apoptosis actively destroys cells, axonal degeneration results from a cellular program that actively removes the damaged axon. In certain diseases, the program may be inappropriately triggered.
“We want to understand axonal degeneration at the same level that we understand programmed cell death, in the hopes of developing drugs to block the process when it becomes overactive,” DiAntonio says.
DiAntonio’s major collaborators in this project include Jeffrey D. Milbrandt, MD, PhD, the James S. McDonnell Professor and head of the Department of Genetics, and first author Elisabetta Babetto, PhD, postdoctoral research scholar.
Studying mice, the researchers found that a gene called Phr1 plays a major role in governing the self-destruction of injured axons. When they removed Phr1 from adult mice, the severed portion of the axons remained intact for much longer than in genetically normal mice.
In the normal mice, a severed axon degenerated entirely after two days. In mice without Phr1, they found that about 75 percent of the severed axons remained at five days, with a quarter persisting at least 10 days after being cut. The mice showed no side effects and suffered no obvious problems due to the missing Phr1.
The findings raise the possibility that blocking the Phr1 protein with a drug could keep damaged axons alive and functional when the body would normally cause the axons to self-destruct.
DiAntonio emphasizes that he is not trying to save axons that have no connection to the rest of the nerve. The paradigm is simply a good way to model nerve injury. In many instances, such as a crush injury or disease processes in which the axon is not severed, blocking the Phr1 protein could potentially preserve an attached axon that would otherwise self-destruct.
Importantly, the research team also looked at optic nerves of the central nervous system, which are damaged in glaucoma, and found similar protective effects from the loss of Phr1.
“This is not the first gene identified whose loss protects mammalian axons from degeneration,” DiAntonio says. “But it is the first one that shows evidence of working in the central nervous system. So it could be important in conditions like glaucoma, multiple sclerosis and other neurodegenerative diseases where the central nervous system is the primary problem.”
DiAntonio also points out possible ways to help cancer patients. Many chemotherapy drugs cause damage to peripheral axons, which may limit the doses a patient can tolerate.
As part of the new study, the researchers showed that intact axons without Phr1 were protected from the damage caused by vincristine, a chemotherapy drug used to treat leukemia, neuroblastoma, Hodgkin’s disease and non-Hodgkin’s lymphoma, among other cancers.
“In this case, the loss of axons is not caused by disease,” DiAntonio says. “It’s caused by the drug doctors are giving. You know the date it will start. You know the date it will stop. This is probably where I am most optimistic that we could make an impact.”
(Source: news.wustl.edu)
Experience leads to the growth of new brain cells
A new study examines how individuality develops
The DFG-Center for Regenerative Therapies Dresden - Cluster of Excellence at the TU Dresden (CRTD), the Dresden site of the German Center for Neurodegenerative Diseases (DZNE), and the Max Planck Institute for Human Development in Berlin played a pivotal role in the study.
The adult brain continues to grow with the challenges that it faces; its changes are linked to the development of personality and behavior. But what is the link between individual experience and brain structure? Why do identical twins not resemble each other perfectly even when they grew up together? To shed light on these questions, the scientists observed forty genetically identical mice that were kept in an enclosure offering a large variety of activity and exploration options.
"The animals were not only genetically identical, they were also living in the same environment," explains principal investigator Gerd Kempermann, Professor for Genomics of Regeneration, CRTD, and Site Speaker of the DZNE in Dresden. "However, this environment was so rich that each mouse gathered its own individual experiences in it. Over time, the animals therefore increasingly differed in their realm of experience and behavior."
New neurons for individualized brains
Each of the mice was equipped with a special micro-chip emitting electromagnetic signals. This allowed the scientists to construct the mice’s movement profiles and to quantify their exploratory behavior. The result: Despite a common environment and identical genes the mice showed highly individualized behavioral patterns. They reacted to their environment differently. In the course of the three-month experiment these differences increased in size.
"Though the animals shared the same life space, they increasingly differed in their activity levels. These differences were associated with differences in the generation of new neurons in the hippocampus, a region of the brain that supports learning and memory," says Kempermann. "Animals that explored the environment to a greater degree also grew more new neurons than animals that were more passive."
Adult neurogenesis, that is, the generation of new neurons in the hippocampus, allows the brain to react to new information flexibly. With this study, the authors show for the first time that personal experiences and ensuing behavior contribute to the „individualization of the brain.” The individualization they observed cannot be reduced to differences in environment or genetic makeup.
"Adult neurogenesis also occurs in the hippocampus of humans," says Kempermann. "Hence we assume that we have tracked down a neurobiological foundation for individuality that also applies to humans."
Impulses for discussion across disciplines
"The finding that behavior and experience contribute to differences between individuals has implications for debates in psychology, education science, biology, and medicine," states Prof. Ulman Lindenberger, Director of the Center for Lifespan Psychology at the Max Planck Institute for Human Development (MPIB) in Berlin. "Our findings show that development itself contributes to differences in adult behavior. This is what many have assumed, but now there is direct neurobiological evidence in support of this claim. Our results suggest that experience influences the aging of the human mind."
In the study, a control group of animals housed in a relatively unattractive enclosure was also examined; on average, neurogenesis in these animals was lower than in the experimental mice. „When viewed from educational and psychological perspectives, the results of our experiment suggest that an enriched environment fosters the development of individuality,” comments Lindenberger.
Interdisciplinary teamwork
The study is also an example of multidisciplinary cooperation — it was made possible because neuroscientists, ethologists, computer scientists, and developmental psychologists collaborated closely in designing the experimental set-up and applying new data analysis methods. Biologist Julia Freund from the CRTD Dresden and computer scientist Dr. Andreas Brandmaier from the MPIB in Berlin share first authorship on the article. In addition to the DZNE, CRTD, and the MPIB, the German Research Center for Artificial Intelligence in Saarbrücken and the Institute for Geoinformatics and the Department of Behavioural Biology at the University of Münster were also involved in this project.
Original publication
"Emergence of Individuality in Genetically Identical Mice", Julia Freund, Andreas M. Brandmaier, Lars Lewejohann, Imke Kirste, Mareike Kritzler, Antonio Krüger, Norbert Sachser, Ulman Lindenberger, Gerd Kempermann, Science
(Image: Dr Jonathan Clarke, Wellcome Images)
Researchers Discover Dynamic Behavior Of Progenitor Cells In Brain
By monitoring the behavior of a class of cells in the brains of living mice, neuroscientists at Johns Hopkins discovered that these cells remain highly dynamic in the adult brain, where they transform into cells that insulate nerve fibers and help form scars that aid in tissue repair.
Published online April 28 in the journal Nature Neuroscience, their work sheds light on how these multipurpose cells communicate with each other to maintain a highly regular, grid-like distribution throughout the brain and spinal cord. The disappearance of one of these so-called progenitor cells causes a neighbor to quickly divide to form a replacement, ensuring that cell loss and cell addition are kept in balance.
“There is a widely held misconception that the adult nervous system is static or fixed, and has a limited capacity for repair and regeneration,” says Dwight Bergles, Ph.D., professor of neuroscience and otolaryngology at the Johns Hopkins University School of Medicine. “But we found that these progenitor cells, called oligodendrocyte precursor cells (OPCs), are remarkably dynamic. Unlike most other adult brain cells, they are able to respond to the repair needs around them while maintaining their numbers.”
OPCs can mature to become oligodendrocytes — support cells in the brain and spinal cord responsible for wrapping nerve fibers to create insulation known as myelin. Without myelin, the electrical signals sent by neurons travel poorly and some cells die due to the lack of metabolic support from oligodendrocytes. It is the death of oligodendrocytes and the subsequent loss of myelin that leads to neurological disability in diseases such as multiple sclerosis.
During brain development, OPCs spread throughout the central nervous system and make large numbers of oligodendrocytes. Scientists know that few new oligodendrocytes are born in the healthy adult brain, yet the brain is flush with OPCs. However, the function of OPCs in the adult brain wasn’t clear.
To find out, Bergles and his team genetically modified mice so that their OPCs contained a fluorescent protein along their edges, giving crisp definition to their many fine branches that extend in every direction. Using special microscopes that allow imaging deep inside the brain, the team watched the activity of individual cells in living mice for over a month.
The researchers discovered that, far from being static, the OPCs were continuously moving through the brain tissue, extending their “tentacles” and repositioning themselves. Even though these progenitors are dynamic, each cell maintains its own area by repelling other OPCs when they come in contact.
“The cells seem to sense each other’s presence and know how to control the number of cells in their population,” says Bergles. “It looks like this process goes wrong in multiple sclerosis lesions, where there are reduced numbers of OPCs, a loss that may impair the cells’ ability to sense whether demyelination has occurred. We don’t yet know what molecules are involved in this process, but it’s something we’re actively working on.”
To see if OPCs do more than form new oligodendrocytes in the adult brain, the team tested their response to injury by using a laser to create a small wound in the brain. Surprisingly, OPCs migrated to the injury site and contributed to scar formation, a previously unsuspected role. The empty space in the OPC grid, created by the loss of the scar-forming OPCs, was then filled by cell division of neighboring OPCs, providing an explanation for why brain injury is often accompanied by proliferation of these cells.
“Scar cells are not oligodendrocytes, so the term ‘oligodendrocyte precursor cell’ may now be outdated,” says Bergles. “These cells are likely to have a broader role in tissue regeneration and repair than we thought. Because traumatic brain injuries, multiple sclerosis and other neurodegenerative diseases require tissue regeneration, we are eager to learn more about the functions of these enigmatic cells.”
Unleashing the watchdog protein
Research opens door to new drug therapies for Parkinson’s disease
McGill University researchers have unlocked a new door to developing drugs to slow the progression of Parkinson’s disease. Collaborating teams led by Dr. Edward A. Fon at the Montreal Neurological Institute and Hospital -The Neuro, and Dr. Kalle Gehring in the Department of Biochemistry at the Faculty of Medicine, have discovered the three-dimensional structure of the protein Parkin. Mutations in Parkin cause a rare hereditary form of Parkinson’s disease and are likely to also be involved in more commonly occurring forms of Parkinson’s disease. The Parkin protein protects neurons from cell death due to an accumulation of defective mitochondria. Mitochondria are the batteries in cells, providing the power for cell functions. This new knowledge of Parkin’s structure has allowed the scientists to design mutations in Parkin that make it better at recognizing damaged mitochondria and therefore possibly provide better protection for nerve cells. The research will be published online May 9 in the leading journal Science.
VIDEO: Parkin protein
“The majority of Parkinson’s patients suffer from a sporadic form of the disease that occurs from a complex interplay of genetic and environmental factors which are still not fully understood, explains Dr. Fon, neurologist at The Neuro and head of the McGill Parkinson Program, a National Parkinson Foundation Centre of Excellence. “A minority of patients have genetic mutations in genes such as Parkin that cause the disease. Although there are differences between the genetic and sporadic forms, there is good reason to believe that understanding one will inform us about the other. It’s known that toxins that poison mitochondria can lead to Parkinson’s-like symptoms in humans and animals. Recently, Parkin was shown to be a key player in the cell’s system for identifying and removing damaged mitochondria.”
Dr. Gehring, head of McGill’s structural biology centre, GRASP, likens Parkin to a watchdog for damaged mitochondria. “Our structural studies show that Parkin is normally kept in check by a part of the protein that acts as a leash to restrict Parkin activity. When we made mutations in this specific ‘leash’ region in the protein, we found that Parkin recognized damaged mitochondria more quickly. If we can reproduce this response with a drug rather than mutations, we might be able to slow the progression of disease in Parkinson’s patients.”
Parkin is an enzyme in cells that attaches a small protein, ubiquitin, to other proteins to mark them for degradation. For example, when mitochondria are damaged, Parkin is switched on which leads to the clearing of the dysfunctional mitochondria. This is an important process because damaged mitochondria are a major source of cellular stress and thought to play a central role in the death of neurons in neurodegenerative diseases.
Husband and wife team, Drs. Jean-François Trempe and Véronique Sauvé, are lead authors on the paper. Dr. Sauvé led the Gehring team that used X-ray crystallography to determine the structure of Parkin. Dr. Trempe in the Fon laboratory directed the functional studies of Parkin.
(Source: mcgill.ca)
Scientists Identify Early Predictors of Disease Progression Which Could Speed Huntington’s Disease Drug Trials
Scientists have identified a set of tests that could help identify whether and how Huntington’s disease (HD) is progressing in groups of people who are not yet showing symptoms. The latest findings from the TRACK-HD study*, published Online First in The Lancet Neurology, could be used to assess whether potential new treatments are slowing the disease up to 10 years before the development of noticeable symptoms.
“Currently, the effectiveness of a new drug is decided by its ability to treat symptoms. These new tests could be used in future preventative drug trials in individuals who are gene positive for HD but are not yet showing overt motor symptoms. These people have the most to gain by initiating treatment early to delay the start of these overt symptoms and give them a high quality of life for a longer period of time”, explains lead author Sarah Tabrizi from University College London’s Institute of Neurology.
The TRACK-HD investigators have previously reported a range of tests that could be used in clinical trials to assess the effectiveness of potential disease-modifying drugs in people who already show signs of the disease. But in individuals without noticeable symptoms there was little evidence of a decline in function over two years, limiting the ability to test new drugs early in the disease course.
HD is caused by the mutation of a single gene on chromosome 4, which causes a part of the DNA (known as a CAG motif) to repeat many more times than it is supposed to. The length of the CAG repeat is known to be a major determinant of the age at which symptoms of the disease are likely to start, but its contribution to progression is unclear.
Here the TRACK-HD investigators extend the study to a third year with the aim of identifying some of the earliest biological changes in individuals with presymptomatic HD, giving additional power to predict how the disease may progress beyond that already expected from age and CAG length.
Over 3 years, baseline measures derived from brain imaging were the clearest markers of disease progression and future diagnosis, above and beyond the effect of age and CAG count, in gene carriers up to 20 years before they were expected to show symptoms.
In particular, the investigators suggest that measuring volume change in white matter and the caudate and putamen regions might be future endpoints for treatment trials.
In individuals up to 10 years away from developing symptoms, there was also significant deterioration in performance on a number of motor (movement) and cognitive (intellectual function) tasks compared with controls, and the frequency of apathy increased. Finger tapping was the most sensitive of the motor assessments, while the symbol digit modality test proved to be the most sensitive of the cognitive measures.
According to Tabrizi, “A new generation of drugs will be ready for human trials in the very near future. Diagnosis in HD is something of an artificial construct at onset of motor symptoms, and this study now gives us a number of other, more well-defined parameters that correlate with disease progression. Something that suggests we’re moving towards a more biological, as opposed to physical, definition of disease progression that reduces the importance of an ‘onset event’ is great news. By extending the reach of clinical trials to include individuals who are currently free of overt symptoms there is a realistic future possibility that treatments in the pipeline can significantly improve the quality of life for patients and families.”**
Writing in a linked Comment, Francis O. Walker, M.D., from Wake Forest School of Medicine in the USA says that the TRACK-HD investigators have set the standard for observational studies in other neurodegenerative diseases, adding that, “Virtual roadmaps of disease in the minds of practitioners are good for care in the framework of the traditional patient encounter, but it takes substantial effort, teamwork, and genius to turn them into rigorous, quantifiable timelines that can be used to test efficacy in future therapeutic trials.”
* The Track-HD study was established to identify differences between people carrying the HD mutation at different stages and healthy controls that could be used to accurately predict the progression of HD using a variety of techniques to assess changes in brain function, motor function, behaviour, and cognition. 366 individuals from Canada, France, the Netherlands and the UK were enrolled: 120 presymptomatic carriers of the HD gene mutation, 123 patients with early symptomatic HD, and 123 healthy controls.
(Source: newswise.com)
Hit a 95 mph baseball? Scientists pinpoint how we see it coming
How does San Francisco Giants slugger Pablo Sandoval swat a 95 mph fastball, or tennis icon Venus Williams see the oncoming ball, let alone return her sister Serena’s 120 mph serves? For the first time, vision scientists at the University of California, Berkeley, have pinpointed how the brain tracks fast-moving objects.
The discovery advances our understanding of how humans predict the trajectory of moving objects when it can take one-tenth of a second for the brain to process what the eye sees.
That 100-millisecond holdup means that in real time, a tennis ball moving at 120 mph would have already advanced 15 feet before the brain registers the ball’s location. If our brains couldn’t make up for this visual processing delay, we’d be constantly hit by balls, cars and more.
Thankfully, the brain “pushes” forward moving objects so we perceive them as further along in their trajectory than the eye can see, researchers said.
“For the first time, we can see this sophisticated prediction mechanism at work in the human brain,” said Gerrit Maus, a postdoctoral fellow in psychology at UC Berkeley and lead author of the paper published today (May 8) in the journal, Neuron.
A clearer understanding of how the brain processes visual input – in this case life in motion – can eventually help in diagnosing and treating myriad disorders, including those that impair motion perception. People who cannot perceive motion cannot predict locations of objects and therefore cannot perform tasks as simple as pouring a cup of coffee or crossing a road, researchers said.
This study is also likely to have a major impact on other studies of the brain. Its findings come just as the Obama Administration initiates its push to create a Brain Activity Map Initiative, which will further pave the way for scientists to create a roadmap of human brain circuits, as was done for the Human Genome Project.
Using functional Magnetic Resonance Imaging (fMRI) Gerrit and fellow UC Berkeley researchers Jason Fischer and David Whitney located the part of the visual cortex that makes calculations to compensate for our sluggish visual processing abilities. They saw this prediction mechanism in action, and their findings suggest that the middle temporal region of the visual cortex known as V5 is computing where moving objects are most likely to end up.
For the experiment, six volunteers had their brains scanned, via fMRI, as they viewed the “flash-drag effect,”(a, b) a visual illusion in which we see brief flashes shifting in the direction of the motion.
“The brain interprets the flashes as part of the moving background, and therefore engages its prediction mechanism to compensate for processing delays,” Maus said.
The researchers found that the illusion – flashes perceived in their predicted locations against a moving background and flashes actually shown in their predicted location against a still background – created the same neural activity patterns in the V5 region of the brain. This established that V5 is where this prediction mechanism takes place, they said.
In a study published earlier this year, Maus and his fellow researchers pinpointed the V5 region of the brain as the most likely location of this motion prediction process by successfully using transcranial magnetic stimulation, a non-invasive brain stimulation technique, to interfere with neural activity in the V5 region of the brain, and disrupt this visual position-shifting mechanism.
“Now not only can we see the outcome of prediction in area V5,” Maus said. “But we can also show that it is causally involved in enabling us to see objects accurately in predicted positions.”
On a more evolutionary level, the latest findings reinforce that it is actually advantageous not to see everything exactly as it is. In fact, it’s necessary to our survival:
“The image that hits the eye and then is processed by the brain is not in sync with the real world, but the brain is clever enough to compensate for that,” Maus said. “What we perceive doesn’t necessarily have that much to do with the real world, but it is what we need to know to interact with the real world.”
(Source: newscenter.berkeley.edu)
Research determines how the brain computes tool use
With a goal of helping patients with spinal cord injuries, Jason Gallivan and a team of researchers at Queen’s University’s Department of Psychology and Centre for Neuroscience Studies are probing deep into the human brain to learn how it manages basic daily tasks.
The team’s most recent research, in collaboration with a group at Western University, investigated how the human brain supports tool use. The researchers were especially interested in determining the extent to which brain regions involved in planning actions with the hand alone would also be involved in planning actions with a tool. They found that although some brain regions were involved in planning actions with either the hand or tool alone, the vast majority were involved in planning both hand- and tool-related movements. In a subset of these latter brain areas the researchers further determined that the tool was in fact being represented as an extension of the hand.
“Tool use represents a defining characteristic of high-level cognition and behaviour across the animal kingdom but studying how the brain – and the human brain in particular – supports tool use remains a significant challenge for neuroscientists” says Dr. Gallivan. “This work is a considerable step forward in our understanding of how tool-related actions are planned in humans.”
Over the course of one year, human participants had their brain activity scanned using functional magnetic resonance imaging (fMRI) as they reached towards and grasped objects using either their hand or a set of plastic tongs. The tongs had been designed so they opened whenever participants closed their grip, requiring the participants to perform a different set of movements to use the tongs as opposed to when using their hand alone.
The team found that mere seconds before the action began, that the neural activity in some brain regions was predictive of the type of action to be performed upon the object, regardless of whether the hand or tool was to be used (and despite the different movements being required). By contrast, the predictive neural activity in other brain regions was shown to represent hand and tool actions separately. Specifically, some brain regions only coded actions with the hand whereas others only coded actions with the tool.
“Being able to decode desired tool use behaviours from brain signals takes us one step closer to using those signals to control those same types of actions with prosthetic limbs,” says Dr. Gallivan. “This work uncovers the brain organization underlying the planning of movements with the hand and hand-operated tools and this knowledge could help people suffering from spinal cord injuries.”
The research was recently published in eLife.
(Source: queensu.ca)
Look! Something Shiny! How Some Textbook Visuals can Hurt Learning
Adding captivating visuals to a textbook lesson to attract children’s interest may sometimes make it harder for them to learn, a new study suggests.
Researchers found that 6- to 8-year-old children best learned how to read simple bar graphs when the graphs were plain and a single color.
Children who were taught using graphs with images (like shoes or flowers) on the bars didn’t learn the lesson as well and sometimes tried counting the images rather than relying on the height of the bars.
“Graphs with pictures may be more visually appealing and engaging to children than those without pictures. However, engagement in the task does not guarantee that children are focusing their attention on the information and procedures they need to learn. Instead, they may be focusing on superficial features,” said Jennifer Kaminski, co-author of the study and research scientist in psychology at The Ohio State University.
Kaminski conducted the study with Vladimir Sloutsky, professor of psychology at Ohio State.
The problem of distracting visuals is not just an academic issue. In the study, the authors cite real-life examples of colorful, engaging – and possibly confusing - bar graphs in educational materials aimed at children, as well as in the popular media.
And when the authors asked 16 kindergarten and elementary school teachers whether they would use the visually appealing graphs featured in this study, all of them said they would. Intuitively, most of these teachers felt that the graphs with the pictures would be more effective for instruction than the graphs without, according to the researchers.
The findings apply beyond learning graphs and mathematics, the authors said.
“When designing instructional material, we need to consider children’s developing ability to focus their attention and make sure that the material helps them focus on the right things,” Kaminski said.
“Any unnecessary visual information may distract children from the very procedures we want them to learn.”
The study appears online in the Journal of Educational Psychology and will appear in a future print edition.
The main study involved 122 students in kindergarten, first and second grade. All were tested individually.
The experiment began with a training phase where a researcher showed each child a graph on a computer screen and taught him or her how to read it. The children were then tested on three graphs to see if they could accurately interpret them.
The graphs in the training phase involved how many shoes were in a lost and found for each of five weeks. Half the students were presented with graphs in which the bars were a solid color. The other students were shown graphs in which the bars contained pictures of shoes. The number of shoes in the bars was equal to the corresponding y-value on the graph. In other words, if there were five shoes in the lost and found, there were five shoes pictured in the bar.
After the training phase, the children were tested on new graphs in which the bars were either solid-colored or contained pictures of objects such as flowers. However, the number of objects pictured did not equal the correct y-value for the bar. In other words, the bar value could equal 14 flowers, but only seven flowers were pictured.
“This allowed us to clearly identify which students learned the correct way to read a bar graph from those who simply counted the number of objects in each bar,” Sloutsky said.
Sure enough, children who trained with the pictures on the graph were more likely than others to get the answers wrong by simply counting the objects in each bar.
All of the first- and second-graders and 75 percent of the kindergarten children who learned on the solid-bar graphs appropriately read the new graphs.
However, those who learned with the more visually appealing shoe graphs did not do nearly as well. In this case, 90 percent of kindergarteners and 72 percent of first-graders responded by counting the number of flowers pictured. Second-graders did better, but still about 30 percent responded by counting.
All the children were then tested again with graphs that featured patterned bars, with either stripes or polka dots within each bar.
Again, those who learned from the more visually appealing graphs did worse at interpreting these patterned graphs.
“To our surprise, some children tried to count all the tiny polka dots or stripes in the bars. They clearly didn’t learn the correct way to read the graphs,” Kaminski said.
The researchers conducted several other related experiments to confirm the results and make sure there weren’t other explanations for the findings. In one experiment, some children were trained on graphs with pictures of objects. But in this case, the number of objects pictured was not even close to the correct value of the bar, so the students could not use counting as a strategy.
Still, these children did not do as well on subsequent tests as did those who learned on the graphs with single-colored bars.
“When teaching children new math concepts, keeping material simple is very important,” Sloutsky said.
“Any extraneous information we provide, even with the best of intentions, to make the lesson more interesting may actually hurt learning because it may be misinterpreted,” he said.
The researchers said these results don’t mean that textbook authors or others can never use interesting visuals or other techniques to capture the interest of students.
“But they need to study how such material will affect students’ attention. You can’t assume that it is beneficial just because it is colorful; in can affect learning by distracting attention from what is relevant,” Sloutsky said.
(Source: researchnews.osu.edu)