Neuroscience

Articles and news from the latest research reports.

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How gut bacteria ensure a healthy brain – and could play a role in treating depression
One of medicine’s greatest innovations in the 20th century was the development of antibiotics. It transformed our ability to combat disease. But medicine in the 21st century is rethinking its relationship with bacteria and concluding that, far from being uniformly bad for us, many of these organisms are actually essential for our health.
Nowhere is this more apparent than in the human gut, where the microbiome – the collection of bacteria living in the gastrointestinal tract – plays a complex and critical role in the health of its host. The microbiome interacts with and influences organ systems throughout the body, including, as research is revealing, the brain. This discovery has led to a surge of interest in potential gut-based treatments for neuropsychiatric disorders and a new class of studies investigating how the gut and its microbiome affect both healthy and diseased brains.
The microbiome consists of a startlingly massive number of organisms. Nobody knows exactly how many or what type of microbes there might be in and on our bodies, but estimates suggest there may be anywhere from three to 100 times more bacteria in the gut than cells in the human body. The Human Microbiome Project, co-ordinated by the US National Institutes of Health (NIH), seeks to create a comprehensive database of the bacteria residing throughout the gastrointestinal tract and to catalogue their properties.
The lives of the bacteria in our gut are intimately entwined with our immune, endocrine and nervous systems. The relationship goes both ways: the microbiome influences the function of these systems, which in turn alter the activity and composition of the bacterial community. We are starting to unravel this complexity and gain insight into how gut bacteria interface with the rest of the body and, in particular, how they affect the brain.
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How gut bacteria ensure a healthy brain – and could play a role in treating depression

One of medicine’s greatest innovations in the 20th century was the development of antibiotics. It transformed our ability to combat disease. But medicine in the 21st century is rethinking its relationship with bacteria and concluding that, far from being uniformly bad for us, many of these organisms are actually essential for our health.

Nowhere is this more apparent than in the human gut, where the microbiome – the collection of bacteria living in the gastrointestinal tract – plays a complex and critical role in the health of its host. The microbiome interacts with and influences organ systems throughout the body, including, as research is revealing, the brain. This discovery has led to a surge of interest in potential gut-based treatments for neuropsychiatric disorders and a new class of studies investigating how the gut and its microbiome affect both healthy and diseased brains.

The microbiome consists of a startlingly massive number of organisms. Nobody knows exactly how many or what type of microbes there might be in and on our bodies, but estimates suggest there may be anywhere from three to 100 times more bacteria in the gut than cells in the human body. The Human Microbiome Project, co-ordinated by the US National Institutes of Health (NIH), seeks to create a comprehensive database of the bacteria residing throughout the gastrointestinal tract and to catalogue their properties.

The lives of the bacteria in our gut are intimately entwined with our immune, endocrine and nervous systems. The relationship goes both ways: the microbiome influences the function of these systems, which in turn alter the activity and composition of the bacterial community. We are starting to unravel this complexity and gain insight into how gut bacteria interface with the rest of the body and, in particular, how they affect the brain.

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Filed under microbiome gut bacteria gut depression neuroscience science

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New front in war on Alzheimer’s, other protein-folding diseases
A surprise discovery that overturns decades of thinking about how the body fixes proteins that come unraveled greatly expands opportunities for therapies to prevent diseases such as Alzheimer’s and Parkinson’s, which have been linked to the accumulation of improperly folded proteins in the brain.
“This finding provides a whole other outlook on protein-folding diseases; a new way to go after them,” said Andrew Dillin, the Thomas and Stacey Siebel Distinguished Chair of Stem Cell Research in the Department of Molecular and Cell Biology and Howard Hughes Medical Institute investigator at the University of California, Berkeley.
Dillin, UC Berkeley postdoctoral fellows Nathan A. Baird and Peter M. Douglas and their colleagues at the University of Michigan, The Scripps Research Institute and Genentech Inc., will publish their results in the Oct. 17 issue of the journal Science.
Cells put a lot of effort into preventing proteins – which are like a string of beads arranged in a precise three-dimensional shape – from unraveling, since a protein’s activity as an enzyme or structural component depends on being properly shaped and folded. There are at least 350 separate molecular chaperones constantly patrolling the cell to refold misfolded proteins. Heat is one of the major threats to proteins, as can be demonstrated when frying an egg – the clear white albumen turns opaque as the proteins unfold and then tangle like spaghetti.
Heat shock
For 35 years, researchers have worked under the assumption that when cells undergo heat shock, as with a fever, they produce a protein that triggers a cascade of events that field even more chaperones to refold unraveling proteins that could kill the cell. The protein, HSF-1 (heat shock factor-1), does this by binding to promoters upstream of the 350-plus chaperone genes, upping the genes’ activity and launching the army of chaperones, which originally were called “heat shock proteins.”
Injecting animals with HSF-1 has been shown not only to increase their tolerance of heat stress, but to increase lifespan.
Because an accumulation of misfolded proteins has been implicated in aging and in neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s diseases, scientists have sought ways to artificially boost HSF-1 in order to reduce the protein plaques and tangles that eventually kill brain cells. To date, such boosters have extended lifespan in lab animals, including mice, but greatly increased the incidence of cancer.
Dillin’s team found in experiments on the nematode worm C. elegans that HSF-1 does a whole lot more than trigger release of chaperones. An equal if not more important function is to stabilize the cell’s cytoskeleton, which is the highway that transports essential supplies – healing chaperones included – around the cell.
“We are suggesting that, rather than making more of HSF-1 to prevent diseases like Huntington’s, we should be looking for ways to make the actin cytoskeleton better,” Dillin said. Such tactics might avoid the carcinogenic side effects of upping HSF-1.
Dillin is codirector of the Paul F. Glenn Center for Aging Research, a new collaboration between UC Berkeley and UC San Francisco supported by the Glenn Foundation for Medical Research. Center investigators will study the many ways that proteins malfunction within cells, ideally paving the way for novel treatments for neurodegenerative diseases.
A cell at war
Dillin compares a cell experiencing heat shock to a country under attack. In a war, an aggressor first cuts off all communications, such as roads, train and bridges, which prevents the doctors from treating the wounded. Similarly, heat shock disrupts the cytoskeletal highway, preventing the chaperone “doctors” from reaching the patients, the misfolded proteins.
“We think HSF-1 not only makes more chaperones, more doctors, but also insures that the roadways stay intact to keep everything functional and make sure the chaperones can get to the sick and wounded warriors,” he said.
The researchers found specifically that HSF-1 up-regulates another gene, pat-10, that produces a protein that stabilizes actin, the building blocks of the cytoskeleton.
By boosting pat-10 activity, they were able to cure worms that had been altered to express the Huntington’s disease gene, and also extend the lifespan of normal worms.
Dillin suspects that HSF-1’s main function is, in fact, to protect the actin cytoskeleton. He and his team mutated HSF-1 so that it no longer boosted chaperones, demonstrating, he said, that “you can survive heat shock with the normal level of heat shock proteins, as long as you make your cytoskeleton work better.”
He noted that the team’s results – that boosting chaperones is not essential to surviving heat stress – were so contradictory to current thinking that “I made my post-docs’ lives hell for three years” insisting on more experiments to rule out errors. Yet, when Dillin presented the results recently to members of the protein-folding community, he said the first reaction of many was, “That makes perfect sense.”

New front in war on Alzheimer’s, other protein-folding diseases

A surprise discovery that overturns decades of thinking about how the body fixes proteins that come unraveled greatly expands opportunities for therapies to prevent diseases such as Alzheimer’s and Parkinson’s, which have been linked to the accumulation of improperly folded proteins in the brain.

“This finding provides a whole other outlook on protein-folding diseases; a new way to go after them,” said Andrew Dillin, the Thomas and Stacey Siebel Distinguished Chair of Stem Cell Research in the Department of Molecular and Cell Biology and Howard Hughes Medical Institute investigator at the University of California, Berkeley.

Dillin, UC Berkeley postdoctoral fellows Nathan A. Baird and Peter M. Douglas and their colleagues at the University of Michigan, The Scripps Research Institute and Genentech Inc., will publish their results in the Oct. 17 issue of the journal Science.

Cells put a lot of effort into preventing proteins – which are like a string of beads arranged in a precise three-dimensional shape – from unraveling, since a protein’s activity as an enzyme or structural component depends on being properly shaped and folded. There are at least 350 separate molecular chaperones constantly patrolling the cell to refold misfolded proteins. Heat is one of the major threats to proteins, as can be demonstrated when frying an egg – the clear white albumen turns opaque as the proteins unfold and then tangle like spaghetti.

Heat shock

For 35 years, researchers have worked under the assumption that when cells undergo heat shock, as with a fever, they produce a protein that triggers a cascade of events that field even more chaperones to refold unraveling proteins that could kill the cell. The protein, HSF-1 (heat shock factor-1), does this by binding to promoters upstream of the 350-plus chaperone genes, upping the genes’ activity and launching the army of chaperones, which originally were called “heat shock proteins.”

Injecting animals with HSF-1 has been shown not only to increase their tolerance of heat stress, but to increase lifespan.

Because an accumulation of misfolded proteins has been implicated in aging and in neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s diseases, scientists have sought ways to artificially boost HSF-1 in order to reduce the protein plaques and tangles that eventually kill brain cells. To date, such boosters have extended lifespan in lab animals, including mice, but greatly increased the incidence of cancer.

Dillin’s team found in experiments on the nematode worm C. elegans that HSF-1 does a whole lot more than trigger release of chaperones. An equal if not more important function is to stabilize the cell’s cytoskeleton, which is the highway that transports essential supplies – healing chaperones included – around the cell.

“We are suggesting that, rather than making more of HSF-1 to prevent diseases like Huntington’s, we should be looking for ways to make the actin cytoskeleton better,” Dillin said. Such tactics might avoid the carcinogenic side effects of upping HSF-1.

Dillin is codirector of the Paul F. Glenn Center for Aging Research, a new collaboration between UC Berkeley and UC San Francisco supported by the Glenn Foundation for Medical Research. Center investigators will study the many ways that proteins malfunction within cells, ideally paving the way for novel treatments for neurodegenerative diseases.

A cell at war

Dillin compares a cell experiencing heat shock to a country under attack. In a war, an aggressor first cuts off all communications, such as roads, train and bridges, which prevents the doctors from treating the wounded. Similarly, heat shock disrupts the cytoskeletal highway, preventing the chaperone “doctors” from reaching the patients, the misfolded proteins.

“We think HSF-1 not only makes more chaperones, more doctors, but also insures that the roadways stay intact to keep everything functional and make sure the chaperones can get to the sick and wounded warriors,” he said.

The researchers found specifically that HSF-1 up-regulates another gene, pat-10, that produces a protein that stabilizes actin, the building blocks of the cytoskeleton.

By boosting pat-10 activity, they were able to cure worms that had been altered to express the Huntington’s disease gene, and also extend the lifespan of normal worms.

Dillin suspects that HSF-1’s main function is, in fact, to protect the actin cytoskeleton. He and his team mutated HSF-1 so that it no longer boosted chaperones, demonstrating, he said, that “you can survive heat shock with the normal level of heat shock proteins, as long as you make your cytoskeleton work better.”

He noted that the team’s results – that boosting chaperones is not essential to surviving heat stress – were so contradictory to current thinking that “I made my post-docs’ lives hell for three years” insisting on more experiments to rule out errors. Yet, when Dillin presented the results recently to members of the protein-folding community, he said the first reaction of many was, “That makes perfect sense.”

Filed under neurodegenerative diseases proteins HSF-1 chaperones medicine science

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Presence of Enzyme May Worsen Effects of Spinal Cord Injury and Impair Long-term Recovery
Traumatic spinal cord injury (SCI) is a devastating condition with few treatment options. Studies show that damage to the barrier separating blood from the spinal cord can contribute to the neurologic deficits that arise secondary to the initial trauma. Through a series of sophisticated experiments, researchers reporting in The American Journal of Pathology suggest that matrix metalloproteinase-3 (MMP-3) plays a pivotal role in disruption of the brain/spinal cord barrier (BSCB), cell death, and functional deficits after SCI. This link also presents new therapeutic possibilities.
“Matrix metalloproteinases (MMPs) are enzymes known to degrade the extracellular matrix and other extracellular proteins and are essential for remodeling of the extracellular matrix and wound healing. Excessive proteolytic activity of MMPs can be detrimental, leading to numerous pathological conditions, including blood brain barrier (BBB)/BSCB disruption after injury,” explains Tae Young Yune, PhD, of the Department of Biochemistry and Molecular Biology, School of Medicine, Kyung Hee University, Seoul, Korea. Although other MMPs have been linked to SCI (i.e. MMP-2, MMP-9, and MMP-12), there has been no previous direct evidence of a similar role for MMP-3.
By comparing mice that underwent spinal cord injury to a control group, investigators found that both MMP3 messenger RNA (mRNA) and MMP-3 protein levels in spinal cord segments were increased after SCI, peaking one day after surgery in the experimental group, whereas no changes were seen in the controls. MMP-3 immunoreactivity was detected in cells within the lesion site, invading neutrophils, and blood vessel endothelial cells in the area outside of the initial injured area (the penumbra).
Another series of experiments focused on the role of MMP-3 in BSCB permeability, using dye to visualize leakage through the BSCB. Similar to MMP-3 mRNA and protein levels, dye leakage reached a maximum one day after SCI. Leakage was lower in Mmp3 knockout mice that were genetically altered to be deficient in MMP-3 as well as in mice injected with either Mmp3 small interfering RNA (siRNA) or a general MMP inhibitor. Injection of MMP-3 into normal spinal cord also significantly increased dye leakage.
MMP-3 was found to contribute to the degradation of tight junction proteins that are responsible for maintaining the integrity of the BSCB barrier. In addition, the researchers reported that MMP-3 induced blood cell infiltration and hemorrhage after SCI in wild-type mice, but not in Mmp3 knockout mice.  MMP-3 also mediated activation of other MMPs (MMP-2 and MMP-9) that are up-regulated after SCI. “This is the first study to demonstrate that MMP-3 is involved in MMP-9 activation in central nervous system injury,” says Dr. Yune.
A significant finding was that mice deficient in MMP-3 showed significantly better functional recovery 14 and 28 days after injury than non-deficient mice. Histological analysis showed that after SCI the mice deficient in MMP-3 had smaller volumes of injured tissue and more healthy axons than non-deficient wild-type mice.
“The evidence suggests that BBB/BSCB disruption plays a pivotal role in acute and chronic neurological disorders. The inhibition of MMP-3 may be a promising therapeutic target for human central nervous system disease, including SCI,” notes Dr. Yune.

Presence of Enzyme May Worsen Effects of Spinal Cord Injury and Impair Long-term Recovery

Traumatic spinal cord injury (SCI) is a devastating condition with few treatment options. Studies show that damage to the barrier separating blood from the spinal cord can contribute to the neurologic deficits that arise secondary to the initial trauma. Through a series of sophisticated experiments, researchers reporting in The American Journal of Pathology suggest that matrix metalloproteinase-3 (MMP-3) plays a pivotal role in disruption of the brain/spinal cord barrier (BSCB), cell death, and functional deficits after SCI. This link also presents new therapeutic possibilities.

“Matrix metalloproteinases (MMPs) are enzymes known to degrade the extracellular matrix and other extracellular proteins and are essential for remodeling of the extracellular matrix and wound healing. Excessive proteolytic activity of MMPs can be detrimental, leading to numerous pathological conditions, including blood brain barrier (BBB)/BSCB disruption after injury,” explains Tae Young Yune, PhD, of the Department of Biochemistry and Molecular Biology, School of Medicine, Kyung Hee University, Seoul, Korea. Although other MMPs have been linked to SCI (i.e. MMP-2, MMP-9, and MMP-12), there has been no previous direct evidence of a similar role for MMP-3.

By comparing mice that underwent spinal cord injury to a control group, investigators found that both MMP3 messenger RNA (mRNA) and MMP-3 protein levels in spinal cord segments were increased after SCI, peaking one day after surgery in the experimental group, whereas no changes were seen in the controls. MMP-3 immunoreactivity was detected in cells within the lesion site, invading neutrophils, and blood vessel endothelial cells in the area outside of the initial injured area (the penumbra).

Another series of experiments focused on the role of MMP-3 in BSCB permeability, using dye to visualize leakage through the BSCB. Similar to MMP-3 mRNA and protein levels, dye leakage reached a maximum one day after SCI. Leakage was lower in Mmp3 knockout mice that were genetically altered to be deficient in MMP-3 as well as in mice injected with either Mmp3 small interfering RNA (siRNA) or a general MMP inhibitor. Injection of MMP-3 into normal spinal cord also significantly increased dye leakage.

MMP-3 was found to contribute to the degradation of tight junction proteins that are responsible for maintaining the integrity of the BSCB barrier. In addition, the researchers reported that MMP-3 induced blood cell infiltration and hemorrhage after SCI in wild-type mice, but not in Mmp3 knockout mice.  MMP-3 also mediated activation of other MMPs (MMP-2 and MMP-9) that are up-regulated after SCI. “This is the first study to demonstrate that MMP-3 is involved in MMP-9 activation in central nervous system injury,” says Dr. Yune.

A significant finding was that mice deficient in MMP-3 showed significantly better functional recovery 14 and 28 days after injury than non-deficient mice. Histological analysis showed that after SCI the mice deficient in MMP-3 had smaller volumes of injured tissue and more healthy axons than non-deficient wild-type mice.

“The evidence suggests that BBB/BSCB disruption plays a pivotal role in acute and chronic neurological disorders. The inhibition of MMP-3 may be a promising therapeutic target for human central nervous system disease, including SCI,” notes Dr. Yune.

Filed under spinal cord spinal cord injury matrix metalloproteinase CNS neuroscience science

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How the brain leads us to believe we have sharp vision
We assume that we can see the world around us in sharp detail. In fact, our eyes can only process a fraction of our surroundings precisely. In a series of experiments, psychologists at Bielefeld University have been investigating how the brain fools us into believing that we see in sharp detail. The results have been published in the scientific magazine ‘Journal of Experimental Psychology: General.’ Its central finding is that our nervous system uses past visual experiences to predict how blurred objects would look in sharp detail.
"In our study we are dealing with the question of why we believe that we see the world uniformly detailed," says Dr. Arvid Herwig from the Neuro-Cognitive Psychology research group of the Faculty of Psychology and Sports Science. The group is also affiliated to the Cluster of Excellence Cognitive Interaction Technology (CITEC) of Bielefeld University and is led by Professor Dr. Werner X. Schneider.
Only the fovea, the central area of the retina, can process objects precisely. We should therefore only be able to see a small area of our environment in sharp detail. This area is about the size of a thumb nail at the end of an outstretched arm. In contrast, all visual impressions which occur outside the fovea on the retina become progressively coarse. Nevertheless, we commonly have the impression that we see large parts of our environment in sharp detail.
Herwig and Schneider have been getting to the bottom of this phenomenon with a series of experiments. Their approach presumes that people learn through countless eye movements over a lifetime to connect the coarse impressions of objects outside the fovea to the detailed visual impressions after the eye has moved to the object of interest. For example, the coarse visual impression of a football (blurred image of a football) is connected to the detailed visual impression after the eye has moved. If a person sees a football out of the corner of her eye, her brain will compare this current blurred picture with memorised images of blurred objects. If the brain finds an image that fits, it will replace the coarse image with a precise image from memory. This blurred visual impression is replaced before the eye moves. The person thus thinks that she already sees the ball clearly, although this is not the case.
The psychologists have been using eye-tracking experiments to test their approach. Using the eye-tracking technique, eye movements are measured accurately with a specific camera which records 1000 images per second. In their experiments, the scientists have recorded fast balistic eye movements (saccades) of test persons. Though most of the participants did not realise it, certain objects were changed during eye movement. The aim was that the test persons learn new connections between visual stimuli from inside and outside the fovea, in other words from detailed and coarse impressions. Afterwards, the participants were asked to judge visual characteristics of objects outside the area of the fovea. The result showed that the connection between a coarse and detailed visual impression occurred after just a few minutes. The coarse visual impressions became similar to the newly learnt detailed visual impressions.
"The experiments show that our perception depends in large measure on stored visual experiences in our memory," says Arvid Herwig. According to Herwig and Schneider, these experiences serve to predict the effect of future actions ("What would the world look like after a further eye movement"). In other words: "We do not see the actual world, but our predictions."

How the brain leads us to believe we have sharp vision

We assume that we can see the world around us in sharp detail. In fact, our eyes can only process a fraction of our surroundings precisely. In a series of experiments, psychologists at Bielefeld University have been investigating how the brain fools us into believing that we see in sharp detail. The results have been published in the scientific magazine ‘Journal of Experimental Psychology: General.’ Its central finding is that our nervous system uses past visual experiences to predict how blurred objects would look in sharp detail.

"In our study we are dealing with the question of why we believe that we see the world uniformly detailed," says Dr. Arvid Herwig from the Neuro-Cognitive Psychology research group of the Faculty of Psychology and Sports Science. The group is also affiliated to the Cluster of Excellence Cognitive Interaction Technology (CITEC) of Bielefeld University and is led by Professor Dr. Werner X. Schneider.

Only the fovea, the central area of the retina, can process objects precisely. We should therefore only be able to see a small area of our environment in sharp detail. This area is about the size of a thumb nail at the end of an outstretched arm. In contrast, all visual impressions which occur outside the fovea on the retina become progressively coarse. Nevertheless, we commonly have the impression that we see large parts of our environment in sharp detail.

Herwig and Schneider have been getting to the bottom of this phenomenon with a series of experiments. Their approach presumes that people learn through countless eye movements over a lifetime to connect the coarse impressions of objects outside the fovea to the detailed visual impressions after the eye has moved to the object of interest. For example, the coarse visual impression of a football (blurred image of a football) is connected to the detailed visual impression after the eye has moved. If a person sees a football out of the corner of her eye, her brain will compare this current blurred picture with memorised images of blurred objects. If the brain finds an image that fits, it will replace the coarse image with a precise image from memory. This blurred visual impression is replaced before the eye moves. The person thus thinks that she already sees the ball clearly, although this is not the case.

The psychologists have been using eye-tracking experiments to test their approach. Using the eye-tracking technique, eye movements are measured accurately with a specific camera which records 1000 images per second. In their experiments, the scientists have recorded fast balistic eye movements (saccades) of test persons. Though most of the participants did not realise it, certain objects were changed during eye movement. The aim was that the test persons learn new connections between visual stimuli from inside and outside the fovea, in other words from detailed and coarse impressions. Afterwards, the participants were asked to judge visual characteristics of objects outside the area of the fovea. The result showed that the connection between a coarse and detailed visual impression occurred after just a few minutes. The coarse visual impressions became similar to the newly learnt detailed visual impressions.

"The experiments show that our perception depends in large measure on stored visual experiences in our memory," says Arvid Herwig. According to Herwig and Schneider, these experiences serve to predict the effect of future actions ("What would the world look like after a further eye movement"). In other words: "We do not see the actual world, but our predictions."

Filed under vision eye movements fovea visual acuity saccades psychology neuroscience science

181 notes

Study finds action video games bolster sensorimotor skills

A study led by University of Toronto psychology researchers has found that people who play action video games such as Call of Duty or Assassin’s Creed seem to learn a new sensorimotor skill more quickly than non-gamers do.

image

A new sensorimotor skill, such as learning to ride a bike or typing, often requires a new pattern of coordination between vision and motor movement. With such skills, an individual generally moves from novice performance, characterized by a low degree of coordination, to expert performance, marked by a high degree of coordination. As a result of successful sensorimotor learning, one comes to perform these tasks efficiently and perhaps even without consciously thinking about them.

“We wanted to understand if chronic video game playing has an effect on sensorimotor control, that is, the coordinated function of vision and hand movement,” said graduate student Davood Gozli, who led the study with supervisor Jay Pratt.

To find out, they set up two experiments. In the first, 18 gamers (those who played a first-person shooter game at least three times per week for at least two hours each time in the previous six months) and 18 non-gamers (who had little or no video game use in the past two years) performed a manual tracking task. Using a computer mouse, they were instructed to keep a small green square cursor at the centre of a white square moving target which moved in a very complicated pattern that repeated itself. The task probes sensorimotor control, because participants see the target movement and try to coordinate their hand movements with what they see.

In the early stages of doing the tasks, the gamers’ performance was not significantly better than non-gamers. “This suggests that while chronically playing action video games requires constant motor control, playing these games does not give gamers a reliable initial advantage in new and unfamiliar sensorimotor tasks,” said Gozli.

By the end of the experiment, all participants performed better as they learned the complex pattern of the target. The gamers, however, were significantly more accurate in following the repetitive motion than the non-gamers. “This is likely due to the gamers’ superior ability in learning a novel sensorimotor pattern, that is, their gaming experience enabled them to learn better than the non-gamers.”

In the next experiment, the researchers wanted to test whether the superior performance of the gamers was indeed a result of learning rather than simply having better sensorimotor control. To eliminate the learning component of the experiment, they required participants to again track a moving dot, but in this case the patterns of motion changed throughout the experiment. The result this time: neither the gamers nor the non-gamers improved as time went by, confirming that learning was playing a key role and the gamers were learning better.

One of the benefits of playing action games may be an enhanced ability to precisely learn the dynamics of new sensorimotor tasks. Such skills are key, for example, in laparoscopic surgery which involves high precision manual control of remote surgery tools through a computer interface.

(Source: media.utoronto.ca)

Filed under video games motor movement vision learning eye-hand coordination neuroscience science

384 notes

Myth-conceptions: How myths about the brain are hampering teaching
Teachers in the UK, Holland, Turkey, Greece and China were presented with seven so-called ‘neuromyths’ and asked whether they believe them to be true.
A quarter or more of teachers in the UK and Turkey believe a student’s brain would shrink if they drank less than six to eight glasses of water a day, while around half or more of those surveyed believe a student’s brain is only 10 per cent active and that children are less attentive after sugary drinks and snacks.
Over 70 per cent of teachers in all countries wrongly believe a student is either left-brained or right-brained, peaking at 91 per cent in the UK.
And almost all teachers (over 90 per cent in each country) feel that teaching to a student’s preferred learning style - auditory, kinaesthetic or visual - is helpful, despite no convincing evidence to support this approach.
The new research from the University of Bristol, published in Nature Reviews Neuroscience, calls for better communication between neuroscientists and educators.
Dr Paul Howard-Jones, author of the article from Bristol University’s Graduate School of Education, said: “These ideas are often sold to teachers as based on neuroscience – but modern neuroscience cannot be used support them. These ideas have no educational value and are often associated with poor practice in the classroom.”
The report blames wishfulness, anxiety and a bias towards simple explanations as typical factors that distort neuroscientific fact into neuromyth.
Such factors also appear to be hampering recent efforts of neuroscientists to communicate the true meaning of their work to educators.
Dr Howard-Jones added: “Although the increased dialogue between neuroscience and education is encouraging, we see new neuromyths on the horizon and old ones returning in new forms.
“Sometimes, transmitting ‘boiled-down’ messages about the brain to educators can just lead to misunderstanding, and confusions about concepts such as brain plasticity are common in discussions about education policy.”
The report highlights several areas where new findings from neuroscience are becoming misinterpreted by education, including brain-related ideas regarding early educational investment, adolescent brain development and learning disorders such as dyslexia and ADHD.
Hopes that education will draw genuine benefit from neuroscience may rest on a new but rapidly growing field of ‘neuroeducational’ research that combines both fields.
The review concludes that, in the future, such collaboration will be greatly needed if education is to be enriched rather than misled by neuroscience.

Myth-conceptions: How myths about the brain are hampering teaching

Teachers in the UK, Holland, Turkey, Greece and China were presented with seven so-called ‘neuromyths’ and asked whether they believe them to be true.

A quarter or more of teachers in the UK and Turkey believe a student’s brain would shrink if they drank less than six to eight glasses of water a day, while around half or more of those surveyed believe a student’s brain is only 10 per cent active and that children are less attentive after sugary drinks and snacks.

Over 70 per cent of teachers in all countries wrongly believe a student is either left-brained or right-brained, peaking at 91 per cent in the UK.

And almost all teachers (over 90 per cent in each country) feel that teaching to a student’s preferred learning style - auditory, kinaesthetic or visual - is helpful, despite no convincing evidence to support this approach.

The new research from the University of Bristol, published in Nature Reviews Neuroscience, calls for better communication between neuroscientists and educators.

Dr Paul Howard-Jones, author of the article from Bristol University’s Graduate School of Education, said: “These ideas are often sold to teachers as based on neuroscience – but modern neuroscience cannot be used support them. These ideas have no educational value and are often associated with poor practice in the classroom.”

The report blames wishfulness, anxiety and a bias towards simple explanations as typical factors that distort neuroscientific fact into neuromyth.

Such factors also appear to be hampering recent efforts of neuroscientists to communicate the true meaning of their work to educators.

Dr Howard-Jones added: “Although the increased dialogue between neuroscience and education is encouraging, we see new neuromyths on the horizon and old ones returning in new forms.

“Sometimes, transmitting ‘boiled-down’ messages about the brain to educators can just lead to misunderstanding, and confusions about concepts such as brain plasticity are common in discussions about education policy.”

The report highlights several areas where new findings from neuroscience are becoming misinterpreted by education, including brain-related ideas regarding early educational investment, adolescent brain development and learning disorders such as dyslexia and ADHD.

Hopes that education will draw genuine benefit from neuroscience may rest on a new but rapidly growing field of ‘neuroeducational’ research that combines both fields.

The review concludes that, in the future, such collaboration will be greatly needed if education is to be enriched rather than misled by neuroscience.

Filed under neuromyths education neuroscience science

108 notes

Brain’s Compass Relies on Geometric Relationships

The brain has a complex system for keeping track of which direction you are facing as you move about; remembering how to get from one place to another would otherwise be impossible. Researchers from the University of Pennsylvania have now shown how the brain anchors this mental compass.

Their findings provide a neurological basis for something that psychologists have long observed about navigational behavior: people use geometrical relationships to orient themselves.

The research, which is related to the work that won this year’s Nobel Prize in Physiology or Medicine, adds new dimensions to our understanding of spatial memory and how it helps us to build memories of events.           

The study was led by Russell Epstein, a professor of psychology in Penn’s School of Arts & Sciences, and Steven Marchette, a postdoctoral fellow in Epstein’s lab. Also contributing to the study were lab members Lindsay Vass, a graduate student, and Jack Ryan, a research specialist.

It was published in Nature Neuroscience.  

Read more

Filed under spatial navigation spatial memory retrosplenial complex orientation neuroscience science

91 notes

Researcher adds to evidence linking autism to air pollutants

A researcher at the University of Wisconsin-Milwaukee (UWM) has added to a growing body of evidence that links autism to air pollutants such as those generated by cars and trucks.

Amy Kalkbrenner’s study, published this week online at the journal Epidemiology, showed that pollution’s impact on autism rates in North Carolina is similar to results of pollution-autism studies in California – despite weather and climate differences between the two states.

In addition, the work of Kalkbrenner and her colleagues, building on previous studies, showed that women in the third trimester of pregnancy were more susceptible to the damaging effects of air pollution on their unborn child.

“It adds another piece supporting the hypothesis that environmental chemicals are part of the autism puzzle,” says Kalkbrenner, an assistant professor in UWM’s Joseph J. Zilber School of Public Health. Autism, a spectrum of disorders affecting interpersonal relations and work achievement, now affects some 1 in 68 children in the U.S.

Her research team focused on exposure to coarse and fine particulate matter, known as PM10, which arises in part from traffic-related air pollution. The study evaluated records in the two states, covering pre-conception through the first birthday for 87,000 children in North Carolina and 77,500 in California born in the mid-to-late 1990s. Key regions in each state were selected based on researchers’ ability to simultaneously measure the level of particulate matter present, and know which children had autism in these regions.

Researchers used a new, more exact tool to measure the levels of particulate matter in smaller slices of time, based on pollution at the family’s address during pregnancy. With this method, they were able to compare exposures during specific weeks of pregnancy. The approximately one thousand children who later developed some form of autism spectrum disorders were then compared to all other children.

Kalkbrenner says it was important to look at eastern states because of the differences in climate, seasonal weather patterns and the chemical make-up of the particulate matter that might impact brain development. “Evidence for a link between a chemical exposure and a health impact like autism is stronger when it can be shown in more than one region.” The team found that the concentration of particulate matter was highest among children born in summer months in North Carolina and those born in fall and winter months in California.

Reasons for increased susceptibility in the third trimester of pregnancy are not known at this time. However, Kalkbrenner says this finding is consistent with theories that show links between autism and altered brain network development, specifically synaptic connections that are developing during the final months of pregnancy.

“We’ve now had three solid studies saying the same thing. The evidence is pretty compelling that something is going on with air pollution and autism,” says Kalkbrenner, who adds that further study is needed to determine the neurodevelopmental impacts of specific chemical pollutants during precise developmental windows.

(Source: www5.uwm.edu)

Filed under autism air pollution particulate matter brain development pregnancy neuroscience science

216 notes

Male and female brains aren’t equal when it comes to fatResearchers have found that male and female brains respond in remarkably different ways to high-fat meals. Those differences in the brain lead to greater inflammation and increased health risks in males that indulge on fatty foods in comparison to females, a new study in mice shows. The findings reported in the Cell Press journal Cell Reports on October 16th may help to explain observed differences in obesity outcomes between women and men – premenopausal women carrying extra weight fare better than men do – and suggest that dietary advice should be made more sex-specific.
"Our findings, for the first time, suggest that males and females respond to high-fat diets differently," said Deborah Clegg of the Cedar-Sinai Diabetes And Obesity Research Institute in Los Angeles. "The data would suggest that is probably ‘ok’ for females to occasionally have a high-fat meal, where it is not recommended for males.
"The way we treat patients and provide dietary and nutritional advice should be altered. We might be less concerned about an occasional hamburger for women, but for men, we might more strongly encourage avoidance, especially if they have pre-existing diseases such as heart disease or type 2 diabetes."
Earlier data from Clegg’s team and others had suggested that inflammation in the brain is tied to overeating, blood sugar imbalances, and increased inflammation in other parts of the body, including fat tissue. Those effects can be triggered, in males in particular, by short-term exposure to a high-fat diet.
The researchers say they were initially shocked to discover that male and female brains differ in their fatty acid composition. When they manipulated male mouse brains to have the fatty acid profile of females, they found that those animals were protected from the ill effects of a diet high in fat.
When males with average male brains entered an inflammatory state after eating diets high in fat, they also suffered from reduced cardiac function in a way that female animals in the study did not. Those sex differences in the brain’s response to fat are related to differences between females and males in estrogen and estrogen receptor status.
Clegg says her team is now working out a strategy to confirm whether the findings in mice apply to people too. If they do, there will be some very immediate practical implications for what men and women should put on their plates.
"We have always had ‘one size fits all’ with respect to our nutritional information and our pharmaceutical approach," Clegg said. "Our data begin to suggest that sex should be factored in, and men should be more closely monitored for fat intake and inflammation than women."
(Image: Shutterstock)

Male and female brains aren’t equal when it comes to fat

Researchers have found that male and female brains respond in remarkably different ways to high-fat meals. Those differences in the brain lead to greater inflammation and increased health risks in males that indulge on fatty foods in comparison to females, a new study in mice shows. The findings reported in the Cell Press journal Cell Reports on October 16th may help to explain observed differences in obesity outcomes between women and men – premenopausal women carrying extra weight fare better than men do – and suggest that dietary advice should be made more sex-specific.

"Our findings, for the first time, suggest that males and females respond to high-fat diets differently," said Deborah Clegg of the Cedar-Sinai Diabetes And Obesity Research Institute in Los Angeles. "The data would suggest that is probably ‘ok’ for females to occasionally have a high-fat meal, where it is not recommended for males.

"The way we treat patients and provide dietary and nutritional advice should be altered. We might be less concerned about an occasional hamburger for women, but for men, we might more strongly encourage avoidance, especially if they have pre-existing diseases such as heart disease or type 2 diabetes."

Earlier data from Clegg’s team and others had suggested that inflammation in the brain is tied to overeating, blood sugar imbalances, and increased inflammation in other parts of the body, including fat tissue. Those effects can be triggered, in males in particular, by short-term exposure to a high-fat diet.

The researchers say they were initially shocked to discover that male and female brains differ in their fatty acid composition. When they manipulated male mouse brains to have the fatty acid profile of females, they found that those animals were protected from the ill effects of a diet high in fat.

When males with average male brains entered an inflammatory state after eating diets high in fat, they also suffered from reduced cardiac function in a way that female animals in the study did not. Those sex differences in the brain’s response to fat are related to differences between females and males in estrogen and estrogen receptor status.

Clegg says her team is now working out a strategy to confirm whether the findings in mice apply to people too. If they do, there will be some very immediate practical implications for what men and women should put on their plates.

"We have always had ‘one size fits all’ with respect to our nutritional information and our pharmaceutical approach," Clegg said. "Our data begin to suggest that sex should be factored in, and men should be more closely monitored for fat intake and inflammation than women."

(Image: Shutterstock)

Filed under obesity sex differences fatty acid inflammation diet neuroscience science

110 notes

Are Male Brains Wired to Ignore Food for Sex?

Choosing between two good things can be tough. When animals must decide between feeding and mating, it can get even trickier. In a discovery that might ring true even for some humans, researchers have shown that male brains – at least in nematodes – will suppress the ability to locate food in order to instead focus on finding a mate.

image

(Image caption: C. elegans male (top) and hermaphrodite (bottom))

The results, which appear today in the journal Current Biology, may point to how subtle changes in the brain’s circuitry dictate differences in behavior between males and females. 

“While we know that human behavior is influenced by numerous factors, including cultural and social norms, these findings point to basic biological mechanisms that may not only help explain some differences in behavior between males and females, but why different sexes may be more susceptible to certain neurological disorders,” said Douglas Portman, Ph.D., an associate professor in the Department of Biomedical Genetics and Center for Neural Development and Disease at the University of Rochester and lead author of the study.

The findings were made in experiments involving C. elegans, a microscopic roundworm that has long been used by researchers to understand fundamental mechanisms in biology. Many of the discoveries made using C. elegans apply throughout the animal kingdom and this research has led to a broader understanding of human biology. In fact, three Nobel Prizes in medicine and chemistry have been awarded for discoveries involving C. elegans.  

C. elegans is particularly useful in the study of the nervous system and scientists understand in great detail the development, function, and multiple connections of its entire neural network. 

The study published today focuses on the activity of a single pair of neurons found in C. elegans – called AWA – that control smell. Smell, along with taste and touch, are critical sensory factors that dictate how C. elegans understands and navigates its environment, including finding food, avoiding danger, and locating a mate.

There are two sexes of C. elegans, males and hermaphrodites. Though the hermaphrodites are able to self-fertilize, they are also mating partners for males, and are considered to be modified females.  

It has been previously observed that males and hermaphrodites act differently when exposed to food. If placed at a food source, the hermaphrodites tend to stay there. Males, however, will leave food source and “wander” – scientist believe they do this because they are in search of a mate. 

The Rochester researchers discovered that the sensory mechanisms – called chemoreceptors – of the AWA neurons were regulated by the sexual identity of these cells, which, in turn, controls the expression of a receptor called ODR-10. These receptors bind to a chemical scent that is given off by food and other substances.  

In hermaphrodites, more of the ODR-10 receptors are produced, making the worms more sensitive – and thereby attracted – to the presence of food. In males, fewer of these receptors are active, essentially suppressing their ability – and perhaps desire – to find food. However, when males were deprived of food, they produced dramatically higher levels of this receptor, allowing them to temporarily focus on finding food.

To confirm the role of these genetic differences between the sexes on behavior, the researchers designed a series of experiments in which they observed the activity of C. elegans when placed in a petri-dish and confronted with the option to either feed or go in search of a mate. The hermaphrodites were place in the center of the dish at a food source and, as expected, they stayed put. 

The males were placed in their own individual food sources at the periphery of the dish. As a further obstacle between the males and their potential mates, an additional ring of food surrounded the hermaphrodites in the center of the dish. The males in the experiment consisted of two categories, one group with a normal genetic profile and another group that had been engineered by the researchers to overexpress the ODR-10 receptor, essentially making them more sensitive to the smell of food.

The researchers found that the normal worms left their food source and eventually made their way to the center of the dish where they mated with the hermaphrodites. The genetically engineered males were less successful at finding a mate, presumably because they were more interested in feeding. By examining the genetic profile of the resulting offspring, the scientists observed that the normal males out-produced the genetically engineered males by 10 to one. 

In separate experiments, the researchers were also able to modify the behavior of the hermaphrodites by suppressing the ODR-10 receptors, causing them to act like males and abandon their food source.

“These findings show that by tuning the properties of a single cell, we can change behavior,” said Portman. “This adds to a growing body of evidence that sex-specific regulation of gene expression may play an important role in neural plasticity and, consequently, influence differences in behaviors – and in disease susceptibility – between the sexes.”

(Source: urmc.rochester.edu)

Filed under C. elegans neural circuits chemoreceptors neurons hermaphrodites olfaction neuroscience science

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