Posts tagged science
Articles and news from the latest research reports.
The Hidden Costs of Cognitive Enhancement
Gentle electrical zaps to the brain can accelerate learning and boost performance on a wide range of mental tasks, scientists have reported in recent years. But a new study suggests there may be a hidden price: Gains in one aspect of cognition may come with deficits in another.
Researchers who study transcranial electrical stimulation, which uses electrodes placed on the scalp, see it as a potentially promising way to enhance cognition in neurological patients, struggling students, and perhaps even ordinary people. Scientists have used it to speed up rehab in people whose speech or movement has been affected by a stroke, and DARPA has studied it as a way to accelerate learning in intelligence analysts or soldiers on the lookout for bad guys and bombs.
Until now, the papers coming out of this field have reported one good-news finding after another.
“This is the first paper to my knowledge to show a cost associated with the gains in cognitive function,” said neuropsychologist Rex Jung of the University of New Mexico, who was not associated with the study. “It’s a really nice demonstration.”
Cognitive neuroscientist Roi Cohen Kadosh of the University of Oxford, who led the study, has been investigating brain stimulation to boost mathematical abilities. He has applied for a patent on a brain stimulator he hopes could help math-challenged students get a better grip on the basics, or even help the mathematically inclined perform even better.
Cohen Kadosh and his colleague Teresa Iuculano investigated 19 volunteers as they learned a new numerical system by trial and error. The new system was based on arbitrary symbols: A cylinder represented the number five, for example, and a triangle represented the number nine. In several training sessions the volunteers viewed pairs of symbols on a computer screen and pressed a key to indicate which one represented a bigger quantity. At first they had to guess, but they eventually learned which symbols corresponded with which numbers.
All of the volunteers wore electrodes on their scalp during these training session. Some received mild electrical stimulation that targeted the posterior parietal cortex, an area implicated in previous studies of numerical cognition. Others received stimulation of the dorsolateral prefrontal cortex, an area involved in a wide range of functions, including learning and memory. A third group received sham stimulation that caused a slight tingling of the skin but no change in brain activity.
Those who had the parietal area involved in numerical cognition stimulated learned the new number system more quickly than those who got sham stimulation, the researchers report in the Journal of Neuroscience. But at the end of the weeklong study their reaction times were slower when they had to put their newfound knowledge to use to solve a new task that they hadn’t seen during the training sessions. ”They had trouble accessing what they’d learned,” Cohen Kadosh said.
The volunteers who had the prefrontal area involved in learning and memory stimulated showed the opposite pattern. They were slower than the control group to learn the new numerical system, but they performed faster on the new test at the end of the experiment. The bottom line, says Cohen Kadosh, is that stimulating either brain region had both benefits and drawbacks. ”Just like with drugs, there seem to be side effects,” he said.
Going forward, Cohen Kadosh says, more work is needed on how to maximize the benefits and minimize the costs of electrical brain stimulation. He thinks the approach has promise, but only when it’s used strategically, by picking the right brain regions to target and stimulating them while a person is training on the skill they want to improve. ”I think it’s going to be useless unless you pair it with some type of cognitive training,” he said.
But that’s not stopping some people from giving it a try on their own. Although it should be obvious that DIY brain stimulation is a bad idea, both Jung and Cohen Kadosh say there seems to be growing interest in the general public in using it for cognitive enhancement.
“There are some do it yourself websites I’ve stumbled across that are pretty frightening,” Jung said. “People are definitely tinkering around with this in their garage.”
The new study suggests one way that could backfire. And that’s not all, said Jung. ”You can burn yourself if nothing else.”
Mutated Gene Causes Nerve Cell Death
The British astrophysicist Stephen Hawking is likely to be the world’s most famous person living with amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease. ALS is a progressive disease affecting motor neurons, nerve cells that control muscle function, and nearly always leads to death. Researchers at the Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA) in Vienna have now identified a completely new mechanism in the onset of motor neuron diseases. Their findings could be the basis for future treatments for these presently incurable diseases.
A new principle on motor neuron death
The IMBA scientists, working with an international team of researchers under the leadership of Josef Penninger and Javier Martinez, discovered a completely new fundamental mechanism that triggers the death of motor neurons. Motor neurons are nerve cells responsible for stimulating muscles. The loss of these motor neurons in mice with a genetic mutation in a gene named CLP11 leads to severe and progressive muscular paralysis and, in some cases, to death.
"We’ve been working on resolving the function of the CLP1 gene in a living organism for a long time. To do that, we developed model mice in which the function of CLP1 was genetically inactivated. To our utter surprise we discovered that deactivating CLP1 increases the sensitivity of cell die when exposed to oxidative stress2. That leads to enhanced activity of the p53 protein3 and then to the permanent destruction of motor neurons," says Toshikatsu Hanada, a postdoctoral researcher working in the lab of Josef Penninger and first author of the study along with Stefan Weitzer.
Stephen Hawking - a most renowned patient
Motor neuron diseases (MNDs), such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA), are chronic disorders of the neuromuscular system. These diseases are caused by damage in the motor nerve cells in the brain and spinal cord, and the nerves can no longer stimulate motion in the muscles. The primary symptoms are muscular weakness, muscular dystrophy, and problems swallowing or speaking. Stephen Hawking was diagnosed with ALS 50 years ago. But not all ALS patients live so long with the disease: so far there are no treatments for ALS. Nearly all ALS patients die of paralysis of respiratory muscles within a few years.
Completely new disease mechanism
Javier Martinez, an IMBA team leader and co-author of the study, is a specialist in the field of ribonucleic acid (RNA) research. His research group had discovered the CLP1 gene in an earlier study, published in Nature in 2007. Until now, the exact essential function of CLP1 in RNA biology was unclear. “By deactivating CLP1, we have discovered a previously unknown new species of RNA,” says Javier Martinez about the scientific relevance of the work. “The accumulation of this RNA is a consequence of increased oxidative stress in the cell. We see this as one of the triggers for the loss of motor neurons that occurs in ALS and other neuromuscular diseases. Thus our findings describe a completely new mechanism of motor neuron diseases.”
Seminal findings
Josef Penninger, scientific director at the IMBA and last-author of the study, is excited about the researchers’ findings: “This surprising discovery of a role of CLP1 in the onset of motor neuron diseases is an entirely new principle in how RNA talks to oxidative stress. Nearly all genetic mutations found in ALS patients affect either RNA metabolism or oxidative stress, suggesting a possibly unifying principle for these diseases. Our work may have revealed the ‘missing link’ in how these two biological systems communicate and trigger incurable diseases like ALS.”
Stefan Weitzer sees tremendous potential for these findings: “We’ve discovered a new mechanism that leads to the death of motor neurons. If this holds true for other neuronal disease, our results could be one day used to drive the development of treatments for previously incurable diseases. In our work we also describe how the p53 protein regulates the loss of motor neurons. Removing p53 saves mice with CLP1 mutations from certain death.” If scientists are successful in applying these findings to people, the researchers may have discovered a treatment approach to cure ALS and similar diseases. The authors, however, caution that more studies will be needed to translate their findings to human medicine.
This study was performed in collaboration with research groups from the Medical Universities of Vienna and Innsbruck, the University Medical Center at Hamburg-Eppendorf in Germany, the Harvard Medical School, the Harvard Stem Cell Institute, the Boston Children’s and Massachusetts General Hospitals, the Keio University School of Medicine in Tokyo, Oita University in Japan, and the Weizmann Institute of Science in Rehovot in Israel.
Their work, “CLP1 links tRNA metabolism to progressive motor-neuron loss”, was published on March 10, 2013 in “Nature”, an internationally renowned journal.
(Source: imba.oeaw.ac.at)
When most of us admire a piece of art, it triggers a cascade of complex neural activity; a wash of emotion and meaning that fills our brains and prompts deep thought. But does that happen for people with neurological conditions, too?
Forthcoming Oxford-based exhibition Affecting Perception seeks to explore that very question, through a combination of art, seminars and school workshops. Organised by Martha Crawford, Cosima Gretton and Rachel Stratton, who together form the AXNS collective, the aim is to understand how artists and their work are affected by neurological conditions.
The team is working with the University’s Department of Experimental Psychology and artists who suffer from conditions ranging from dementia to brain damage, in order to help the public understand how art and neuroscience are intertwined. “We’re trying to engage the community with the kind of learning usually kept in the University,” explains Martha Crawford.
Helping them achieve that are Prof. Glyn Humphreys and Prof. Charles Spence, both from the University’s Department of Experimental Psychology. Individually, they’ll be leading seminars during the exhibition which explore the overlap between academia and art. “There’s a coarse level of understanding of neuropsychology outside of academia, which means people are sometimes scared of neurological conditions,” explains Professor Glyn Humphreys. “I think anything we can do to raise awareness has to be a good thing.”
During the course of the four-week exhibition, Prof. Humprheys will talk about visual agnosia: a condition where patients can’t associate visual stimulus with meaning. It’s a rare condition, but it’s of interest to artists and scientists alike. Separating meaning and aesthetic is a trick used by artists to explore the two more thoughtfully; Humphreys’ patients still have little choice but to face the world that way.
Elsewhere, Prof. Spence will talk about subtle forms of synesthesia, called cross-modal correspondences, which affect us all. Synesthesia is that odd condition where stimulating one sense leads to automatic experiences in a second; cross-modal correspondences are more subtle, like the way red stars make many of us think of bitter flavours. Plenty of famous creatives have used the phenomenon to great effect — and during his talk, Spence will explain how it can help amplify our enjoyment of art.
There’s no denying that these are weighty subject indeed. But by understanding them just a little better we can achieve a better grasp on the neurological conditions that many suffer — and break down the stigma attached to them, too.
Affecting Perception runs from 4th-31st March 2013 at venues across Oxford. Admission is free. For more information, visit http://axnscollective.org.
Kinect + Brain Scan = Augmented Reality for Neurosurgeons
With a little duct tape, a touch screen tablet, and their new Kinect API, the Microsoft Research Cambridge team built an augmented reality system to help brain surgeons visualize 3D brain scans. Kinect Fusion supplies 3D modeling of anything, which could fuel some seriously neat medical innovations. (The Cambridge team also built KinEtre, which lets you posses anything.) At the 13th annual Microsoft TechFest, Ben Glocker demoed a prototype system that would allow neurosurgeons to prepare for surgery by looking inside a patient’s brain before they cut it open. Doctors could see the skeleton, brain, blood vessels, and the targeted tumor on a tablet—which they can move around the patient’s head—helping them to plot the best brain surgery path.
The Fusion API will be released in the next Kinect for Windows SDK, which researchers say will be out very soon.
Patient has 75 per cent of his skull replaced by 3D-printed implant
A man has had 75 per cent of his skull replaced with a custom-made 3D-printed implant.
The un-named patient in the United States had his head imaged by a 3D scanner before the plastic prosthetic was crafted to suit his features.
Oxford Performance Materials in Connecticut then gained approval from US regulators before the printed bone replacement was inserted in his skull during a surgical procedure earlier this week.
The ground-breaking operation has only now been revealed.
The company says it can now provide the 3D printouts to replace bone damaged by disease or trauma after the US Food and Drug Administration granted approval on February 18.
The implant is more than a simple moulded plastic plate: Tiny surface details are etched into the polyetherketoneketone to encourage the growth of cells and bone.
The company says about 500 people in the US could make use of the technology each month, with recipients ranging from injured construction workers through to wounded soldiers.
It says it can produce an implant within two weeks of obtaining 3D scans of the affected area.
Right-Handed Males, Left-Handed Females?
This is true for sugar gliders (Petaurus breviceps) and grey short-tailed opossums (Monodelphis domestica), say biologists from Saint Petersburg State University, Russia.
Their study, published in the open access journal BMC Evolutionary Biology, shows that handedness in marsupials is dependent on gender.
This preference of one hand over another has developed despite the absence of a corpus callosum, the part of the brain, which in placental mammals allows one half of the brain to communicate with the other.
Many animals show a distinct preference for using one hand (paw, hoof) over another. This is often related to posture – an animal is more likely to show manual laterality if it is upright, related to the difficulty of the task, more complex tasks show a handed preference, or even with age. As an example of all three: crawling human babies show less hand preference than toddlers.
Some species also show a distinct sex effect in handedness but among non-marsupial mammals this tendency is for left-handed males and right-handed females.
In contrast, the team from Russia shows that male quadruped marsupials, such as who walk on all fours, tend to be right-handed while the females are left-handed, especially as tasks became more difficult.
“Marsupials do not have a corpus callosum – which connects the two halves of the mammalian brain together. Reversed sex related handedness is an indication of how the marsupial brain has developed different ways of the two halves of the brain communicating in the absence of the corpus callosum,” explains senior author Dr Yegor Malashichev.
Researchers explain the goals and structure of a new brain-mapping project
A proposed effort to map brain activity on a large scale, expected to be announced by the White House later this month, could help neuroscientists understand the origins of cognition, perception, and other phenomena. These brain activities haven’t been well understood to date, in part because they arise from the interaction of large sets of neurons whose coördinated efforts scientists cannot currently track.
“There are all kinds of remarkable tools to study the microscopic world of individual cells,” says John Donoghue, a neuroscientist at Brown and a participant in the project. “And on the macroscopic end, we have tools like MRI and EEG that tell us about the function of the brain and its structure, but at a low resolution. There is a gap in the middle. We need to record many, many neurons exactly as they operate with temporal precision and in large areas,” he says.
An article published Thursday in Science online expands the project’s already ambitious goals beyond just recording the activity of all individual neurons in a brain circuit simultaneously. Researchers should also find ways to manipulate the neurons within those circuits and understand circuit function through new methods of data analysis and modeling, the authors write.
Understanding how neurons communicate with one another across large regions of the brain will be critical to understanding how the brain works, according to participants in the project. Other efforts to map out the physical connections in the brain are already under way (see “TR10: Connectomics” and “Mapping the Brain on a Massive Scale”), but these projects look at static brains or can only get a rough view of how regions of the brain communicate. The new project will probably start applying its novel and yet unknown technologies on simpler brains, such as those of flies, and will probably take decades to achieve its goals.
Numerous leaders from the fields of neuroscience, nanotechnology, and synthetic biology are expected to collaborate on the effort. “We need something large scale to try to build tools for the future,” says Rafael Yuste, a neurobiologist at Columbia University and a member of the project. “We view ourselves as tool builders. I think we could provide to the scientific community the methods that could be used for the next stage in neuroscience.”
In addition to deepening fundamental understanding of the brain, the project may also lead to new treatments for psychiatric and neurological disorders. “If we truly understand how things like thoughts, cognition, and other features of the brain emerge, then we should have a better understanding of mood disorders, Parkinson’s, epilepsy and other conditions that are thought to arise from brain-wide circuitry problems,” says Donoghue.
Details about which technology ideas will be given the green light and how much money will support their development are expected to be revealed in the White House announcement that is still to come. The project is likely to be supported by the National Institutes of Health, the National Science Foundation, the Defense Advanced Research Projects Agency, the Office of Science and Technology Policy, and private foundations, participants say. It’s not yet clear how much money will be needed or which technologies will be given priority.
Whichever particular technologies emerge, nanotechnology is likely to be involved, in part because of the need for smaller and faster sensors to record neuronal activity across the brain. Existing sensors can record the electrical activity of neurons, but these chips can typically monitor fewer than 100 neurons at a time and can’t record activity from neighboring neurons, which would be necessary to understand how neurons interact with one another. Paul Weiss, director of the California NanoSystems Institute at the University of California, Los Angeles, a participant in the project, says that nanofabrication techniques could address this problem, with smaller chips bearing smaller electrical and even chemical probes. “We’ve had over a decade a fairly substantial investment in science and technology to develop the capability … to control how what we make interacts with the chemical, physical, and biological worlds,” he says.
Novel optical techniques could also aid the mapping project. Currently, many research groups use calcium-sensitive fluorescent dyes to study neuron firing, but Yuste wants to develop an optical technique that uses voltage-sensitive fluorescent dyes for a faster readout. “Neurons communicate using voltage,” he says. “We would like to develop voltage imaging so we will be able to measure neuronal activity directly.”
While many things about the project are uncertain, one thing is clear—there is going to be a lot of data to store, share, and analyze. “We have just begun to scratch the surface of how you deal with data in high-dimensional spaces,” says Terry Sejnowski, a computational neuroscientist at the Salk Institute. “If you are talking about one million neurons, no one can even imagine what that looks like–it is way beyond what we can perceive in three dimensions.”
The Science article also sketches out a rough time line. Within five years, it should be possible to monitor tens of thousands of neurons; in 15 years, one million neurons should be possible. A fly’s brain has about 100,000 neurons, a mouse’s about 75 million, and a human’s about 85 billion. “With one million neurons, scientists will be able to evaluate the function of the entire brain of the zebrafish or several areas from the cerebral cortex of the mouse,” the authors write.
Chewing gum helps you concentrate for longer
Chewing gum can help you stay focused for longer on tasks that require continuous monitoring.
This is the finding of new research by Kate Morgan and colleagues from Cardiff University published in the British Journal of Psychology.
Previous research has shown that chewing gum can improve concentration in visual memory tasks. This study focussed on the potential benefits of chewing gum during an audio memory task.
Kate Morgan, author of the study explained: “It’s been well established by previous research that chewing gum can benefit some areas of cognition. In our study we focussed on an audio task that involved short-term memory recall to see if chewing gum would improve concentration; especially in the latter stages of the task.”
The study involved 38 participants being split in to two groups. Both groups completed a 30 minute audio task that involved listening to a list of numbers from 1-9 being read out in a random manner. Participants were scored on how accurately and quickly they were able to detect a sequence of odd-even-odd numbers, such as 7-2-1. Participants also completed questionnaires on their mood both before and after the task.
The results showed that participants who chewed gum had quicker reaction times and more accurate results than the participants who didn’t chew gum. This was especially the case towards the latter parts of the task.
Kate explained: “Interestingly participants who didn’t chew gum performed slightly better at the beginning of the task but were overtaken by the end. This suggests that chewing gum helps us focus on tasks that require continuous monitoring over a longer amount of time.”
The study was discussed in Radio Four Today programme.
(Image: iStock)
Scientists Identify Buphenyl as a Possible Drug for Alzheimer’s disease
Buphenyl, an FDA-approved medication for hyperammonemia, may protect memory and prevent the progression of Alzheimer’s disease. Hyperammonemia is a life-threatening condition that can affect patients at any age. It is caused by abnormal, high levels of ammonia in the blood.
Studies in mice with Alzheimer’s disease (AD) have shown that sodium phenylbutyrate, known as Buphenyl, successfully increases factors for neuronal growth and protects learning and memory, according to neurological researchers at the Rush University Medical Center.
Results from the National Institutes of Health funded study, recently were published in the Journal of Biological Chemistry.
“Understanding how the disease works is important to developing effective drugs that protect the brain and stop the progression of Alzheimer’s disease,” said Kalipada Pahan, PhD, the Floyd A. Davis professor of neurology at Rush and lead investigator of this study.
A family of proteins known as neurotrophic factors help in survival and function of neurons. Past research indicates that these proteins are drastically decreased in the brain of patients with Alzheimer’s disease (AD).
“Neurotrophic factor proteins could be increased in the brain by direct injection or gene delivery,” said Pahan. “However, using an oral medication to increase the level of these protein may be the best clinical option and a cost effective way to increase the level of these proteins directly in the brain.”
“Our study found that after oral feeding, Buphenyl enters into the brain, increases these beneficial proteins in the brain, protects neurons, and improves memory and learning in mice with AD-like pathology,” said Pahan.
In the brain of a patient with AD, two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. While neurons die, other brain cells like astroglia do not die.
The study findings indicate that Buphenyl increases neurotrophic factors from astroglia. Buphenyl stimulates memory-related protein CREB (cyclic AMP response element-binding protein) using another protein known as Protein Kinase C (PKC) and increases neurotrophic factors in the brain.
"Now we need to translate this finding to the clinic and test Buphenyl in Alzheimer’s disease patients,” said Pahan. “If these results are replicated in Alzheimer’s disease patients, it would open up a promising avenue of treatment of this devastating neurodegenerative disease.”
Low incidence of venous insufficiency in MS
Results of a study using several imaging methods showed that CCSVI (chronic cerebrospinal venous insufficiency) occurs at a low rate in both people with multiple sclerosis (MS) and non-MS volunteers, contrary to some previous studies. The research by an interdisciplinary team at The University of Texas Health Science Center at Houston (UTHealth) was published in a recent early online edition of the Annals of Neurology.
“Our results in this phase of the study suggest that findings in the major veins that drain the brain consistent with CCSVI are uncommon in individuals with MS and quite similar to those found in our non-MS volunteers,” said Jerry Wolinsky, M.D., principal investigator and the Bartels Family and Opal C. Rankin Professor of Neurology at The UTHealth Medical School. “This makes it very unlikely that CCSVI could be the cause of MS, or contribute in an important manner to how the disease can worsen over time.” Wolinsky is also a member of the faculty of The University of Texas Graduate School of Biomedical Sciences at Houston and director of the UTHealth MS Research Group.
CCSVI has been described by Italian neurosurgeon Paolo Zamboni, M.D., as a new disorder in which veins draining the central nervous system are abnormal. Zamboni’s published research linked CCSVI to MS. Not all researchers have been able to duplicate his results.
UTHealth was one of three institutions in the United States to receive an initial grant to study CCSVI in multiple sclerosis (MS). The grant was part of a $2.3 million joint commitment from the National MS Society and the MS Society of Canada.
The UTHealth team tested several imaging methods including ultrasound, magnetic resonance imaging with an intravenous contrast agent, and direct radiologic investigation of the major veins by direct injection of veins with radio-opaque contrast. The goal was to validate a consistent, reliable diagnostic approach for CCSVI, determine whether CCSVI was specific to MS and if CCSVI contributed to disease activity.
The team was blinded to the participant’s diagnosis throughout the study. Doppler ultrasound was used to investigate venous drainage in 276 people with and without MS. Using the criteria described by Zamboni for the diagnosis of CCVSI, UTHealth researchers found less prevalence of CCVSI than in some previous studies and no statistical difference between those with MS and those without MS. Detailed experience with the other imaging approaches are being readied for publication.
Multiple sclerosis is an unpredictable, often disabling disease of the central nervous system, interrupting the flow of information within the brain and from the brain to the body. It affects more than 400,000 people in the United States and 2.1 million in the world.