Posts tagged science
Articles and news from the latest research reports.
Breakthrough Offers First Direct Measurement of Spinal Cord Myelin in Multiple Sclerosis
Real-time Imaging Technique Provides Essential Molecular Picture of Protective Nerve Sheath
Researchers have made an exciting breakthrough – developing a first-of-its-kind imaging tool to examine myelin damage in multiple sclerosis (MS). An extremely difficult disease to diagnose, the tool will help physicians diagnose patients earlier, monitor the disease’s progression, and evaluate therapy efficacy.
Case Western Reserve University School of Medicine scientists have developed a novel molecular probe detectable by positron emission tomography (PET) imaging. The new molecular marker, MeDAS, offers the first non-invasive visualization of myelin integrity of the entire spinal cord at the same time, as published today in an article in the Annals of Neurology.
“While MS originates in the immune system, the damage occurs to the myelin structure of the central nervous system. Our discovery brings new hope to clinicians who may be able to make an accurate diagnosis and prognosis in as little as a few hours compared to months or even years,” said Yanming Wang, PhD, senior author of study and associate professor of radiology at Case Western Reserve University School of Medicine. “Because of its shape and size, it is particularly difficult to directly detect myelin damage in the spinal cord; this is the first time we have been able to image its function at the molecular level.”
As the most common acquired autoimmune disease currently affecting more than two million people worldwide, MS is characterized by destruction of myelin, the membrane that protects nerves. Once damaged, it inhibits the nerves’ ability to transmit electrical impulses, causing cognitive impairment and mobility dysfunction. So far, there is no cure for MS, therapies are only available that modify the symptoms.
In addition to its role in monitoring the effects of myelin-repair drugs currently under development, the new imaging tool offers a real-time quantitative clinical diagnosis of MS. A long lag exists between the onset of disease, physical symptoms in the patient and diagnosis via behavioral testing and magnetic resonance imaging (MRI). The lesions, or plaques, as detected by a MRI in the brain and spinal cord are not myelin specific and thus poorly associated with a patient’s disease severity or progression. There is an urgent need to find a new imaging marker that correlates with a patient’s pathology.
“This discovery has open the door to develop new drugs that can truly restore nerve function, not just modify the symptoms,” said Robert Miller, PhD, co-author on the study, vice president for research for Case Western Reserve and the Allen C. Holmes Professor of Neurological Diseases at the School of Medicine. “A cure for MS requires both repairing myelin and a tool to measure the mechanism.”
For the past 20 years, Miller’s lab has been working tirelessly to create new myelin-repair therapies that would restore nerve function. Successful translation of new drugs from animal studies to human clinical trials is contingent upon researchers’ ability to measure and evaluate the effectiveness of a therapy.
Created by Wang’s laboratory, the MeDAS molecular probe works like a homing device. Injected into the body intravenously, it is programmed to seek out and bind only to myelin in the central nervous system, i.e., the brain, spinal cord and optic nerves. A positron-emitting radioisotope label on the molecule allows a PET scanner to detect the targets and quantify their intensity and location. The data can then be reconstructed into an image as shown in the article: http://onlinelibrary.wiley.com/doi/10.1002/ana.23965/abstract.
“This is an indispensable tool to help find a new way to treat MS down the road” said Chunying Wu, PhD, first author of the study and instructor of radiology at Case Western Reserve. “It can also be used as a platform technology to unlock the mysteries of other myelin related diseases such as spinal cord injury.”
(Source: casemed.case.edu)
Why don’t apes have musical talent, while humans, parrots, small birds, elephants, whales, and bats do? Matz Larsson, senior physician at the Lung Clinic at Örebro University Hospital, attempts to answer this question in the scientific publication Animal Cognition.
In his article, he asserts that the ability to mimic and imitate things like music and speech is the result of the fact that synchronised group movement quite simply makes it possible to perceive sounds from the surroundings better.
The hypothesis is that the evolution of vocal learning, that is musical traits, is influenced by the need of a species to deal with the disturbing sounds that are created in connection with locomotion. These sounds can affect our hearing only when we move.
“When several people with legs of roughly the same length move together, we tend to unconsciously move in rhythm. When our footsteps occur simultaneously, a brief interval of silence occurs. In the middle of each stride we can hear our surroundings better. It becomes easier to hear a pursuer, and perhaps easier to conduct a conversation as well,” explains Larsson.
A behaviour that has survival value tends to produce dopamine, the “reward molecule”. In dangerous terrain, this could result in the stimulation of rhythmic movements and enhanced listening to surrounding sounds in nature. If that kind of synchronized behaviour was rewarding in dangerous environments it may as well have been rewarding for the brain in relative safety, resulting in activities such as hand- clapping, foot-stamping and yelping around the campfire. From there it is just a short step to dance and rhythm. The hormone dopamine flows when we listen to music.
Brain may rely on computer-like mechanism to make sense of novel situations
Our brains give us the remarkable ability to make sense of situations we’ve never encountered before—a familiar person in an unfamiliar place, for example, or a coworker in a different job role—but the mechanism our brains use to accomplish this has been a longstanding mystery of neuroscience.
Now, researchers at the University of Colorado Boulder have demonstrated that our brains could process these new situations by relying on a method similar to the “pointer” system used by computers. “Pointers” are used to tell a computer where to look for information stored elsewhere in the system to replace a variable.
For the study, published today in the Proceedings of the National Academy of Sciences, the research team relied on sentences with words used in unique ways to test the brain’s ability to understand the role familiar words play in a sentence even when those words are used in unfamiliar, and even nonsensical, ways.
For example, in the sentence, “I want to desk you,” we understand the word “desk” is being used as a verb even though our past experience with the word “desk” is as a noun.
“The fact that you understand that the sentence is grammatically well formed means you can process these completely novel inputs,” said Randall O’Reilly, a professor in CU-Boulder’s Department of Psychology and Neuroscience and co-author of the study. “But in the past when we’ve tried to get computer models of a brain to do that, we haven’t been successful.”
This shows that human brains are able to understand the sentence as a structure with variables—a subject, a verb and often, an object—and that the brain can assign a wide variety of words to those variables and still understand the sentence structure. But the way the brain does this has not been understood.
Computers routinely complete similar tasks. In computer science, for example, a computer program could create an email form letter that has a pointer in the greeting line. The pointer would then draw the name information for each individual recipient into the greeting being sent to that person.
In the new study, led by Trenton Kriete, a postdoctoral researcher in O’Reilly’s lab, the scientists show that the connections in the brain between the prefrontal cortex and the basal ganglia could play a similar role to the pointers used in computer science. The researchers added new information about how the connections between those two regions of the brain could work into their model.
The result was that the model could be trained to understand simple sentences using a select group of words. After the training period, the researchers fed the model new sentences using familiar words in novel ways and found that the model could still comprehend the sentence structure.
While the results show that a pointer-like system could be at play in the brain, the function is not identical to the system used in computer science, the scientists said. It’s similar to comparing an airplane’s wing and a bird’s wing, O’Reilly said. They’re both used for flying but they work differently.
In the brain, for example, the pointer-like system must still be learned. The brain has to be trained, in this case, to understand sentences while a computer can be programmed to understand sentences immediately.
“As your brain learns, it gets better and better at processing these novel kinds of information,” O’Reilly said.
(Source: colorado.edu)
Researchers erase human brain tumor cells in mice
Working with mice, Johns Hopkins researchers have discovered that weeks of treatment with a repurposed FDA-approved drug halted the growth of — and ultimately left no detectable trace of — brain tumor cells taken from adult human patients.
The scientists targeted a mutation in the IDH1 gene first identified in human brain tumors called gliomas by a team of Johns Hopkins cancer researchers in 2008. This mutation was found in 70 to 80 percent of lower-grade and progressive forms of the brain cancer. The change occurs within a single spot along a string of thousands of genetic coding letters, and is disruptive enough to keep the seemingly innocuous protein from playing its role in converting glucose into energy. Instead, the mutation hijacks the protein to make a new molecule not normally found in the cell, which is apparently a linchpin in the process of forming and maintaining cancer cells.
Encouraged by the new findings, described online Sept. 16 in the open-access journal Oncotarget, the Johns Hopkins researchers say they want to work quickly to design a clinical trial to bring what they learned in mice to humans with gliomas. Despite the growing understanding of IDH1 mutant gliomas, the development of effective therapies has proven challenging, they say.
"Usually in the lab, we’re happy to see a drug slow down tumor growth," says Alexandra Borodovsky, a graduate student in the Cellular and Molecular Medicine Program at the Johns Hopkins University School of Medicine who performed the experiments. "We never expect tumors to regress, but that is exactly what happened here."
"This therapy has worked amazingly well in these mice," says study leader Gregory J. Riggins, M.D., Ph.D., a professor of neurosurgery and oncology at the Johns Hopkins University School of Medicine. "We have spoken with neurosurgeons here, and as soon as possible, we want to start discussing the parameters of a clinical trial to see if this will work in our patients as a follow-up to surgery."
The researchers caution that many treatments have cured cancers in mice, and then failed in humans.
The IDH1 gene, whose name stands for isocitrate dehydrogenase 1, produces an enzyme that regulates cell metabolism. Mutations, or changes in the DNA code, force the IDH1 gene to increase production of a flawed version of the enzyme. The flawed enzyme produces large amounts of an entirely new molecule, called 2-hydroxyglutarate. This molecule is believed to cause groups of atoms called methyl groups to latch onto the DNA strand.
Although methylation is a normal cellular process, when too many methyl groups glom onto the DNA, Riggins says, this can interfere with normal cell biology and eventually contribute to cancer formation and growth.
Borodovsky, Riggins and their colleagues — including Timothy A. Chan, M.D., Ph.D., of Memorial Sloan-Kettering Cancer Center in New York — thought that a drug that could strip those methyl groups might be able to reverse the cancer process in those cancers with IDH1 mutations. They chose 5-azacytidine, which is approved to treat a pre-leukemia condition called myelodysplastic syndrome and is being tested on lung and other cancers at Johns Hopkins and elsewhere.
Riggins notes that one of the difficulties in developing treatments for IDH1 mutant brain cancers is finding a model in which to study them. Cell lines containing the IDH1 mutation are difficult to grow in the laboratory, for example. Borodovsky worked with Johns Hopkins neurosurgeons to obtain tumor cells from glioma patients likely to have IDH1 mutations and injected them under the skins of mice. She did this for months, before finally getting the tumor cells to grow.
Once the tumors grew, the researchers injected the mice with 5-azacytidine for 14 weeks and saw a dramatic reduction in growth and what appeared to be complete regression. Then they withdrew therapy. Seven weeks later, the tumors had not regrown. The researchers, however, said they do expect the tumors to regrow at some point, and are still monitoring the mice.
The type of tumor targeted by the researchers eventually progresses to a subtype of glioblastoma multiform — the deadliest form of brain cancer — known as progressive or secondary glioblastoma. They arise as a lower-grade glioma and are initially treated with surgery alone, but eventually they progress to the more lethal form of tumor. Survival is longer than with glioblastoma, but it is found in younger patients, those under the age of 50. While both types of tumor look the same at the end, they look very different at the molecular level, Riggins says, leading researchers to believe they may have a better chance at targeting the progressive tumors, which are more likely to have the IDH1 mutation.
Chan’s team at Sloan-Kettering simultaneously published a paper in Oncotarget, along with Borodovsky and Riggins, which describes similar results in a different animal model using a similar drug. This is further evidence that the strategy is a sound one, Riggins says.
(Source: eurekalert.org)
Addiction: Can You Ever Really Completely Leave It Behind?
A new study in Biological Psychiatry suggests the answer is no
It is often said that once people develop an addiction, they can never completely eliminate their attraction to the abused substance. New findings provide further support for this notion by suggesting that even long-term abstinence from cocaine does not result in a complete normalization of brain circuitry.
Scientists are currently trying to answer some of the ‘chicken and egg’ questions surrounding the abuse of drugs. In particular, one of those questions is whether individuals who abuse psychostimulants like cocaine are more impulsive and show alterations in brain reward circuits as a consequence of using the drug, or whether such abnormalities existed prior to their drug use. In the former case, one might expect brain alterations to normalize following prolonged drug abstinence.
To address these questions, Krishna Patel at Institute of Living/Hartford Hospital and colleagues compared neural responses between three groups of people who were asked to complete a task that resembles bidding on eBay items. The 3 groups consisted of 47 healthy controls, 42 currently drug-abusing cocaine users, and 35 former cocaine users who had been abstinent an average of 4 years. They also compared all three groups on their levels of impulsivity and reward responding.
They found that active users showed abnormal activation in multiple brain regions involved with reward processing, and that the abstinent individuals who were previously cocaine dependent manifested differences in a subset of those regions. Both current and former cocaine users displayed similarly elevated impulsivity measures compared to healthy controls, which may indicate that these individuals had a pre-existing risk for addiction. Indeed, the degree of impulsivity correlated with several of the brain activation abnormalities.
These findings suggest that prolonged abstinence from cocaine may normalize only a subset of the brain abnormalities associated with active drug use.
"The knowledge that some neural changes associated with addiction persist despite long periods of abstinence is important because it supports clinical wisdom that recovery from addiction is a lifelong process," says Dr. John Krystal, Editor of Biological Psychiatry. "Further, it is the start of a deeper question: How do these persisting changes develop and how can they be reversed?"
The authors agree that further studies will be needed to investigate such questions, including the continued attempt to determine the extent to which differences in former cocaine users reflect aspects of pre-existing features, exposure to cocaine, or recovery.
(Image: Shutterstock)
Caffeine consumption slows down brain development
Humans and other mammals show particularly intensive sleeping patterns during puberty. The brain also matures fastest in this period. But when pubescent rats are administered caffeine, the maturing processes in their brains are delayed. This is the result of a study supported by the Swiss National Science Foundation (SNSF).
Children’s and young adults’ average caffeine consumption has increased by more than 70 per cent over the past 30 years, and an end to this rise is not in sight: the drinks industry is posting its fastest-growing sales in the segment of caffeine-laden energy drinks. Not everybody is pleased about this development. Some people are worried about possible health risks caused in young consumers by the pick-me-up.
Researchers led by Reto Huber of the University Children’s Hospital Zurich are now adding new arguments to the debate. In their recently published study conducted on rats, the conclusions call for caution: in pubescent rodents, caffeine intake equating to three to four cups of coffee per day in humans results in reduced deep sleep and a delayed brain development.
Peak level during puberty
Both in humans and in rats, the duration and intensity of deep sleep as well as the number of synapses or connections in the brain increase during childhood, reaching their highest level during puberty and dropping again in adult age. “The brain of children is extremely plastic due to the many connections,” says Huber. When the brain then begins to mature during puberty, a large number of these connections are lost. “This optimisation presumably occurs during deep sleep. Key synapses extend, others are reduced; this makes the network more efficient and the brain more powerful,” says Huber.
Timid instead of curious
Huber’s group of researchers administered moderate quantities of caffeine to 30-day-old rats over five days and measured the electrical current generated by their brains. The deep sleep periods, which are characterised by slow waves, were reduced from day 31 until day 42, i.e. well beyond the end of administering caffeine. Compared to the rats being given pure drinking water, the researchers found far more neural connections in the brains of the caffeine-drinking animals at the end of the study. The slower maturing process in the brain also had an impact on behaviour: rats normally become more curious with age, but the rats consuming caffeine remained timid and cautious.
The brain goes through a delicate maturing phase in puberty, during which many mental diseases can break out. And even if the rat brain differs clearly from that of humans, the many parallels in how the brains develop raise the question as to whether children’s and young adults’ caffeine intake really is harmless or whether it might be wiser to abstain from consuming the pick-me-up. “There is still need for research in this area,” says Huber.
(Source: snf.ch)
Propofol Discovery May Aid Development of New Anesthetics
Researchers at Washington University School of Medicine in St. Louis and Imperial College London have identified the site where the widely used anesthetic drug propofol binds to receptors in the brain to sedate patients during surgery.
Until now, it hasn’t been clear how propofol connects with brain cells to induce anesthesia. The researchers believe the findings, reported online in the journal Nature Chemical Biology, eventually will lead to the development of more effective anesthetics with fewer side effects.
“For many years, the mechanisms by which anesthetics act have remained elusive,” explained co-principal investigator Alex S. Evers, MD, the Henry E. Mallinckrodt Professor and head of the Department of Anesthesiology at Washington University. “We knew that intravenous anesthetics, like propofol, act on an important receptor on brain cells called the GABA-A receptor, but we didn’t really know exactly where they bound to that receptor.”
Propofol is a short-acting anesthetic often used in patients having surgery. It wears off quickly and is less likely to cause nausea than many other anesthetics. But the drug isn’t risk-free. Its potentially dangerous side effects include lowering blood pressure and interfering with breathing.
In an attempt to understand how propofol induces anesthesia during surgery, scientists have tried to identify its binding site within the gamma-aminobutyric acid type A (GABA-A) receptor on brain cells. Activating these receptors — with propofol, for example — depresses a cell’s activity.
Researchers have altered the amino acids that make up the GABA-A receptor in attempts to find propofol’s binding site, but Evers said those methods couldn’t identify the precise site with certainty.
“In previous work to directly identify anesthetic binding sites, GABA-A receptors had to be extracted from membranes and purified prior to performing the binding studies,” he said. “Our method allowed us to study propofol binding to the intact receptor in its native membrane environment.”
Having developed the techniques to analyze the interactions between anesthetics and GABA-A receptors in their native environment, Evers’ laboratory teamed up with a group at Imperial College that had been taking the same approach. Led by Nicholas P. Franks, PhD, professor of biophysics and anaesthetics, the group has spent years creating a photoanalogue of propofol that both behaves in precisely the same way as propofol and contains a labeling group that permanently attaches to its binding site on the GABA-A receptor when exposed to a specific wavelength of light.
In creating the analogue of propofol, it’s as if the researchers put a tiny hook onto the molecule so that when it binds to the GABA-A receptor, it grabs onto the receptor and won’t let go.
“Normally, an anesthetic drug binds to the GABA-A receptor transiently,” Franks explained. “But for the purposes of this research, we wanted to create an analogue that behaved exactly like propofol except that we could activate this chemical hook to permanently bind the drug to the receptor. The next step was then to extract the receptor, cut it into pieces and identify the precise piece of the protein where the propofol analogue had attached to the receptor. This was the tricky step that the Evers group at Washington University had perfected.”
Evers and Franks believe this technique has implications beyond propofol and other anesthetics.
“Anesthetics have desirable effects — they induce anesthesia, for example — but they also have undesirable effects,” Evers said. “Propofol can lower blood pressure or interfere with breathing, for example. By understanding precisely what the binding sites look like on the proteins that induce those potential problems, we eventually hope to design and select for drugs that have the benefits we want without dangerous side effects.”
Using the techniques they have developed, Evers and Franks now plan to identify binding sites of other anesthetic agents. They believe their approach also can be used to study other types of drugs, such as psychiatric agents and anti-seizure drugs.
First evidence that fear memories can be reduced during sleep
A fear memory was reduced in people by exposing them to the memory over and over again while they slept. It’s the first time that emotional memory has been manipulated in humans during sleep, report Northwestern Medicine® scientists.
The finding potentially offers a new way to enhance the typical daytime treatment of phobias through exposure therapy by adding a nighttime component. Exposure therapy is a common treatment for phobia and involves a gradual exposure to the feared object or situation until the fear is extinguished.
"It’s a novel finding," said Katherina Hauner, a postdoctoral fellow in neurology at Northwestern University Feinberg School of Medicine. "We showed a small but significant decrease in fear. If it can be extended to pre-existing fear, the bigger picture is that, perhaps, the treatment of phobias can be enhanced during sleep."
Hauner did the research in the lab of Jay Gottfried, associate professor of neurology at Feinberg and senior author of the paper.
The study will be published Sept. 22 in the journal Nature Neuroscience.
Previous projects have shown that spatial learning and motor sequence learning can be enhanced during sleep. It wasn’t previously known that emotions could be manipulated during sleep, Northwestern investigators said.
In the study, 15 healthy human subjects received mild electric shocks while seeing two different faces. They also smelled a specific odorant while viewing each face and being shocked, so the face and the odorant both were associated with fear. Subjects received different odorants to smell with each face such as woody, clove, new sneaker, lemon or mint.
Then, when a subject was asleep, one of the two odorants was re-presented, but in the absence of the associated faces and shocks. This occurred during slow wave sleep when memory consolidation is thought to occur. Sleep is very important for strengthening new memories, noted Hauner, also a research scientist at the Rehabilitation Institute of Chicago.
"While this particular odorant was being presented during sleep, it was reactivating the memory of that face over and over again which is similar to the process of fear extinction during exposure therapy," Hauner said.
When the subjects woke up, they were exposed to both faces. When they saw the face linked to the smell they had been exposed to during sleep, their fear reactions were lower than their fear reactions to the other face.
Fear was measured in two ways: through small amounts of sweat in the skin, similar to a lie detector test, and through neuroimaging with fMRI (functional magnetic resonance imaging). The fMRI results showed changes in regions associated with memory, such as the hippocampus, and changes in patterns of brain activity in regions associated with emotion, such as the amygdala. These brain changes reflected a decrease in reactivity that was specific to the targeted face image associated with the odorant presented during sleep.
![Is this my finger? Sensory illusion study provides new insight for body representation brain disorders
People can be easily tricked into believing an artificial finger is their own, shows a study published today [23 September] in The Journal of Physiology. The results reveal that the brain does not require multiple signals to build a picture body ownership, as this is the first time the illusion has been created using sensory inputs from the muscle alone.
The discovery provides new insight into clinical conditions where body representation in the brain is disrupted due to changes in the central or peripheral nervous systems e.g. stroke, schizophrenia and phantom limb syndrome following amputation.
Professor Simon Gandevia, Deputy Director of Neuroscience Research Australia (NeuRA), says:
“It may seem silly to ask yourself whether your index finger is part of your body. However, our current findings demonstrate that this question has led to important insights into key brain functions.
“These findings could lead to new clinical interventions where the addition or the removal of specific sensory stimuli is used to change someone’s body image.”
In the experiment, subjects held an artificial finger with their left hand that was located 12 cm above their right index finger. Vision was eliminated and anaesthesia was used to numb the skin and remove feelings of joint movement. When the artificial finger and the right index finger were moved synchronously, subjects reported they were holding their own index finger: the brain incorrectly incorporated the artificial finger into its internal body representation.
The human brain uses sensory signals to maintain and update internal representation of the body, to plan and generate movements and interact with the world. The study gives new understanding as to how the brain decides what is part of our own body and where it is located. Contrary to previous theories which used multiple sensory inputs including touch and vision, these results demonstrate that messages coming from muscle receptors are enough to change the internal body representation.
The team additionally found a new type of sensory ‘grasp illusion’ in which perceived distances between index fingers decreases when subjects hold an artificial finger. This implies that the brain generates possible scenarios and tests them against available sensory information.
Professor Gandevia says:
“Grasping the artificial finger induces a sensation in some subjects that their hands are level with one another, despite being 12 cm apart. This illusion demonstrates that our brain is a thoughtful (yet at times gullible!) decision maker: it uses available sensory information and memories of past experiences to decide what scenario is most likely (i.e. ‘my hands are level’).”](http://40.media.tumblr.com/1fff97edccc65cb160d971ab6a2bde30/tumblr_mtkv0pPXPU1rog5d1o1_500.jpg)
People can be easily tricked into believing an artificial finger is their own, shows a study published today [23 September] in The Journal of Physiology. The results reveal that the brain does not require multiple signals to build a picture body ownership, as this is the first time the illusion has been created using sensory inputs from the muscle alone.
The discovery provides new insight into clinical conditions where body representation in the brain is disrupted due to changes in the central or peripheral nervous systems e.g. stroke, schizophrenia and phantom limb syndrome following amputation.
Professor Simon Gandevia, Deputy Director of Neuroscience Research Australia (NeuRA), says:
“It may seem silly to ask yourself whether your index finger is part of your body. However, our current findings demonstrate that this question has led to important insights into key brain functions.
“These findings could lead to new clinical interventions where the addition or the removal of specific sensory stimuli is used to change someone’s body image.”
In the experiment, subjects held an artificial finger with their left hand that was located 12 cm above their right index finger. Vision was eliminated and anaesthesia was used to numb the skin and remove feelings of joint movement. When the artificial finger and the right index finger were moved synchronously, subjects reported they were holding their own index finger: the brain incorrectly incorporated the artificial finger into its internal body representation.
The human brain uses sensory signals to maintain and update internal representation of the body, to plan and generate movements and interact with the world. The study gives new understanding as to how the brain decides what is part of our own body and where it is located. Contrary to previous theories which used multiple sensory inputs including touch and vision, these results demonstrate that messages coming from muscle receptors are enough to change the internal body representation.
The team additionally found a new type of sensory ‘grasp illusion’ in which perceived distances between index fingers decreases when subjects hold an artificial finger. This implies that the brain generates possible scenarios and tests them against available sensory information.
Professor Gandevia says:
“Grasping the artificial finger induces a sensation in some subjects that their hands are level with one another, despite being 12 cm apart. This illusion demonstrates that our brain is a thoughtful (yet at times gullible!) decision maker: it uses available sensory information and memories of past experiences to decide what scenario is most likely (i.e. ‘my hands are level’).”
Virginia Tech to Host Neuroscience Workshop in Switzerland
Neuroscientists will discuss cognition, computation, decisions
Nearly two dozen of the world’s leading neuroscientists will gather in Switzerland next month to share their latest findings on the mysteries of how the brain processes information and makes decisions.
The Virginia Tech Carilion Research Institute European–U.S. Workshop on the Neuroscience of Cognition, Computation, and Decisions will be held at Virginia Tech’s Center for European Studies and Architecture at Riva San Vitale in Ticino on Oct. 16 to Oct. 18.
“We have two principal goals for this intensive workshop,” said Michael Friedlander, associate provost for health sciences at Virginia Tech and executive director of the Virginia Tech Carilion Research Institute. “First, we want to identify new and powerful integrated approaches to bridge multiple levels of understanding brain function. We are also hoping to lay the foundations for pioneering innovative and disruptive approaches to transcending disciplines and technologies across teams of leading European brain researchers and Virginia Tech Carilion Research Institute neuroscientists.”
The workshop will convene 10 neuroscientists from the institute and 13 neuroscientists from prominent brain-research institutions in five European countries, includinbg the Centre National de la Recherche Scientifique and École Polytechnique in France; the Central Institute of Mental Health Mannheim, Freie Universität Berlin, the Max Planck Institute for Biological Cybernetics, the Max Planck Institute for Human Development, and the University of Heidelberg in Germany; the International School for Advanced Studies in Trieste, Italy; École Polytechnique Fédérale de Lausanne, ETH Zürich, and the University of Zurich in Switzerland; and University College London in the United Kingdom.
Workshop participants will address emerging views of how neuronal and synaptic networks in the brain assemble, process, store, and access information and how large-scale networks of interconnected neurons perform in humans and other mammals. The participants will also consider the functional architecture that underlies the brain’s decision-making capacity, the neural basis of social interactions, the effects of the environment on information processing, and the consequences of a range of disorders on the function of the human brain.
Participants will share their newest discoveries in multiple sessions of several speakers each, followed by in-depth discussions to identify congruent perspectives and converging insights from multiple disciplines.
The discoveries will represent a broad array of technological and conceptual approaches, including analysis of detailed structural and functional properties of individual neurons and synaptic networks obtained with powerful electrophysiological, genetic, and optical imaging methods; functional brain imaging and behavioral studies in individuals and groups of interacting humans; and computational analysis and modeling of brain function and behavior.
Additional experts will address economics and game theory applications to human brain function and behavior in health and in disease; analysis of development, aging, and educational interventions on brain function; and the modulation of brain function acutely and over time in health and in various disorders that affect behavior, neural information processing, and decision-making.
“This workshop is taking place at a confluence of important national and international milestones in brain research in both Europe and the United States,” Friedlander said. “The Blue Brain Project in Europe represents a major international coalition to support large-scale, detailed analysis of the circuitry of the brain, while in the United States, President Barack Obama’s BRAIN Initiative will support innovative new approaches to high-resolution, large-scale functional mapping of the brain. We’re hoping to harness the wisdom of experts on both continents to develop new approaches and better technologies for diagnosing and treating neurological and psychiatric disorders that affect people worldwide.”