Posts tagged science

June 24, 2012 by SETH BORENSTEIN

(AP) — The more we study animals, the less special we seem.

In this Dec. 13, 2006 photo provided by the Primate Research Institute of Kyoto University, a 5 1/2-year-old chimpanzee named Ayumu performs a memory test with randomly-placed consecutive Arabic numerals, which are later masked, accurately duplicating the lineup on a touch screen computer in Kyoto, Japan. The young chimpanzees in the study titled “Working memory of numerals in chimpanzees” by Sana Inoue and Tetsuro Matsuzawa could memorize the nine numerals much faster and more accurately than human adults. The evidence that animals are more intelligent and more social than we thought seems to grow each year, especially when it comes to primates. It’s an increasingly hot scientific field with the number of ape and monkey cognition studies doubling in recent years, often with better technology and neuroscience paving the way to unusual discoveries. (AP Photo/Primate Research Institute of Kyoto University) PART OF A SEVEN-PICTURE PACKAGE WITH “ANIMAL SCIENCES”

Baboons can distinguish between written words and gibberish. Monkeys seem to be able to do multiplication. Apes can delay instant gratification longer than a human child can. They plan ahead. They make war and peace. They show empathy. They share.

"It’s not a question of whether they think — it’s how they think," says Duke University scientist Brian Hare. Now scientists wonder if apes are capable of thinking about what other apes are thinking.

The evidence that animals are more intelligent and more social than we thought seems to grow each year, especially when it comes to primates. It’s an increasingly hot scientific field with the number of ape and monkey cognition studies doubling in recent years, often with better technology and neuroscience paving the way to unusual discoveries.

Read more …

ScienceDaily (June 24, 2012) — The blood-brain barrier — the filter that governs what can and cannot come into contact with the mammalian brain — is a marvel of nature. It effectively separates circulating blood from the fluid that bathes the brain, and it keeps out bacteria, viruses and other agents that could damage it.

But the barrier can be disrupted by disease, stroke and multiple sclerosis, for example, and also is a big challenge for medicine, as it can be difficult or impossible to get therapeutic molecules through the barrier to treat neurological disorders.

Now, however, the blood-brain barrier may be poised to give up some of its secrets as researchers at the University of Wisconsin-Madison have created in the laboratory dish the cells that make up the brain’s protective barrier. Writing in the June 24, 2012 edition of the journal Nature Biotechnology, the Wisconsin researchers describe transforming stem cells into endothelial cells with blood-brain barrier qualities.

Access to the specialized cells “has the potential to streamline drug discovery for neurological disease,” says Eric Shusta, a UW-Madison professor of chemical and biological engineering and one of the senior authors of the new study. “You can look at tens of thousands of drug candidates and just ask the question if they have a chance to get into the brain. There is broad interest from the pharmaceutical industry.”

The blood-brain barrier depends on the unique qualities of endothelial cells, the cells that make up the lining of blood vessels. In many parts of the body, the endothelial cells that line capillaries are spaced so that substances can pass through. But in the capillaries that lead to the brain, the endothelial cells nestle in tight formation, creating a semi-permeable barrier that allows some substances — essential nutrients and metabolites — access to the brain while keeping others — pathogens and harmful chemicals — locked out.

The cells described in the new Wisconsin study, which was led by Ethan S. Lippmann, now a postdoctoral fellow at the Wisconsin Institute for Discovery, and Samira M. Azarin, now a postdoctoral fellow at Northwestern University, exhibit both the active and passive regulatory qualities of those cells that make up the capillaries of the intact brain.

The research team coaxed both embryonic and induced pluripotent stem cells to form the endothelial cells of the blood-brain barrier. The use of induced cells, which can come from patients with specific neurological conditions, may be especially important for modeling disorders that compromise the blood-brain barrier. What’s more, because the cells can be mass produced, they could be used to devise high-throughput screens for molecules that may have therapeutic value for neurological conditions or to identify existing drugs that may have neurotoxic qualities.

"The nice thing about deriving endothelial cells from induced pluripotent stem cells is that you can make disease-specific models of brain tissue that incorporate the blood-brain barrier," explains Sean Palecek, a UW-Madison professor of chemical and biological engineering and a senior author of the new report. "The cells you create will carry the genetic information of the condition you want to study."

The generation of the specialized blood-brain barrier endothelial cells, the Wisconsin researchers note, has never been done with stem cells. In addition to the potential applications to screen drugs and model pathologies of the blood-brain barrier, they may also provide a novel window for developmental biologists who are interested in how the barrier comes together and co-develops with the brain.

"Neurons develop at the same time as the endothelial cells," Shusta says, noting that, in development, the cells secrete chemical cues that help determine organ specificity.

"We don’t know what all those factors are," Lippmann says. "But with this model, we can go back and look." Identifying all of the molecular factors at play as blank slate stem cells differentiate to become specialized endothelial cells could one day have clinical significance to treat stroke or tamp down the ability of brain tumors to recruit blood vessels needed to sustain cancer.

Source: Science Daily

ScienceDaily (June 24, 2012) — Every day the human brain is presented with tasks ranging from the trivial to the complex. How much mental effort and attention are devoted to each task is usually determined in a split second and without conscious awareness. Now a study from Massachusetts General Hospital (MGH) researchers finds that a structure deep within the brain, believed to play an important role in regulating conscious control of goal-directed behavior, helps to optimize behavioral responses by predicting how difficult upcoming tasks will be. The report is receiving advance online publication in Nature.

"The dorsal anterior cingulate cortex (dACC), which lies deep beneath the outer layer of the frontal lobes, is part of an ancient and enigmatic part of the brain," says Emad Eskandar, MD, of the MGH Department of Neurosurgery, senior author of the Nature paper. “Some have speculated that it plays a role in detecting errors or monitoring for conflicting demands, but exactly how it contributes to regulating behavioral responses is unclear, so we used a variety of scientific techniques to get a better picture of its function.”

The study enrolled six participants who were scheduled to undergo cingulotomy — a procedure in which a small, precisely placed lesion is created within the ACC — to treat severe obsessive compulsive disorder (OCD) that has not responded to other types of treatment. A standard part of the cingulotomy procedure involves microelectrode recordings of the activity of single neurons in the area where the lesion is to be placed. To evaluate dACC function, the investigators recorded brain activity from several neurons within the structure while participants performed a behavioral task testing their reactions to visual images.

The task presented participants with a random series of images of three numerals, which could be 0, 1, 2, or 3. In each image, two of the numerals were identical. Participants responded by pressing one of three buttons, the position of which would indicate the identity of the number that was different, with the left button indicating 1, the middle 2 and the right button 3. Each image was ranked in difficulty depending on how much the position of the target numeral or the identity of the duplicate numerals might distract participants from the correct response. For example, when presented with 3-3-2, the correct response would be to press the middle button for number 2; and that image would be ranked more difficult than 3-2-3, in which both the target number and the correct button were in the same position.

Functional magnetic resonance imaging (fMRI) of four participants performing the behavioral task prior to the cingulotomy procedure revealed that the task increased metabolic activity within the dACC, a result seen in previous fMRI studies. The fMRI images also revealed that responding to more difficult images produced greater activity levels within the dACC and in other structures known to be involved in decision making. Intraoperative microelectrode recordings of all participants demonstrated that this apparent increase in metabolic activity corresponded with an increase in neuronal activity, linking for the first time the increased activation revealed by fMRI with increased neuronal firing.

Analysis of individual neuron activity indicated that dACC neuronal activity remained elevated immediately after difficult trials. Moreover, participant reaction time revealed that the difficulty of the prior trial had an impact on the next trial: if the preceding trial was of the same level of difficulty, reaction time was shorter; if the two tests were of different difficulty levels — even if the second test was easier — reaction time was longer. By anticipating the difficulty of upcoming tasks, the authors note, it appears that the dACC speeds up responses when difficulty levels are constant but slows response time down when faced with changing demands in order to promote accuracy.

While behavioral tests conducted after the cingulotomy procedure — which destroys tissue within the dACC — did not indicate a change in participants’ ability to perform the test accurately, the impact of preceding trials on reaction time appeared to vanish. “Participants could still perform the task, but the dACC’s role of priming the system based on immediate prior experience was gone,” Eskandar explains. “We believe this result indicates an important role for the dACC in rapidly adjusting to different cognitive demands, possibly by recruiting other areas of the brain to solve particular problems.”

An associate professor of Surgery at Harvard Medical School, Eskandar adds that, while significant cognitive changes have not been reported in patients undergoing cingulotomy, the apparent role of the dACC in adapting to changing situations implies a possible role for the structure in several psychiataric disorders. “A lack of behavior flexibility and adjustment is characteristic of OCD, for example. Whether or not our findings directly relate to these disorders remains to be determined, but we hope that continued study using complex tasks, such as the behavioral test used here, will be helpful in diagnosing or monitoring psychiatric disorders.”

Source: Science Daily

ScienceDaily (June 24, 2012) — Hemimegalencephaly is a rare but dramatic condition in which the brain grows asymmetrically, with one hemisphere becoming massively enlarged. Though frequently diagnosed in children with severe epilepsy, the cause of hemimegalencephaly is unknown and current treatment is radical: surgical removal of some or all of the diseased half of the brain.

This image depicts hemimegalencephaly. (Credit: UC San Diego School of Medicine)

In a paper published in the June 24, 2012 online issue of Nature Genetics, a team of doctors and scientists, led by researchers at the University of California, San Diego School of Medicine and the Howard Hughes Medical Institute, say de novo somatic mutations in a trio of genes that help regulate cell size and proliferation are likely culprits for causing hemimegalencephaly, though perhaps not the only ones.

De novo somatic mutations are genetic changes in non-sex cells that are neither possessed nor transmitted by either parent. The scientists’ findings — a collaboration between Joseph G. Gleeson, MD, professor of neurosciences and pediatrics at UC San Diego School of Medicine and Rady Children’s Hospital-San Diego; Gary W. Mathern, MD, a neurosurgeon at UC Los Angeles’ Mattel Children’s Hospital; and colleagues — suggest it may be possible to design drugs that inhibit or turn down signals from these mutated genes, reducing or even preventing the need for surgery.

Gleeson’s lab studied a group of 20 patients with hemimegalencephaly upon whom Mathern had operated, analyzing and comparing DNA sequences from removed brain tissue with DNA from the patients’ blood and saliva.

"Mathern had reported a family with identical twins, in which one had hemimegalencephaly and one did not. Since such twins share all inherited DNA, we got to thinking that there may be a new mutation that arose in the diseased brain that causes the condition," said Gleeson. Realizing they shared the same ideas about potential causes, the physicians set out to tackle this question using new exome sequencing technology, which allows sequencing of all of the protein-coding exons of the genome at the same time.

The researchers ultimately identified three gene mutations found only in the diseased brain samples. All three mutated genes had previously been linked to cancers.

"We found mutations in a high percentage of the cells in genes regulating the cellular growth pathways in hemimegalencephaly," said Gleeson. "These same mutations have been found in various solid malignancies, including breast and pancreatic cancer. For reasons we do not yet understand, our patients do not develop cancer, but rather this unusual brain condition. Either there are other mutations required for cancer propagation that are missing in these patients, or neurons are not capable of forming these types of cancers."

The mutations were found in 30 percent of the patients studied, indicating other factors are involved. Nonetheless, the researchers have begun investigating potential treatments that address the known gene mutations, with the clear goal of finding a way to avoid the need for surgery.

"Although counterintuitive, hemimegalencephaly patients are far better off following the functional removal or disconnection of the enlarged hemisphere," said Mathern. "Prior to the surgery, most patients have devastating epilepsy, with hundreds of seizures per day, completely resistant to even our most powerful anti-seizure medications. The surgery disconnects the affected hemisphere from the rest of the brain, causing the seizures to stop. If performed at a young age and with appropriate rehabilitation, most children suffer less language or cognitive delay due to neural plasticity of the remaining hemisphere."

But a less-invasive drug therapy would still be more appealing.

"We know that certain already-approved medications can turn down the signaling pathway used by the mutated genes in hemimegalencephaly," said lead author and former UC San Diego post-doctoral researcher Jeong Ho Lee, now at the Korea Advanced Institute of Science and Technology. "We would like to know if future patients might benefit from such a treatment. Wouldn’t it be wonderful if our results could prevent the need for such radical procedures in these children?"

Source: Science Daily

ScienceDaily (June 24, 2012) — Researchers at Yale School of Medicine have zeroed in on a set of neurons in the part of the brain that controls hunger, and found that these neurons are not only associated with overeating, but also linked to non-food associated behaviors, like novelty-seeking and drug addiction.

A lean animal and a control were both exposed to a novelty item (center). The lean animal spent more time exploring the novelty, as shown by the higher concentration of yellow in the slide. (Credit: Image courtesy of Yale University)

Published in the June 24 online issue of Nature Neuroscience, the study was led by Marcelo O. Dietrich, postdoctoral associate, and Tamas L. Horvath, the Jean and David W. Wallace Professor of Biomedical Research and chair of comparative medicine at Yale School of Medicine.

In attempts to develop treatments for metabolic disorders such as obesity and diabetes, researchers have paid increasing attention to the brain’s reward circuits located in the midbrain, with the notion that in these patients, food may become a type of “drug of abuse” similar to cocaine. Dietrich notes, however, that this study flips the common wisdom on its head.

"Using genetic approaches, we found that increased appetite for food can actually be associated with decreased interest in novelty as well as in cocaine, and on the other hand, less interest in food can predict increased interest in cocaine," said Dietrich.

Horvath and his team studied two sets of transgenic mice. In one set, they knocked out a signaling molecule that controls hunger-promoting neurons in the hypothalamus. In the other set, they interfered with the same neurons by eliminating them selectively during development using diphtheria toxin. The mice were given various non-invasive tests that measured how they respond to novelty, and anxiety, and how they react to cocaine.

"We found that animals that have less interest in food are more interested in novelty-seeking behaviors and drugs like cocaine," said Horvath. "This suggests that there may be individuals with increased drive of the reward circuitry, but who are still lean. This is a complex trait that arises from the activity of the basic feeding circuits during development, which then impacts the adult response to drugs and novelty in the environment."

Horvath and his team argue that the hypothalamus, which controls vital functions such as body temperature, hunger, thirst fatigue and sleep, is key to the development of higher brain functions. “These hunger-promoting neurons are critically important during development to establish the set point of higher brain functions, and their impaired function may be the underlying cause for altered motivated and cognitive behaviors,” he said.

"There is this contemporary view that obesity is associated with the increased drive of the reward circuitry," Horvath added. "But here, we provide a contrasting view: that the reward aspect can be very high, but subjects can still be very lean. At the same time, it indicates that a set of people who have no interest in food, might be more prone to drug addiction."

Source: Science Daily

ScienceDaily (June 24, 2012) — Want to nail that tune that you’ve practiced and practiced? Maybe you should take a nap with the same melody playing during your sleep, new provocative Northwestern University research suggests.

Want to nail that tune that you’ve practiced and practiced? Maybe you should take a nap with the same melody playing during your sleep. (Credit: © Anton Maltsev / Fotolia)

The research grows out of exciting existing evidence that suggests that memories can be reactivated during sleep and storage of them can be strengthened in the process.

In the Northwestern study, research participants learned how to play two artificially generated musical tunes with well-timed key presses. Then while the participants took a 90-minute nap, the researchers presented one of the tunes that had been practiced, but not the other.

"Our results extend prior research by showing that external stimulation during sleep can influence a complex skill," said Ken A. Paller, professor of psychology in the Weinberg College of Arts and Sciences at Northwestern and senior author of the study.

By using EEG methods to record the brain’s electrical activity, the researchers ensured that the soft musical “cues” were presented during slow-wave sleep, a stage of sleep previously linked to cementing memories. Participants made fewer errors when pressing the keys to produce the melody that had been presented while they slept, compared to the melody not presented.

"We also found that electrophysiological signals during sleep correlated with the extent to which memory improved," said lead author James Antony of the Interdepartmental Neuroscience Program at Northwestern. "These signals may thus be measuring the brain events that produce memory improvement during sleep."

The age-old myth that you can learn a foreign language while you sleep is sure to come to mind, said Paul J. Reber, associate professor of psychology at Northwestern and a co-author of the study.

"The critical difference is that our research shows that memory is strengthened for something you’ve already learned," Reber said. "Rather than learning something new in your sleep, we’re talking about enhancing an existing memory by re-activating information recently acquired."

The researchers, he said, are now thinking about how their findings could apply to many other types of learning.

"If you were learning how to speak in a foreign language during the day, for example, and then tried to reactivate those memories during sleep, perhaps you might enhance your learning."

Paller said he hopes the study will help them learn more about the basic brain mechanisms that transpire during sleep to help preserve memory storage.

"These same mechanisms may not only allow an abundance of memories to be maintained throughout a lifetime, but they may also allow memory storage to be enriched through the generation of novel connections among memories," he said.

The study opens the door for future studies of sleep-based memory processing for many different types of motor skills, habits and behavioral dispositions, Paller said.

Source: Science Daily

ScienceDaily (June 23, 2012) — The commonly-used epilepsy drug, valproic acid (VPA), can have a highly beneficial effect on some babies born with spinal muscular atrophy (SMA), the number one genetic killer during early infancy. But in about two-thirds of such cases it is either damaging or simply has no effect. Now, for the first time, researchers have found a way to identify which patients are likely to respond well to VPA prior to starting treatment. Their results have major implications, not just for SMA patients, but for other conditions treated with the drug such as migraine and epilepsy, and may even provide the conditions for turning VPA non-responders into responders, the researchers say.

Dr. Lutz Garbes, from the Institute of Human Genetics, University of Cologne, Germany, will tell the annual conference of the European Society of Human Genetics on June 24 that he and his colleagues had analysed blood RNA samples from a small group of SMA patients who had been treated with VPA. They found, as expected, that only about one third of patients responded well. In an attempt to discover whether blood sampling was the most appropriate test method to use, they also looked at VPA response in another tissue — fibroblasts (a type of skin cell). They found that the response in blood and in skin was the same in 60% of cases.

The researchers then generated pluripotent stem cells from fibroblasts of both a VPA responder and a non-responder, and differentiated them into GABAergic neurons (neurons that produce the amino acid GABA, the chief neurotransmitter in the mammalian nervous system). These neurons, when treated with VPA, exhibited a similar response to that previously found in blood and fibroblasts.

"This indicates for the first time that response to VPA is the same among blood and skin and suggests that monitoring blood for VPA therapy is indeed feasible in central nervous system diseases," says Dr. Garbes. "But, even more importantly, by using the SMA patients’ fibroblasts we were able to identify a decisive factor in the suppression of the positive response to VPA treatment. Utilising transcriptome-wide microarray profiling*, we found that high levels of the fatty acid transporter protein CD36 are associated with the lack of positive response to treatment.

"The implications of this discovery are far-reaching. First, we have been able to prove that monitoring blood is a reliable method for doctors to determine response to VPA treatment in many central nervous system diseases, since our findings are not specific to SMA. Second, the identification of CD36 as the crucial factor in suppressing response to treatment provides a simple way of appraising whether a patient will respond to therapy before treatment starts. And third, in the long run we may find a way to target CD36 in order to be able to change a non-VPA responder into a responder."

Knowing that CD36 is a crucial factor here means that the current, potentially dangerous, ‘trial and error’ approach to VPA treatment is now obsolete, the researchers say. Screening of patients for CD36 prior to treatment would mean that only those who would respond positively to VPA would be given it. This is important because, in some cases, VPA can cause life-threatening side-effects such as impairment of liver, blood cell and pancreatic function, especially in those just starting the treatment. “But we still do not understand how CD36 suppresses response to VPA, only that it does so,” says Dr. Garbes. “A greater understanding of its effects could also lead to the detection of even better targets to overcome the problem. “

In the case of SMA, VPA works by inhibiting enzymes called histone deacetylase (HDACs) which are involved in regulating the packaging of DNA. HDACs lead to a denser DNA packaging whereby protein production from genes is reduced. Other enzymes called histone acetyltransferases (HATs) lead to a more relaxed DNA structure, producing more protein. By inhibiting HDACs with VPA, the DNA packaging balance shifts towards the more relaxed structure and thus genes get activated and proteins produced. In SMA, the crucial gene is SMN2, a copy gene of the disease-determining gene SMN1. In healthy individuals, SMN1 is the major source of SMN protein, but SMN2 cannot fully compensate for the loss of SMN1 in SMA patients. By increasing SMN2 activity, it will produce more SMN protein and ameliorate the condition.

"Avoiding needless VPA treatment of non-responders would have a major effect on healthcare costs and improve quality of life for patients," Dr. Garbes will say. "Half of the babies born with SMA will die within two years, but the other half can live to twenty or even longer, so this is an important finding for them. Our findings may also help identify patients who are candidates for VPA treatment in many other diseases of the central nervous system, some of them very common.

"In the EU, approximately 550 SMA babies are born each year, and there are about 311,000 new cases of epilepsy per year. It is estimated that, in Europe, migraine affects up to 28% of people at some time in their lives. We are happy that we may have been able to contribute to the development of personalised medicine for so many people," he will conclude.

*A transcriptome-wide microarray profile provides a way of identifying all the genes that are differentially expressed in distinct cell populations or subtypes, allowing the effects of treatment to be monitored.

Source: Science Daily

ScienceDaily (June 22, 2012) — Some dementia patients show symptoms of a malfunctioning immune system and can receive appropriate treatment.

Scientists at Charité — Universitätsmedizin Berlin have succeeded in recommending a new type of therapeutic approach to dementia. The study published in the journal Neurology shows that immune reactions against the body’s own nerve cells can be the cause of advanced dementia and an appropriate immune suppressive therapy can develop with significant effectiveness.

Dementia burdens society with high costs, and those affected by it and their family members carry a tremendous psychosocial burden. Dementia is increasingly perceived as a sword of Damocles over an aging society due to its often unclear origin, difficult prevention and unsatisfactory therapies.

Together with a workgroup and cooperation partners in Germany and the US, Dr. Harald Prüß, physician at the Klinik für Neurologie of the Charité, was able to prove that dementia is also caused by the immune system. As an accessory symptom of an autoimmune disease, dementia can thus be treated. This approach to diagnostic criteria has been overlooked until now. It was proven that a number of patients in this study who suffered from advanced memory loss had developed an immune defense response with antibodies against an ion channel in the brain, a so-called NMDA-type glutamate channel. Particular proteins in the nerve cell membrane are reduced leading to the characteristic disruption in nerve function and synapsis loss. Those affected exhibit memory problems and abnormalities in mood and emotion. Eliminating these antibodies through hemodialysis improved the symptoms in cerebral metabolism in the hippocampus region — a part of the brain that is relevant for memory performance and particularly affected by dementia.

"Through the study results, a completely new approach to diagnosing dementia can possibly result. At the moment we are working on a follow-up study with larger test groups in order to verify our approach even further," explains Harald Prüß. He adds: "The potential promise of this new approach is that completely new perspectives could result for an entire group of people suffering from dementia for whom no specific therapeutic option exists."

Source: Science Daily

ScienceDaily (June 22, 2012) — A longstanding question in brain research is how information is processed in the brain. Neuroscientists at the Charité — Universitätsmedizin Berlin, Cluster of Excellence NeuroCure and University of Newcastle have made a contribution towards answering this question. In a new study, they have shown that signals are generated not only in the cell body of nerve cells, but also in their output extension, the axon. A specific filter cell regulates signal propagation.

These findings have now been published in the journal Science.

Until now it has been assumed that information flow in nerve cells proceeds along a “one-way street.” Electrical impulses are initiated at the cell body and propagate along the axon to the next neuron, where they are received by extensions, the dendrites, acting as antennae. However, the team around Charité researchers Tengis Gloveli and Tamar Dugladze has demonstrated that this model needs to be revised. They discovered that signals can also be initiated in axons, i.e. outside the cell body. This happens during highly synchronous neuronal activity as, for example, in a state of heightened attention. Moreover, these axonally generated signals flow bidirectionally and represent a new principle of information processing: on the one hand, impulses propagate from their origin towards other nerve cells; on the other hand, the signals also backpropagate towards the cell body, i.e. in the “wrong direction” down the one-way street. A potential problem is that backpropagating signals could lead to excessive cell activation.

However, the researchers found that backpropagating signals do not reach the cell body under normal conditions. The reason for this, the scientists discovered, is a natural filter that prevents these signals from passing. “Axo-axonic cells, an inhibitory cell type, regulate signal propagation and thus occupy an outstanding strategic position,” explains Tamar Dugladze. Through the filter function, these cells allow signals initiated at the cell body to pass, but suppress backpropagating impulses generated in the axon. By this means, excessive activation of the cell body is prevented. In experiments, the scientists could show that when this filter function is deactivated, backpropagating signals are allowed to pass, resulting in higher cell activation.

These filter cells can become damaged in various neurological diseases. The consequent misregulation of signal flow, in turn, has fatal effects on information processing in the brain. “Results of this study shed new light on the central question of how signals are processed in the brain. In addition, these findings could help us better understand the development and progress of neuronal diseases such as epilepsy, which involves excessive hypersynchronous activity of large sets of neurons. This knowledge could open up new therapeutic approaches,” says Tengis Gloveli. The neuroscientists will therefore focus their future research on both basic understanding of the mechanisms of signal flow in the nervous system, and the relevance of these mechanisms in the genesis of epilepsy.

Source: Science Daily