Posts tagged science
Articles and news from the latest research reports.
Study reveals how ecstasy acts on the brain and hints at therapeutic uses
Brain imaging experiments have revealed for the first time how ecstasy produces feelings of euphoria in users.
Results of the study at Imperial College London, parts of which were televised in Drugs Live on Channel 4 in 2012, have now been published in the journal Biological Psychiatry.
The findings hint at ways that ecstasy, or MDMA, might be useful in the treatment of anxiety and post-traumatic stress disorder (PTSD).
MDMA has been a popular recreational drug since the 1980s, but there has been little research on which areas of the brain it affects. The new study is the first to use functional magnetic resonance imaging (fMRI) on resting subjects under its influence.
Twenty-five volunteers underwent brain scans on two occasions, one after taking the drug and one after taking a placebo, without knowing which they had been given.
The results show that MDMA decreases activity in the limbic system – a set of structures involved in emotional responses. These effects were stronger in subjects who reported stronger subjective experiences, suggesting that they are related.
Communication between the medial temporal lobe and medial prefrontal cortex, which is involved in emotional control, was reduced. This effect, and the drop in activity in the limbic system, are opposite to patterns seen in patients who suffer from anxiety.
MDMA also increased communication between the amygdala and the hippocampus. Studies on patients with PTSD have found a reduction in communication between these areas.
The project was led by David Nutt, the Edmond J. Safra Professor of Neuropsychopharmacology at Imperial College London, and Professor Val Curran at UCL.
Dr Robin Carhart-Harris from the Department of Medicine at Imperial, who performed the research, said: “We found that MDMA caused reduced blood flow in regions of the brain linked to emotion and memory. These effects may be related to the feelings of euphoria that people experience on the drug.”
Professor Nutt added: “The findings suggest possible clinical uses of MDMA in treating anxiety and PTSD, but we need to be careful about drawing too many conclusions from a study in healthy volunteers. We would have to do studies in patients to see if we find the same effects.”
MDMA has been investigated as an adjunct to psychotherapy in the treatment of PTSD, with a recent pilot study in the US reporting positive preliminary results.
As part of the Imperial study, the volunteers were asked to recall their favourite and worst memories while inside the scanner. They rated their favourite memories as more vivid, emotionally intense and positive after MDMA than placebo, and they rated their worst memories less negatively. This was reflected in the way that parts of the brain were activated more or less strongly under MDMA. These results were published in the International Journal of Neuropsychopharmacology.
Dr Carhart-Harris said: “In healthy volunteers, MDMA seems to lessen the impact of painful memories. This fits with the idea that it could help patients with PTSD revisit their traumatic experiences in psychotherapy without being overwhelmed by negative emotions, but we need to do studies in PTSD patients to see if the drug affects them in the same way.”
![[Figure 1: Synaptic signaling occurs when neurotransmitter molecules (glutamate) released by the presynaptic neuron travel through the synaptic cleft to activate glutamate receptors, including NMDA receptors, on the postsynaptic neuron. Image courtesy of the National Institute on Aging]
Amplifying communication between neurons
Neurons send signals to each other across small junctions called synapses. Some of these signals involve the flow of potassium, calcium and sodium ions through channel proteins that are embedded within the membranes of neurons. However, it was unclear whether the flow of potassium ions into the synaptic cleft had a physiological purpose. An international team of researchers including Alexey Semyanov from the RIKEN Brain Science Institute has now revealed that potassium ions that leak out of channel proteins and spill into the synapse augment synaptic signaling between neurons, potentially fulfilling a reinforcement mechanism in learning and memory.
Synaptic communication between neurons begins when calcium ions enter the axon terminal of one neuron—the presynaptic neuron—causing the release of neurotransmitter molecules, such as glutamate, which travel across the synaptic cleft and bind to receptor proteins on the surface of the receiving or postsynaptic neuron (Fig. 1). When the glutamate binds to a receptor known as the NMDA receptor, a channel in the receptor protein opens and calcium flows in, which initiates activation of the postsynaptic neuron.
Semyanov and his colleagues found that the opening of the NMDA receptor channel on the postsynaptic neuron also allows potassium ions to flow out of that neuron and into the synaptic cleft. Blocking the NMDA receptor prevented the rise in potassium ions within the synaptic cleft.
The NMDA receptor is generally blocked by magnesium ions, but these ions can be released from the receptor channel upon repetitive stimulation of the postsynaptic neuron. Through mathematical modeling and subsequent experiments, Semyanov and his colleagues found that potassium levels in the synaptic cleft could increase dramatically on removal of magnesium or during repeated activation of the postsynaptic neuron.
The rise in potassium in the synaptic cleft was shown to increase calcium entry into the presynaptic neuron axon terminal when the postsynaptic neuron was stimulated, and enhanced the probability that the glutamate neurotransmitter would be released from the presynaptic neuron. In this way, repeated activation of a given neuronal network, such as during learning, could augment the strength of communication between neurons, making it more likely that a given stimulus would trigger the activation of postsynaptic neurons.
"New memories are associated with long-term changes in synaptic strength following repetitive activation of the synapse, commonly known as synaptic plasticity," explains Semyanov. "Potassium accumulation and the consequent increase in probability of glutamate release can potentially aid the induction of synaptic plasticity, thus facilitating learning and memory," he says.](http://41.media.tumblr.com/30b513e4e381ba41d3d127b44a3ff534/tumblr_mzlu960kOT1rog5d1o1_500.jpg)
[Figure 1: Synaptic signaling occurs when neurotransmitter molecules (glutamate) released by the presynaptic neuron travel through the synaptic cleft to activate glutamate receptors, including NMDA receptors, on the postsynaptic neuron. Image courtesy of the National Institute on Aging]
Amplifying communication between neurons
Neurons send signals to each other across small junctions called synapses. Some of these signals involve the flow of potassium, calcium and sodium ions through channel proteins that are embedded within the membranes of neurons. However, it was unclear whether the flow of potassium ions into the synaptic cleft had a physiological purpose. An international team of researchers including Alexey Semyanov from the RIKEN Brain Science Institute has now revealed that potassium ions that leak out of channel proteins and spill into the synapse augment synaptic signaling between neurons, potentially fulfilling a reinforcement mechanism in learning and memory.
Synaptic communication between neurons begins when calcium ions enter the axon terminal of one neuron—the presynaptic neuron—causing the release of neurotransmitter molecules, such as glutamate, which travel across the synaptic cleft and bind to receptor proteins on the surface of the receiving or postsynaptic neuron (Fig. 1). When the glutamate binds to a receptor known as the NMDA receptor, a channel in the receptor protein opens and calcium flows in, which initiates activation of the postsynaptic neuron.
Semyanov and his colleagues found that the opening of the NMDA receptor channel on the postsynaptic neuron also allows potassium ions to flow out of that neuron and into the synaptic cleft. Blocking the NMDA receptor prevented the rise in potassium ions within the synaptic cleft.
The NMDA receptor is generally blocked by magnesium ions, but these ions can be released from the receptor channel upon repetitive stimulation of the postsynaptic neuron. Through mathematical modeling and subsequent experiments, Semyanov and his colleagues found that potassium levels in the synaptic cleft could increase dramatically on removal of magnesium or during repeated activation of the postsynaptic neuron.
The rise in potassium in the synaptic cleft was shown to increase calcium entry into the presynaptic neuron axon terminal when the postsynaptic neuron was stimulated, and enhanced the probability that the glutamate neurotransmitter would be released from the presynaptic neuron. In this way, repeated activation of a given neuronal network, such as during learning, could augment the strength of communication between neurons, making it more likely that a given stimulus would trigger the activation of postsynaptic neurons.
"New memories are associated with long-term changes in synaptic strength following repetitive activation of the synapse, commonly known as synaptic plasticity," explains Semyanov. "Potassium accumulation and the consequent increase in probability of glutamate release can potentially aid the induction of synaptic plasticity, thus facilitating learning and memory," he says.
Age no obstacle to nerve cell regeneration
In aging worms at least, it is insulin, not Father Time, that inhibits a motor neuron’s ability to repair itself — a finding that suggests declines in nervous system health may not be inevitable.
All organisms show a declining ability to regenerate damaged nervous systems with age, but the study appearing in the Feb. 5 issue of the journal Neuron suggests this deficit is not due to the ravages of time.
“The nervous system regulates its own response to age, separately from what happens in the rest of the body,” said Marc Hammarlund, assistant professor of genetics and senior author of the new study. “By manipulating the insulin pathway, we can make animals that live longer but have nervous systems that age normally, or conversely, we can make animals that die at a normal age but have a young nervous system.”
Alexandra Byrne, postdoctoral associate in genetics and lead author of the study, identified two genetic pathways that regulate insulin activity and are responsible for age-related declines in a worm’s ability to regenerate neuronal axons, or connective branches. The team pinpointed two other pathways that also regulate a neuron’s ability to regenerate, but that have no connection to the age of the worm.
The worm C. elegans is a well-established model to study the genetics of aging, and manipulation of the family of genes that regulate insulin activity has been shown to dramatically increase lifespan of the organism. The new study reveals that insulin signaling is also directly affecting the nervous system.
“We hope to understand how different pathways coordinately regulate neuronal aging, and more specifically, how to entice an aged neuron to regenerate after injury,” Byrne said.
“The hope is to increase healthspan, not just lifespan,” Hammarlund said.
(Image caption: A daydreaming brain: the yellow areas depict the default mode network from three different perspectives; the coloured fibres show the connections amongst each other and with the remainder of the brain.)
The structure of the human brain is complex, reminiscent of a circuit diagram with countless connections. But what role does this architecture play in the functioning of the brain? To answer this question, researchers at the Max Planck Institute for Human Development in Berlin, in cooperation with colleagues at the Free University of Berlin and University Hospital Freiburg, have for the first time analysed 1.6 billion connections within the brain simultaneously. They found the highest agreement between structure and information flow in the “default mode network,” which is responsible for inward-focused thinking such as daydreaming.
Everybody’s been there: You’re sitting at your desk, staring out the window, your thoughts wandering. Instead of getting on with what you’re supposed to be doing, you start mentally planning your next holiday or find yourself lost in a thought or a memory. It’s only later that you realize what has happened: Your brain has simply “changed channels”—and switched to autopilot.
For some time now, experts have been interested in the competition among different networks of the brain, which are able to suppress one another’s activity. If one of these approximately 20 networks is active, the others remain more or less silent. So if you’re thinking about your next holiday, it is almost impossible to follow the content of a text at the same time.
To find out how the anatomical structure of the brain impacts its functional networks, a team of researchers at the Max Planck Institute for Human Development in Berlin, in cooperation with colleagues at the Free University of Berlin and the University Hospital Freiburg, have analysed the connections between a total of 40,000 tiny areas of the brain. Using functional magnetic resonance imaging, they examined a total of 1.6 billion possible anatomical connections between these different regions in 19 participants aged between 21 and 31 years. The research team compared these connections with the brain signals actually generated by the nerve cells.
Their results showed the highest agreement between brain structure and brain function in areas forming part of the “default mode network“, which is associated with daydreaming, imagination, and self-referential thought. “In comparison to other networks, the default mode network uses the most direct anatomical connections. We think that neuronal activity is automatically directed to level off at this network whenever there are no external influences on the brain,” says Andreas Horn, lead author of the study and researcher in the Center for Adaptive Rationality at the Max Planck Institute for Human Development in Berlin.
Living up to its name, the default mode network seems to become active in the absence of external influences. In other words, the anatomical structure of the brain seems to have a built-in autopilot setting. It should not, however, be confused with an idle state. On the contrary, daydreaming, imagination, and self-referential thought are complex tasks for the brain.
“Our findings suggest that the structural architecture of the brain ensures that it automatically switches to something useful when it is not being used for other activities,” says Andreas Horn. “But the brain only stays on autopilot until an external stimulus causes activity in another network, putting an end to the daydreaming. A buzzing fly, a loud bang in the distance, or focused concentration on a text, for example.”
The researchers hope that their findings will contribute to a better understanding of brain functioning in healthy people, but also of neurodegenerative disorders such as Alzheimer’s disease and psychiatric conditions such as schizophrenia. In follow-up studies, the research team will compare the brain structures of patients with neurological disorders with those of healthy controls.
Nearly 8 million Americans suffer from posttraumatic stress disorder (PTSD), a condition marked by severe anxiety stemming from a traumatic event such as a battle or violent attack.
Many patients undergo psychotherapy designed to help them re-experience their traumatic memory in a safe environment so as to help them make sense of the events and overcome their fear. However, such memories can be so entrenched that this therapy doesn’t always work, especially when the traumatic event occurred many years earlier.
MIT neuroscientists have now shown that they can extinguish well-established traumatic memories in mice by giving them a type of drug called an HDAC2 inhibitor, which makes the brain’s memories more malleable, under the right conditions. Giving this type of drug to human patients receiving psychotherapy may be much more effective than psychotherapy alone, says Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory.
“By inhibiting HDAC2 activity, we can drive dramatic structural changes in the brain. What happens is the brain becomes more plastic, more capable of forming very strong new memories that will override the old fearful memories,” says Tsai, the senior author of a paper describing the findings in the Jan. 16 issue of Cell.
The new study also reveals the molecular mechanism explaining why older memories are harder to extinguish. Lead authors of the paper are former Picower Institute postdoc Johannes Graff and Nadine Joseph, a technical assistant at the Picower Institute.
Genes and memories
Tsai’s lab has previously shown that when memories are formed, neurons’ chromatin — DNA packaged with proteins — undergoes extensive remodeling. These chromatin modifications make it easier to activate the genes necessary to create new memories.
In this study, the researchers focused on chromatin modifications that occur when previously acquired memories are extinguished. To do this, they first trained mice to fear a particular chamber — by administering a mild foot shock — and then tried to recondition the mice so they no longer feared it, which was done by placing the mice in the chamber where they received the shock, without delivering the shock again.
This training proved successful in mice that had experienced the traumatic event only 24 hours before the reconditioning. However, in mice whose memories were 30 days old, it was impossible to eliminate the fearful memory.
The researchers also found that in the brains of mice with 24-hour-old memories, extensive chromatin remodeling occurred during the reconditioning. For several hours after the mice were placed back in the feared chamber, there was a dramatic increase in histone acetylation of memory-related genes, caused by inactivation of the protein HDAC2. That histone acetylation makes genes more accessible, turning on the processes needed to form new memories or overwrite old ones.
In mice with 30-day-old memories, however, there was no change in histone acetylation. This suggests that re-exposure to a fearful memory opens a window of opportunity during which the memory can be altered, but only if the memory has recently been formed, Tsai says.
“If you do something within this window of time, then you have the possibility of modifying the memory or forming a new trace of memory that actually instructs the animal that this is not such a dangerous place,” she says. “However, the older the memory is, the harder it is to really change that memory.”
Based on this finding, the researchers decided to treat mice with 30-day-old memories with an HDAC2 inhibitor shortly after re-exposure to the feared chamber. Following this treatment, the traumatic memories were extinguished just as easily as in the mice with 24-hour-old memories.
The researchers also found that HDAC2 inhibitor treatment turns on a group of key genes known as immediate early genes, which then activate other genes necessary for memory formation. They also saw an increase in the number of connections among neurons in the hippocampus, where memories are formed, and in the strength of communication among these neurons.
“Our experiments really strongly argue that either the old memories are permanently being modified, or a new much more potent memory is formed that completely overwrites the old memory,” Tsai says.
“This could be a very promising way to bring older memories back, process them in the hippocampus, and then extinguish them with the correct paradigm,” says Jelena Radulovic, a professor of psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine who was not part of the research team.
Treating anxiety
Some HDAC2 inhibitors have been approved to treat cancer, and Tsai says she believes it is worth trying such drugs to treat PTSD. “I hope this will convince people to seriously think about taking this into clinical trials and seeing how well it works,” she says.
Such drugs might also be useful in treating people who suffer from phobias and other anxiety disorders, she adds.
Tsai’s lab is now studying what happens to memory traces when re-exposure to traumatic memories occurs at different times. It is already known that memories are formed in the hippocampus and then transferred to the cortex for longer-term storage. It appears that the HDAC2 inhibitor treatment may somehow restore the memory to the hippocampus so it can be extinguished, Tsai says.
How metabolism and brain activity are linked
A new study by scientists at McGill University and the University of Zurich shows a direct link between metabolism in brain cells and their ability to signal information. The research may explain why the seizures of many epilepsy patients can be controlled by a specially formulated diet.
(Image caption: Neurons in the cerebellum. Credit: Bowie Lab/McGill University)
The findings, published Jan. 16 in Nature Communications, reveal that metabolism controls the processes that inhibit brain activity, such as that involved in convulsions. The study uncovers a link between how brain cells make energy and how the same cells signal information – processes that neuroscientists have often assumed to be distinct and separate.
“Inhibition in the brain is commonly targeted in clinical practice,” notes Derek Bowie, Canada Research Chair in Receptor Pharmacology at McGill and corresponding author of the study. “For example, drugs that alleviate anxiety, induce anesthesia, or even control epilepsy work by strengthening brain inhibition. These pharmacological approaches can have their drawbacks, since patients often complain of unpleasant side effects.”
The experiments showed an unexpected link between how the mitochondria of brain cells make energy and how the same cells signal information. Brain cells couple these two independent functions by using small chemical messengers, called reactive oxygen species (or ROS), that are normally associated with signaling cell death. While ROS are known to have roles in diseases of aging, such as Alzheimer’s and Parkinson’s, the new study shows they also play important roles in the healthy brain.
The findings emerged from an ongoing collaboration between Prof. Bowie’s laboratory in McGill’s Department of Pharmacology and Therapeutics and a research team headed by Dr. Jean-Marc Fritschy, Professor of Pharmacology at the University of Zurich and current director of the Neuroscience Center Zurich (ZNZ). The researchers have the longer term aim of trying to understand why the seizures of many epilepsy patients — especially young children – can be treated with a high-fat, low-carbohydrate diet known as the ketogenic diet.
The idea that diet can control seizures was noticed as far back as ancient Greece, during periods of fasting. From the 1920s until the 1950s, the ketogenic diet was widely used to treat epilepsy patients. With the introduction of anticonvulsant drugs in the 1950s, the dietary approach fell out of favour with doctors. But because anticonvulsant drugs don’t work for 20% to 30% of patients, there has been a resurgence in use of the ketogenic diet.
“Since our study shows that brain cells have their own means to strengthen inhibition,” explains Prof Bowie, “our work points to potentially new ways in which to control a number of important neurological conditions including epilepsy.”
(Source: mcgill.ca)
Heavy Drinking in Middle Age May Speed Memory Loss by up to Six Years in Men
Middle-aged men who drink more than 36 grams of alcohol, or two and a half US drinks per day, may speed their memory loss by up to six years later on, according to a study published in the January 15, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology. On the other hand, the study found no differences in memory and executive function in men who do not drink, former drinkers and light or moderate drinkers. Executive function deals with attention and reasoning skills in achieving a goal.
“Much of the research evidence about drinking and a relationship to memory and executive function is based on older populations,” said study author Séverine Sabia, PhD, of the University College London in the United Kingdom. “Our study focused on middle-aged participants and suggests that heavy drinking is associated with faster decline in all areas of cognitive function in men.”
The study involved 5,054 men and 2,099 women whose drinking habits were assessed three times over 10 years. A drink was considered wine, beer or liquor. Then, when the participants were an average age of 56, they took their first memory and executive function test. The tests were repeated twice over the next 10 years.
The study found that there were no differences in memory and executive function decline between men who did not drink and those who were light or moderate drinkers—those who drank less than 20 grams, or less than two US drinks per day. Heavy drinkers showed memory and executive function declines between one-and-a-half to six years faster than those who had fewer drinks per day.
More Than Meets the Eye
Many studies suggest that pushing your brain to multitask — writing emails, for instance, while watching the day’s latest news and eating breakfast — leads to poorer performance and lower productivity. But for at least one everyday task — visual sampling (the act of picking up bits of visual information through short glances) — multitasking is not a problem for the brain. A collaboration between researchers at the UC Santa Barbara and the University of Bristol in the UK has shown that during visual sampling, the brain can handle various visual functions simultaneously.
“We might not realize it, but human vision is rather limited,” said Miguel Eckstein, professor in the Department of Psychological and Brain Sciences at UCSB. “We only see clearly in a small region around our specific focus.” Eckstein’s study, “Foveal analysis and peripheral selection during active visual sampling,” appears in the early Proceedings of the National Academy of Sciences Plus edition.
Head injuries triple long-term risk of early death
Survivors of traumatic brain injuries (TBI) are three times more likely to die prematurely than the general population, often from suicide or fatal injuries, finds an Oxford University-led study.
A TBI is a blow to the head that leads to a skull fracture, internal bleeding, loss of consciousness for longer than an hour or a combination of these symptoms. Michael Schumacher’s recent skiing injury is an example of a TBI. Concussions, sometimes called mild TBIs, do not present with these symptoms and were analysed separately in this study.
Researchers examined Swedish medical records going back 41 years covering 218,300 TBI survivors, 150,513 siblings of TBI survivors and over two million control cases matched by sex and age from the general population. The work was carried out by researchers at Oxford University and the Karolinska Institute in Stockholm.
'We found that people who survive six months after TBI remain three times more likely to die prematurely than the control population and 2.6 times more likely to die than unaffected siblings,' said study leader Dr Seena Fazel, a Wellcome Trust Senior Research Fellow in Oxford University's Department of Psychiatry. 'Looking at siblings who did not suffer TBIs allows us to control for genetic factors and early upbringing, so it is striking to see that the effect remains strong even after controlling for these.'
The results, published in the journal JAMA Psychiatry, show that TBI survivors who also have a history of substance abuse or psychiatric disorders are at highest risk of premature death. Premature deaths were defined as before age 56. The main causes of premature death in TBI survivors are suicide and fatal injuries such as car accidents and falls.
'TBI survivors are more than twice as likely to kill themselves as unaffected siblings, many of whom were diagnosed with psychiatric disorders after their TBI,' said Dr Fazel. 'Current guidelines do not recommend assessments of mental health or suicide risk in TBI patients, instead focusing on short-term survival. Looking at these findings, it may make more sense to treat some TBI patients as suffering from a chronic problem requiring longer term management just like epilepsy or diabetes. TBI survivors should be monitored carefully for signs of depression, substance abuse and other psychiatric disorders, which are all treatable conditions.'
The exact reasons for the increased risk of premature death are unknown but may involve damage to the parts of the brain responsible for judgement, decision making and risk taking. TBI survivors are three times more likely to die from fatal injuries which may be a result of impaired judgement or reactions.
'This study highlights the important and as yet unanswered question of why TBI survivors are more likely to die young, but it may be that serious brain trauma has lasting effects on people's judgement,' suggests Dr Fazel. 'People who have survived the acute effects of TBI should be more informed about these risks and how to reduce their impact.'
'When treating traumatic brain injuries focus is placed on immediate treatment and recovery of patients,' says Dr John Williams, Head of Neuroscience and Mental Health at the Wellcome Trust. 'This new finding offers important insight into the longer-term impact of TBIs on the brain and their effect on survival later in life. We hope that further research into understanding which parts of the brain are responsible will help improve future management programmes and reduce the potential for premature death.'
Even relatively minor brain injuries, concussions, had a significant impact on early mortality. People with concussion were found to be twice as likely to die prematurely as the control population, with suicide and fatal injuries as the main causes of death. This raises issues surrounding concussions in a wide range of sports, from American football, rugby and soccer to baseball and cricket.
(Source: ox.ac.uk)
Speech means using both sides of our brain
We use both sides of our brain for speech, a finding by researchers at New York University and NYU Langone Medical Center that alters previous conceptions about neurological activity. The results, which appear in the journal Nature, also offer insights into addressing speech-related inhibitions caused by stroke or injury and lay the groundwork for better rehabilitation methods.
“Our findings upend what has been universally accepted in the scientific community—that we use only one side of our brains for speech,” says Bijan Pesaran, an associate professor in NYU’s Center for Neural Science and the study’s senior author. “In addition, now that we have a firmer understanding of how speech is generated, our work toward finding remedies for speech afflictions is much better informed.”
Many in the scientific community have posited that both speech and language are lateralized—that is, we use only one side of our brains for speech, which involves listening and speaking, and language, which involves constructing and understanding sentences. However, the conclusions pertaining to speech generally stem from studies that rely on indirect measurements of brain activity, raising questions about characterizing speech as lateralized.
To address this matter, the researchers directly examined the connection between speech and the neurological process.
Specifically, the study relied on data collected at NYU ECoG, a center where brain activity is recorded directly from patients implanted with specialized electrodes placed directly inside and on the surface of the brain while the patients are performing sensory and cognitive tasks. Here, the researchers examined brain functions of patients suffering from epilepsy by using methods that coincided with their medical treatment.
“Recordings directly from the human brain are a rare opportunity,” says Thomas Thesen, director of the NYU ECoG Center and co-author of the study.
“As such, they offer unparalleled spatial and temporal resolution over other imaging technologies to help us achieve a better understanding of complex and uniquely human brain functions, such as language,” adds Thesen, an assistant professor at NYU Langone.
In their examination, the researchers tested the parts of the brain that were used during speech. Here, the study’s subjects were asked to repeat two “non-words”—“kig” and “pob.” Using non-words as a prompt to gauge neurological activity, the researchers were able to isolate speech from language.
An analysis of brain activity as patients engaged in speech tasks showed that both sides of the brain were used—that is, speech is, in fact, bi-lateral.
“Now that we have greater insights into the connection between the brain and speech, we can begin to develop new ways to aid those trying to regain the ability to speak after a stroke or injuries resulting in brain damage,” observes Pesaran. “With this greater understanding of the speech process, we can retool rehabilitation methods in ways that isolate speech recovery and that don’t involve language.”
(Source: nyu.edu)