Neuroscience

Articles and news from the latest research reports.

Posts tagged brain activity

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Brain scans predict which criminals are more likely to reoffend
In a twist that evokes the dystopian science fiction of writer Philip K. Dick, neuroscientists have found a way to predict whether convicted felons are likely to commit crimes again from looking at their brain scans. Convicts showing low activity in a brain region associated with decision-making and action are more likely to be arrested again, and sooner.
Kent Kiehl, a neuroscientist at the non-profit Mind Research Network in Albuquerque, New Mexico, and his collaborators studied a group of 96 male prisoners just before their release. The researchers used functional magnetic resonance imaging (fMRI) to scan the prisoners’ brains during computer tasks in which subjects had to make quick decisions and inhibit impulsive reactions.
The scans focused on activity in a section of the anterior cingulate cortex (ACC), a small region in the front of the brain involved in motor control and executive functioning. The researchers then followed the ex-convicts for four years to see how they fared.
Among the subjects of the study, men who had lower ACC activity during the quick-decision tasks were more likely to be arrested again after getting out of prison, even after the researchers accounted for other risk factors such as age, drug and alcohol abuse and psychopathic traits. Men who were in the lower half of the ACC activity ranking had a 2.6-fold higher rate of rearrest for all crimes and a 4.3-fold higher rate for nonviolent crimes. The results are published in the Proceedings of the National Academy of Sciences.
There is growing interest in using neuroimaging to predict specific behaviour, says Tor Wager, a neuroscientist at the University of Colorado in Boulder. He says that studies such as this one, which tie brain imaging to concrete clinical outcomes, “provide a new and so far very promising way” to find patterns of brain activity that have broader implications for society.But the authors themselves stress that much more work is needed to prove that the technique is reliable and consistent, and that it is likely to flag only the truly high-risk felons and leave the low-risk ones alone. “This isn’t ready for prime time,” says Kiehl.
Wager adds that the part of the ACC examined in this study “is one of the most frequently activated areas in the human brain across all kinds of tasks and psychological states”. Low ACC activity could have a variety of causes — impulsivity, caffeine use, vascular health, low motivation or better neural efficiency — and not all of these are necessarily related to criminal behaviour.
Crime prediction was the subject of Dick’s 1956 short story “The Minority Report” (adapted for the silver screen by Steven Spielberg in 2002), which highlighted the thorny ethics of arresting people for crimes they had yet to commit.
Brain scans are of course a far cry from the clairvoyants featured in that science-fiction story. But even if the science turns out to be reliable, the legal and social implications remain to be explored, the authors warn. Perhaps the most appropriate use for neurobiological markers would be for helping to make low-stakes decisions, such as which rehabilitation treatment to assign a prisoner, rather than high-stakes ones such as sentencing or releasing on parole.
“A treatment of [these clinical neuroimaging studies] that is either too glibly enthusiastic or over-critical,” Wager says, “will be damaging for this emerging science in the long run.”

Brain scans predict which criminals are more likely to reoffend

In a twist that evokes the dystopian science fiction of writer Philip K. Dick, neuroscientists have found a way to predict whether convicted felons are likely to commit crimes again from looking at their brain scans. Convicts showing low activity in a brain region associated with decision-making and action are more likely to be arrested again, and sooner.

Kent Kiehl, a neuroscientist at the non-profit Mind Research Network in Albuquerque, New Mexico, and his collaborators studied a group of 96 male prisoners just before their release. The researchers used functional magnetic resonance imaging (fMRI) to scan the prisoners’ brains during computer tasks in which subjects had to make quick decisions and inhibit impulsive reactions.

The scans focused on activity in a section of the anterior cingulate cortex (ACC), a small region in the front of the brain involved in motor control and executive functioning. The researchers then followed the ex-convicts for four years to see how they fared.

Among the subjects of the study, men who had lower ACC activity during the quick-decision tasks were more likely to be arrested again after getting out of prison, even after the researchers accounted for other risk factors such as age, drug and alcohol abuse and psychopathic traits. Men who were in the lower half of the ACC activity ranking had a 2.6-fold higher rate of rearrest for all crimes and a 4.3-fold higher rate for nonviolent crimes. The results are published in the Proceedings of the National Academy of Sciences.

There is growing interest in using neuroimaging to predict specific behaviour, says Tor Wager, a neuroscientist at the University of Colorado in Boulder. He says that studies such as this one, which tie brain imaging to concrete clinical outcomes, “provide a new and so far very promising way” to find patterns of brain activity that have broader implications for society.

But the authors themselves stress that much more work is needed to prove that the technique is reliable and consistent, and that it is likely to flag only the truly high-risk felons and leave the low-risk ones alone. “This isn’t ready for prime time,” says Kiehl.

Wager adds that the part of the ACC examined in this study “is one of the most frequently activated areas in the human brain across all kinds of tasks and psychological states”. Low ACC activity could have a variety of causes — impulsivity, caffeine use, vascular health, low motivation or better neural efficiency — and not all of these are necessarily related to criminal behaviour.

Crime prediction was the subject of Dick’s 1956 short story “The Minority Report” (adapted for the silver screen by Steven Spielberg in 2002), which highlighted the thorny ethics of arresting people for crimes they had yet to commit.

Brain scans are of course a far cry from the clairvoyants featured in that science-fiction story. But even if the science turns out to be reliable, the legal and social implications remain to be explored, the authors warn. Perhaps the most appropriate use for neurobiological markers would be for helping to make low-stakes decisions, such as which rehabilitation treatment to assign a prisoner, rather than high-stakes ones such as sentencing or releasing on parole.

“A treatment of [these clinical neuroimaging studies] that is either too glibly enthusiastic or over-critical,” Wager says, “will be damaging for this emerging science in the long run.”

Filed under brain brain activity brain scans neuroimaging anterior cingulate cortex neuroscience science

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Parkinsons’ drug helps older people to make decisions

A drug widely used to treat Parkinson’s Disease can help to reverse age-related impairments in decision making in some older people, a study from researchers at the Wellcome Trust Centre for Neuroimaging has shown.

The study, published today in the journal Nature Neuroscience, also describes changes in the patterns of brain activity of adults in their seventies that help to explain why they are worse at making decisions than younger people.

Poorer decision-making is a natural part of the ageing process that stems from a decline in our brains’ ability to learn from our experiences. Part of the decision-making process involves learning to predict the likelihood of getting a reward from the choices that we make.

An area of the brain called the nucleus accumbens is responsible for interpreting the difference between the reward that we’re expecting to get from a decision and the reward that is actually received. These so called ‘prediction errors’, reported by a brain chemical called dopamine, help us to learn from our actions and modify our behaviour to make better choices the next time.

Dr Rumana Chowdhury, who led the study at the Wellcome Trust Centre for Neuroimaging at UCL, said: “We know that dopamine decline is part of the normal aging process so we wanted to see whether it had any effect on reward-based decision making. We found that when we treated older people who were particularly bad at making decisions with a drug that increases dopamine in the brain, their ability to learn from rewards improved to a level comparable to somebody in their twenties and enabled them to make better decisions.”

The team used a combination of behavioural testing and brain imaging techniques, to investigate the decision-making process in 32 healthy volunteers aged in their early seventies compared with 22 volunteers in their mid-twenties. Older participants were tested on and off L-DOPA, a drug that increases levels of dopamine in the brain. L-DOPA, more commonly known as Levodopa, is widely used in the clinic to treat Parkinson’s.

The participants were asked to complete a behavioural learning task called the two-arm bandit, which mimics the decisions that gamblers make while playing slot machines. Players were shown two images and had to choose the one that they thought would give them the biggest reward. Their performance before and after drug treatment was assessed by the amount of money they won in the task.

"The older volunteers who were less able to predict the likelihood of a reward from their decisions, and so performed worst in the task, showed a significant improvement following drug treatment," Dr Chowdhury explains.

The team then looked at brain activity in the participants as they played the game using functional Magnetic Resonance Imaging (fMRI), and measured connections between areas of the brain that are involved in reward prediction using a technique called Diffusor Tensor Imaging (DTI).

The findings reveal that the older adults who performed best in the gambling game before drug treatment had greater integrity of their dopamine pathways. Older adults who performed poorly before drug treatment were not able to adequately signal reward expectation in the brain – this was corrected by L-DOPA and their performance improved on the drug.

Dr John Williams, Head of Neuroscience and Mental Health at the Wellcome Trust, said: “This careful investigation into the subtle cognitive changes that take place as we age offers important insights into what may happen at both a functional and anatomical level in older people who have problems with making decisions. That the team were able to reverse these changes by manipulating dopamine levels offers the hope of therapeutic approaches that could allow older people to function more effectively in the wider community.”

(Source: eurekalert.org)

Filed under brain brain activity parkinson's disease nucleus accumbens aging neuroimaging neuroscience science

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DNA damage occurs as part of normal brain activity
Scientists at the Gladstone Institutes have discovered that a certain type of DNA damage long thought to be particularly detrimental to brain cells can actually be part of a regular, non-harmful process. The team further found that disruptions to this process occur in mouse models of Alzheimer’s disease—and identified two therapeutic strategies that reduce these disruptions.
Scientists have long known that DNA damage occurs in every cell, accumulating as we age. But a particular type of DNA damage, known as a double-strand break, or DSB, has long been considered a major force behind age-related illnesses such as Alzheimer’s. Today, researchers in the laboratory of Gladstone Senior Investigator Lennart Mucke, MD, report in Nature Neuroscience that DSBs in neuronal cells in the brain can also be part of normal brain functions such as learning—as long as the DSBs are tightly controlled and repaired in good time. Further, the accumulation of the amyloid-beta protein in the brain—widely thought to be a major cause of Alzheimer’s disease—increases the number of neurons with DSBs and delays their repair.
"It is both novel and intriguing team’s finding that the accumulation and repair of DSBs may be part of normal learning," said Fred H. Gage, PhD, of the Salk Institute who was not involved in this study. "Their discovery that the Alzheimer’s-like mice exhibited higher baseline DSBs, which weren’t repaired, increases these findings’ relevance and provides new understanding of this deadly disease’s underlying mechanisms."
In laboratory experiments, two groups of mice explored a new environment filled with unfamiliar sights, smells and textures. One group was genetically modified to simulate key aspects of Alzheimer’s, and the other was a healthy, control group. As the mice explored, their neurons became stimulated as they processed new information. After two hours, the mice were returned to their familiar, home environment.
The investigators then examined the neurons of the mice for markers of DSBs. The control group showed an increase in DSBs right after they explored the new environment—but after being returned to their home environment, DSB levels dropped.
"We were initially surprised to find neuronal DSBs in the brains of healthy mice," said Elsa Suberbielle, DVM, PhD, Gladstone postdoctoral fellow and the paper’s lead author. "But the close link between neuronal stimulation and DSBs, and the finding that these DSBs were repaired after the mice returned to their home environment, suggest that DSBs are an integral part of normal brain activity. We think that this damage-and-repair pattern might help the animals learn by facilitating rapid changes in the conversion of neuronal DNA into proteins that are involved in forming memories."
The group of mice modified to simulate Alzheimer’s had higher DSB levels at the start—levels that rose even higher during neuronal stimulation. In addition, the team noticed a substantial delay in the DNA-repair process.
To counteract the accumulation of DSBs, the team first used a therapeutic approach built on two recent studies—one of which was led by Dr. Mucke and his team—that showed the widely used anti-epileptic drug levetiracetam could improve neuronal communication and memory in both mouse models of Alzheimer’s and in humans in the disease’s earliest stages. The mice they treated with the FDA-approved drug had fewer DSBs. In their second strategy, they genetically modified mice to lack the brain protein called tau—another protein implicated in Alzheimer’s. This manipulation, which they had previously found to prevent abnormal brain activity, also prevented the excessive accumulation of DSBs.
The team’s findings suggest that restoring proper neuronal communication is important for staving off the effects of Alzheimer’s—perhaps by maintaining the delicate balance between DNA damage and repair.
"Currently, we have no effective treatments to slow, prevent or halt Alzheimer’s, from which more than 5 million people suffer in the United States alone," said Dr. Mucke, who directs neurological research at Gladstone and is a professor of neuroscience and neurology at the University of California, San Francisco, with which Gladstone is affiliated. "The need to decipher the causes of Alzheimer’s and to find better therapeutic solutions has never been more important—or urgent. Our results suggest that readily available drugs could help protect neurons against some of the damages inflicted by this illness. In the future, we will further explore these therapeutic strategies. We also hope to gain a deeper understanding of the role that DSBs play in learning and memory—and in the disruption of these important brain functions by Alzheimer’s disease."
(Image courtesy: Lulu Qian, Erik Winfree & Jehoshua Bruck | California Institute of Technology)

DNA damage occurs as part of normal brain activity

Scientists at the Gladstone Institutes have discovered that a certain type of DNA damage long thought to be particularly detrimental to brain cells can actually be part of a regular, non-harmful process. The team further found that disruptions to this process occur in mouse models of Alzheimer’s disease—and identified two therapeutic strategies that reduce these disruptions.

Scientists have long known that DNA damage occurs in every cell, accumulating as we age. But a particular type of DNA damage, known as a double-strand break, or DSB, has long been considered a major force behind age-related illnesses such as Alzheimer’s. Today, researchers in the laboratory of Gladstone Senior Investigator Lennart Mucke, MD, report in Nature Neuroscience that DSBs in neuronal cells in the brain can also be part of normal brain functions such as learning—as long as the DSBs are tightly controlled and repaired in good time. Further, the accumulation of the amyloid-beta protein in the brain—widely thought to be a major cause of Alzheimer’s disease—increases the number of neurons with DSBs and delays their repair.

"It is both novel and intriguing team’s finding that the accumulation and repair of DSBs may be part of normal learning," said Fred H. Gage, PhD, of the Salk Institute who was not involved in this study. "Their discovery that the Alzheimer’s-like mice exhibited higher baseline DSBs, which weren’t repaired, increases these findings’ relevance and provides new understanding of this deadly disease’s underlying mechanisms."

In laboratory experiments, two groups of mice explored a new environment filled with unfamiliar sights, smells and textures. One group was genetically modified to simulate key aspects of Alzheimer’s, and the other was a healthy, control group. As the mice explored, their neurons became stimulated as they processed new information. After two hours, the mice were returned to their familiar, home environment.

The investigators then examined the neurons of the mice for markers of DSBs. The control group showed an increase in DSBs right after they explored the new environment—but after being returned to their home environment, DSB levels dropped.

"We were initially surprised to find neuronal DSBs in the brains of healthy mice," said Elsa Suberbielle, DVM, PhD, Gladstone postdoctoral fellow and the paper’s lead author. "But the close link between neuronal stimulation and DSBs, and the finding that these DSBs were repaired after the mice returned to their home environment, suggest that DSBs are an integral part of normal brain activity. We think that this damage-and-repair pattern might help the animals learn by facilitating rapid changes in the conversion of neuronal DNA into proteins that are involved in forming memories."

The group of mice modified to simulate Alzheimer’s had higher DSB levels at the start—levels that rose even higher during neuronal stimulation. In addition, the team noticed a substantial delay in the DNA-repair process.

To counteract the accumulation of DSBs, the team first used a therapeutic approach built on two recent studies—one of which was led by Dr. Mucke and his team—that showed the widely used anti-epileptic drug levetiracetam could improve neuronal communication and memory in both mouse models of Alzheimer’s and in humans in the disease’s earliest stages. The mice they treated with the FDA-approved drug had fewer DSBs. In their second strategy, they genetically modified mice to lack the brain protein called tau—another protein implicated in Alzheimer’s. This manipulation, which they had previously found to prevent abnormal brain activity, also prevented the excessive accumulation of DSBs.

The team’s findings suggest that restoring proper neuronal communication is important for staving off the effects of Alzheimer’s—perhaps by maintaining the delicate balance between DNA damage and repair.

"Currently, we have no effective treatments to slow, prevent or halt Alzheimer’s, from which more than 5 million people suffer in the United States alone," said Dr. Mucke, who directs neurological research at Gladstone and is a professor of neuroscience and neurology at the University of California, San Francisco, with which Gladstone is affiliated. "The need to decipher the causes of Alzheimer’s and to find better therapeutic solutions has never been more important—or urgent. Our results suggest that readily available drugs could help protect neurons against some of the damages inflicted by this illness. In the future, we will further explore these therapeutic strategies. We also hope to gain a deeper understanding of the role that DSBs play in learning and memory—and in the disruption of these important brain functions by Alzheimer’s disease."

(Image courtesy: Lulu Qian, Erik Winfree & Jehoshua Bruck | California Institute of Technology)

Filed under brain activity brain function brain cells dna damage neurons animal model neuroscience science

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Altered brain activity responsible for cognitive symptoms of schizophrenia

Cognitive problems with memory and behavior experienced by individuals with schizophrenia are linked with changes in brain activity; however, it is difficult to test whether these changes are the underlying cause or consequence of these symptoms. By altering the brain activity in mice to mimic the decrease in activity seen in patients with schizophrenia, researchers reporting in the Cell Press journal Neuron on March 20 reveal that these changes in regional brain activity cause similar cognitive problems in otherwise normal mice. This direct demonstration of the link between changes in brain activity and the behaviors associated with schizophrenia could alter how the disease is treated.

"We artificially decreased activity of the mediodorsal thalamus region of the brain in the mouse and found that it is sufficient to lead to deficits in working memory and other schizophrenia-like cognitive deficits," says senior author Dr. Christoph Kellendonk of Columbia University in New York City. "Our findings further suggest that decreased thalamic activity interferes with cognition by disrupting communication between the thalamus and the prefrontal cortex, an area of the brain that has already been shown to be important for working memory," he added.

The researchers made their discovery by giving mice a drug that decreased activity selectively in the mediodorsal thalamus region of the brain. They then tested the animals in various cognitive tasks involving levers and mazes. The investigators found that even a subtle decrease in the activity of the mediodorsal thalamus led to altered connectivity between this brain region and the prefrontal cortex region and that the altered connectivity was associated with a variety of cognitive impairments experienced by patients with schizophrenia.

The findings likely apply to humans because patients with schizophrenia have decreased thalamic activity as well as altered connectivity between the thalamus and the prefrontal cortex. “Our work suggests that these two findings may be linked,” explains co-senior author Dr. Joshua Gordon, also of Columbia University. “One next step would be to examine this relationship in patients. For example, one could ask whether deficits in thalamic activity and connectivity between the thalamus and prefrontal cortex are correlated with each other.”

Cognitive symptoms of schizophrenia include problems with memory and behavioral flexibility, two processes that are essential for activities of daily living. These symptoms are resistant to current treatments, but this study’s findings provide new information for the design of potentially more effective therapies that target the neuronal mechanisms underlying patients’ cognitive problems.

(Source: eurekalert.org)

Filed under schizophrenia neurons brain activity cognitive deficit working memory neuroscience science

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‘Brain waves’ challenge area-specific view of brain activity
Our understanding of brain activity has traditionally been linked to brain areas – when we speak, the speech area of the brain is active. New research by an international team of psychologists led by David Alexander and Cees van Leeuwen (Laboratory for Perceptual Dynamics) shows that this view may be overly rigid. The entire cortex, not just the area responsible for a certain function, is activated when a given task is initiated. Furthermore, activity occurs in a pattern: waves of activity roll from one side of the brain to the other.
The brain can be studied on various scales, researcher David Alexander explains: “You have the neurons, the circuits between the neurons, the Brodmann areas – brain areas that correspond to a certain function – and the entire cortex. Traditionally, scientists looked at local activity when studying brain activity, for example, activity in the Brodmann areas. To do this, you take EEG’s (electroencephalograms) to measure the brain’s electrical activity while a subject performs a task and then you try to trace that activity back to one or more brain areas.”
Activity waves
In this study, the psychologists explore uncharted territory: “We are examining the activity in the cerebral cortex as a whole. The brain is a non-stop, always-active system. When we perceive something, the information does not end up in a specific part of our brain. Rather, it is added to the brain’s existing activity. If we measure the electrochemical activity of the whole cortex, we find wave-like patterns. This shows that brain activity is not local but rather that activity constantly moves from one part of the brain to another. The local activity in the Brodmann areas only appears when you average over many such waves.”
Each activity wave in the cerebral cortex is unique. “When someone repeats the same action, such as drumming their fingers, the motor centre in the brain is stimulated. But with each individual action, you still get a different wave across the cortex as a whole. Perhaps the person was more engaged in the action the first time than he was the second time, or perhaps he had something else on his mind or had a different intention for the action. The direction of the waves is also meaningful. It is already clear, for example, that activity waves related to orienting move differently in children – more prominently from back to front – than in adults. With further research, we hope to unravel what these different wave trajectories mean.”

‘Brain waves’ challenge area-specific view of brain activity

Our understanding of brain activity has traditionally been linked to brain areas – when we speak, the speech area of the brain is active. New research by an international team of psychologists led by David Alexander and Cees van Leeuwen (Laboratory for Perceptual Dynamics) shows that this view may be overly rigid. The entire cortex, not just the area responsible for a certain function, is activated when a given task is initiated. Furthermore, activity occurs in a pattern: waves of activity roll from one side of the brain to the other.

The brain can be studied on various scales, researcher David Alexander explains: “You have the neurons, the circuits between the neurons, the Brodmann areas – brain areas that correspond to a certain function – and the entire cortex. Traditionally, scientists looked at local activity when studying brain activity, for example, activity in the Brodmann areas. To do this, you take EEG’s (electroencephalograms) to measure the brain’s electrical activity while a subject performs a task and then you try to trace that activity back to one or more brain areas.”

Activity waves

In this study, the psychologists explore uncharted territory: “We are examining the activity in the cerebral cortex as a whole. The brain is a non-stop, always-active system. When we perceive something, the information does not end up in a specific part of our brain. Rather, it is added to the brain’s existing activity. If we measure the electrochemical activity of the whole cortex, we find wave-like patterns. This shows that brain activity is not local but rather that activity constantly moves from one part of the brain to another. The local activity in the Brodmann areas only appears when you average over many such waves.”

Each activity wave in the cerebral cortex is unique. “When someone repeats the same action, such as drumming their fingers, the motor centre in the brain is stimulated. But with each individual action, you still get a different wave across the cortex as a whole. Perhaps the person was more engaged in the action the first time than he was the second time, or perhaps he had something else on his mind or had a different intention for the action. The direction of the waves is also meaningful. It is already clear, for example, that activity waves related to orienting move differently in children – more prominently from back to front – than in adults. With further research, we hope to unravel what these different wave trajectories mean.”

Filed under brain brain activity activity waves EEG cerebral cortex neuroscience psychology science

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Wireless, implanted sensor broadens range of brain research
A compact, self-contained sensor recorded and transmitted brain activity data wirelessly for more than a year in early stage animal tests, according to a study funded by the National Institutes of Health. In addition to allowing for more natural studies of brain activity in moving subjects, this implantable device represents a potential major step toward cord-free control of advanced prosthetics that move with the power of thought. The report is in the April 2013 issue of the Journal of Neural Engineering.
“For people who have sustained paralysis or limb amputation, rehabilitation can be slow and frustrating because they have to learn a new way of doing things that the rest of us do without actively thinking about it,” said Grace Peng, Ph.D., who oversees the Rehabilitation Engineering Program of the National Institute of Biomedical Imaging and Bioengineering (NIBIB), part of NIH. “Brain-computer interfaces harness existing brain circuitry, which may offer a more intuitive rehab experience, and ultimately, a better quality of life for people who have already faced serious challenges.”
Recent advances in brain-computer interfaces (BCI) have shown that it is possible for a person to control a robotic arm through implanted brain sensors linked to powerful external computers. However, such devices have relied on wired connections, which pose infection risks and restrict movement, or were wireless but had very limited computing power.
Building on this line of research, David Borton, Ph.D., and Ming Yin, Ph.D., of Brown University, Providence, R.I., and colleagues surmounted several major barriers in developing their sensor. To be fully implantable within the brain, the device needed to be very small and completely sealed off to protect the delicate machinery inside the device and the even more delicate tissue surrounding it. At the same time, it had to be powerful enough to convert the brain’s subtle electrical activity into digital signals that could be used by a computer, and then boost those signals to a level that could be detected by a wireless receiver located some distance outside the body. Like all cordless machines, the device had to be rechargeable, but in the case of an implanted brain sensor, recharging must also be done wirelessly.
The researchers consulted with brain surgeons on the shape and size of the sensor, which they built out of titanium, commonly used in joint replacements and other medical implants. They also fitted the device with a window made of sapphire, which electromagnetic signals pass through more easily than other materials, to assist with wireless transmission and inductive charging, a method of recharging also used in electronic toothbrushes. Inside, the device was densely packed with the electronics specifically designed to function on low power to reduce the amount of heat generated by the device and to extend the time it could work on battery power.
Testing the device in animal models — two pigs and two rhesus macaques — the researchers were able to receive and record data from the implanted sensors in real time over a broadband wireless connection. The sensors could transmit signals more than three feet and have continued to perform for over a year with little degradation in quality or performance.
The ability to remotely record brain activity data as an animal interacts naturally with its environment may help inform studies on muscle control and the movement-related brain circuits, the researchers say. While testing of the current devices continues, the researchers plan to refine the sensor for better heat management and data transmission, with use in human medical care as the goal.
“Clinical applications may include thought-controlled prostheses for severely neurologically impaired patients, wireless access to motorized wheelchairs or other assistive technologies, and diagnostic monitoring such as in epilepsy, where patients currently are tethered to the bedside during assessment,” said Borton.

Wireless, implanted sensor broadens range of brain research

A compact, self-contained sensor recorded and transmitted brain activity data wirelessly for more than a year in early stage animal tests, according to a study funded by the National Institutes of Health. In addition to allowing for more natural studies of brain activity in moving subjects, this implantable device represents a potential major step toward cord-free control of advanced prosthetics that move with the power of thought. The report is in the April 2013 issue of the Journal of Neural Engineering.

“For people who have sustained paralysis or limb amputation, rehabilitation can be slow and frustrating because they have to learn a new way of doing things that the rest of us do without actively thinking about it,” said Grace Peng, Ph.D., who oversees the Rehabilitation Engineering Program of the National Institute of Biomedical Imaging and Bioengineering (NIBIB), part of NIH. “Brain-computer interfaces harness existing brain circuitry, which may offer a more intuitive rehab experience, and ultimately, a better quality of life for people who have already faced serious challenges.”

Recent advances in brain-computer interfaces (BCI) have shown that it is possible for a person to control a robotic arm through implanted brain sensors linked to powerful external computers. However, such devices have relied on wired connections, which pose infection risks and restrict movement, or were wireless but had very limited computing power.

Building on this line of research, David Borton, Ph.D., and Ming Yin, Ph.D., of Brown University, Providence, R.I., and colleagues surmounted several major barriers in developing their sensor. To be fully implantable within the brain, the device needed to be very small and completely sealed off to protect the delicate machinery inside the device and the even more delicate tissue surrounding it. At the same time, it had to be powerful enough to convert the brain’s subtle electrical activity into digital signals that could be used by a computer, and then boost those signals to a level that could be detected by a wireless receiver located some distance outside the body. Like all cordless machines, the device had to be rechargeable, but in the case of an implanted brain sensor, recharging must also be done wirelessly.

The researchers consulted with brain surgeons on the shape and size of the sensor, which they built out of titanium, commonly used in joint replacements and other medical implants. They also fitted the device with a window made of sapphire, which electromagnetic signals pass through more easily than other materials, to assist with wireless transmission and inductive charging, a method of recharging also used in electronic toothbrushes. Inside, the device was densely packed with the electronics specifically designed to function on low power to reduce the amount of heat generated by the device and to extend the time it could work on battery power.

Testing the device in animal models — two pigs and two rhesus macaques — the researchers were able to receive and record data from the implanted sensors in real time over a broadband wireless connection. The sensors could transmit signals more than three feet and have continued to perform for over a year with little degradation in quality or performance.

The ability to remotely record brain activity data as an animal interacts naturally with its environment may help inform studies on muscle control and the movement-related brain circuits, the researchers say. While testing of the current devices continues, the researchers plan to refine the sensor for better heat management and data transmission, with use in human medical care as the goal.

“Clinical applications may include thought-controlled prostheses for severely neurologically impaired patients, wireless access to motorized wheelchairs or other assistive technologies, and diagnostic monitoring such as in epilepsy, where patients currently are tethered to the bedside during assessment,” said Borton.

Filed under brain activity implants prosthetics limb amputation BCI animal model neuroscience science

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New Early Warning System for the Brain Development of Babies
A new research technique, pioneered by Dr. Maria Angela Franceschini, was published in JoVE (Journal of Visualized Experiments) on March 14th. Researchers at Massachusetts General Hospital and Harvard Medical School have developed a non-invasive optical measurement system to monitor neonatal brain activity via cerebral metabolism and blood flow.
Of the nearly four million children born in the United States each year, 12% are born preterm, 8% are born with low birth weight, and 1-2% of infants are at risk for death associated with respiratory distress. The result is an average infant mortality rate of 6 deaths per 1,000 live births. These statistics, though low compared to those of 50 or even 20 years ago, are troubling both to parents and to clinicians. Until recently there were no effective bedside methods to screen for brain injury or monitor injury progression that can contribute to developmental abnormalities or infant mortality. Dr. Franceschini’s new system does both.
“We want to measure cerebral vascular development and brain health in babies,” Dr. Franceschini tells us. Because neuronal metabolism is hard to measure directly, scientists instead evaluate cerebral oxygen metabolism, which highly corresponds to neuronal metabolism. Dr. Franceschini and her team have developed a near infrared optical system to quantify cerebral oxygen metabolism by measuring blood oxygen saturation and blood flow.
The technology is an improvement on continuous-wave near-infrared spectroscopy (CWNIRS), which measures oxygen saturation but does not provide long-term or real time brain monitoring. Instead, frequency-domain near-infrared spectroscopy (FDNIRS) is used in conjunction with diffuse correlation spectroscopy (DCS) to get a more robust evaluation of infant health. Dr. Franceschini explains, “CWNIRS has been used for many years but it only provides relative measurements of blood oxygen saturation. Our technology allows quantification of multiple vascular parameters and evaluation of oxygen metabolism which gives a more direct picture of infant distress.”
“This technology will let us monitor babies who may be having seizures, cerebral hemorrhages, or other cerebral distresses and may allow us to expedite treatment,” says Dr. Franceschini, who plans to develop and streamline this technology to one that nurses can use clinically. “We chose to publish in JoVE because it is important to show how these measurements can be done and this publication lets us reach early adopters.”

New Early Warning System for the Brain Development of Babies

A new research technique, pioneered by Dr. Maria Angela Franceschini, was published in JoVE (Journal of Visualized Experiments) on March 14th. Researchers at Massachusetts General Hospital and Harvard Medical School have developed a non-invasive optical measurement system to monitor neonatal brain activity via cerebral metabolism and blood flow.

Of the nearly four million children born in the United States each year, 12% are born preterm, 8% are born with low birth weight, and 1-2% of infants are at risk for death associated with respiratory distress. The result is an average infant mortality rate of 6 deaths per 1,000 live births. These statistics, though low compared to those of 50 or even 20 years ago, are troubling both to parents and to clinicians. Until recently there were no effective bedside methods to screen for brain injury or monitor injury progression that can contribute to developmental abnormalities or infant mortality. Dr. Franceschini’s new system does both.

“We want to measure cerebral vascular development and brain health in babies,” Dr. Franceschini tells us. Because neuronal metabolism is hard to measure directly, scientists instead evaluate cerebral oxygen metabolism, which highly corresponds to neuronal metabolism. Dr. Franceschini and her team have developed a near infrared optical system to quantify cerebral oxygen metabolism by measuring blood oxygen saturation and blood flow.

The technology is an improvement on continuous-wave near-infrared spectroscopy (CWNIRS), which measures oxygen saturation but does not provide long-term or real time brain monitoring. Instead, frequency-domain near-infrared spectroscopy (FDNIRS) is used in conjunction with diffuse correlation spectroscopy (DCS) to get a more robust evaluation of infant health. Dr. Franceschini explains, “CWNIRS has been used for many years but it only provides relative measurements of blood oxygen saturation. Our technology allows quantification of multiple vascular parameters and evaluation of oxygen metabolism which gives a more direct picture of infant distress.”

“This technology will let us monitor babies who may be having seizures, cerebral hemorrhages, or other cerebral distresses and may allow us to expedite treatment,” says Dr. Franceschini, who plans to develop and streamline this technology to one that nurses can use clinically. “We chose to publish in JoVE because it is important to show how these measurements can be done and this publication lets us reach early adopters.”

Filed under infants brain activity blood flow cerebral metabolism brain injury brain development neuroscience science

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Punishment can enhance performance
The stick can work just as well as the carrot in improving our performance, a team of academics at The University of Nottingham has found.
A study led by researchers from the University’s School of Psychology, published recently in the Journal of Neuroscience, has shown that punishment can act as a performance enhancer in a similar way to monetary reward.
Dr Marios Philiastides, who led the work, said: “This work reveals important new information about how the brain functions that could lead to new methods of diagnosing neural development disorders such as autism, ADHD and personality disorders, where decision-making processes have been shown to be compromised.” 
The Nottingham study aimed at looking at how the efficiency with which we make decisions based on ambiguous sensory information — such as visual or auditory — is affected by the potential for, and severity of, anticipated punishment.
Imposing penalties
To investigate this, they asked participants in the study to perform a simple perceptual task — asking them to judge whether a blurred shape behind a rainy window is a person or something else.
They punished incorrect decisions by imposing monetary penalties. At the same time, they measured the participants’ brain activity in response to different amounts of monetary punishment. Brain activity was recorded, non-invasively, using an EEG machine which detects and amplifies brain signals from the surface of the scalp through a set of small electrodes embedded in a swim-like cap fitted on the participants’ head.
They found that participants’ performance increased systematically as the amount of punishment increased, suggesting that punishment acts as a performance enhancer in a similar way to monetary reward.
At the neural level, the academics identified multiple and distinct brain activations induced by punishment and distributed throughout different areas of the brain. Crucially, the timing of these activations confirmed that the punishment does not influence the way in which the brain processes the sensory evidence but does have an impact on the brain’s decision maker responsible for decoding sensory information at a later stage in the decision-making process.
Incentive-based motivation
Finally, they showed that those participants who showed the greatest improvements in performance also showed the biggest changes in brain activity. This is a key finding as it provides a potential route to study differences between individuals and their personality traits in order to characterise why some may respond better to reward and punishment than others.
A more thorough understanding of the influence of punishment on decision-making and how we make choices could lead to useful information on how to use incentive-based motivation to encourage certain behaviour.
The paper, Temporal Characteristics of the Influence of Punishment on Perceptual Decision Making in the Human Brain, is available online via the Journal of Neuroscience.

Punishment can enhance performance

The stick can work just as well as the carrot in improving our performance, a team of academics at The University of Nottingham has found.

A study led by researchers from the University’s School of Psychology, published recently in the Journal of Neuroscience, has shown that punishment can act as a performance enhancer in a similar way to monetary reward.

Dr Marios Philiastides, who led the work, said: “This work reveals important new information about how the brain functions that could lead to new methods of diagnosing neural development disorders such as autism, ADHD and personality disorders, where decision-making processes have been shown to be compromised.”

The Nottingham study aimed at looking at how the efficiency with which we make decisions based on ambiguous sensory information — such as visual or auditory — is affected by the potential for, and severity of, anticipated punishment.

Imposing penalties

To investigate this, they asked participants in the study to perform a simple perceptual task — asking them to judge whether a blurred shape behind a rainy window is a person or something else.

They punished incorrect decisions by imposing monetary penalties. At the same time, they measured the participants’ brain activity in response to different amounts of monetary punishment. Brain activity was recorded, non-invasively, using an EEG machine which detects and amplifies brain signals from the surface of the scalp through a set of small electrodes embedded in a swim-like cap fitted on the participants’ head.

They found that participants’ performance increased systematically as the amount of punishment increased, suggesting that punishment acts as a performance enhancer in a similar way to monetary reward.

At the neural level, the academics identified multiple and distinct brain activations induced by punishment and distributed throughout different areas of the brain. Crucially, the timing of these activations confirmed that the punishment does not influence the way in which the brain processes the sensory evidence but does have an impact on the brain’s decision maker responsible for decoding sensory information at a later stage in the decision-making process.

Incentive-based motivation

Finally, they showed that those participants who showed the greatest improvements in performance also showed the biggest changes in brain activity. This is a key finding as it provides a potential route to study differences between individuals and their personality traits in order to characterise why some may respond better to reward and punishment than others.

A more thorough understanding of the influence of punishment on decision-making and how we make choices could lead to useful information on how to use incentive-based motivation to encourage certain behaviour.

The paper, Temporal Characteristics of the Influence of Punishment on Perceptual Decision Making in the Human Brain, is available online via the Journal of Neuroscience.

Filed under punishment neurodevelopmental disorders performance decision making brain activity EEG psychology neuroscience science

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Researchers find age-related changes in how autism affects the brain

Newly released findings from Bradley Hospital published in the Journal of the American Academy of Child & Adolescent Psychiatry have found that autism spectrum disorders (ASD) affect the brain activity of children and adults differently.

In the study, titled “Developmental Meta-Analysis of the Functional Neural Correlates of Autism Spectrum Disorders,” Daniel Dickstein, M.D., FAAP, director of the Pediatric Mood, Imaging and Neurodevelopment Program at Bradley Hospital, found that autism-related changes in brain activity continue into adulthood.

"Our study was innovative because we used a new technique to directly compare the brain activity in children with autism versus adults with autism," said Dickstein. "We found that brain activity changes associated with autism do not just happen in childhood, and then stop. Instead, our study suggests that they continue to develop, as we found brain activity differences in children with autism compared to adults with autism. This is the first study to show that."

This new technique, a meta-analysis, which is a study that compiles pre-existing studies, provided researchers with a powerful way to look at potential differences between children and adults with autism.

Dickstein conducted the research through Bradley Hospital’s PediMIND Program. Started in 2007, this program seeks to identify biological and behavioral markers—scans and tests—that will ultimately improve how children and adolescents are diagnosed and treated for psychiatric conditions. Using special computer games and brain scans, including magnetic resonance imaging (MRI), Dickstein hopes to one day make the diagnosis and treatment of autism and other disorders more specific and more effective.

Among autism’s most disabling symptoms is a disruption in social skills, so it is noteworthy that this study found significantly less brain activity in autistic children than autistic adults during social tasks, such as looking at faces. This was true in brain regions including the right hippocampus and superior temporal gyrus—two brain regions associated with memory and other functions.

Dickstein noted, “Brain changes in the hippocampus in children with autism have been found in studies using other types of brain scan, suggesting that this might be an important target for brain-based treatments, including both therapy and medication that might improve how this brain area works.”

Rowland Barrett, Ph.D., chief psychologist at Bradley Hospital and chief-of-service for The Center for Autism and Developmental Disabilities was also part of the team leading the study.

"Autism spectrum disorders, including autistic disorder, Asperger’s disorder, and pervasive developmental disorder not otherwise specified (PDD-NOS), are among the most common and impairing psychiatric conditions affecting children and adolescents today," said Barrett. "If we can identify the shift in the parts of the brain that autism affects as we age, then we can better target treatments for patients with ASD."

(Source: eurekalert.org)

Filed under ASD autism brain activity MRI hippocampus superior temporal gyrus neuroscience science

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Neural “Synchrony” May be Key to Understanding How the Human Brain Perceives
Despite many remarkable discoveries in the field of neuroscience during the past several decades, researchers have not been able to fully crack the brain’s “neural code.” The neural code details how the brain’s roughly 100 billion neurons turn raw sensory inputs into information we can use to see, hear and feel things in our environment.
In a perspective article published in the journal Nature Neuroscience on Feb. 25, 2013, biomedical engineering professor Garrett Stanley detailed research progress toward “reading and writing the neural code.” This encompasses the ability to observe the spiking activity of neurons in response to outside stimuli and make clear predictions about what is being seen, heard, or felt, and the ability to artificially introduce activity within the brain that enables someone to see, hear, or feel something that is not experienced naturally through sensory organs.
Stanley also described challenges that remain to read and write the neural code and asserted that the specific timing of electrical pulses is crucial to interpreting the code. He wrote the article with support from the National Science Foundation (NSF) and the National Institutes of Health (NIH). Stanley has been developing approaches to better understand and control the neural code since 1997 and has published about 40 journal articles in this area.
“Neuroscientists have made great progress toward reading the neural code since the 1990s, but the recent development of improved tools for measuring and activating neuronal circuits has finally put us in a position to start writing the neural code and controlling neuronal circuits in a physiological and meaningful way,” said Stanley, a professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University.
With recent reports that the Obama administration is planning a decade-long scientific effort to examine the workings of the human brain and build a comprehensive map of its activity, progress toward breaking the neural code could begin to accelerate.
The potential rewards for cracking the neural code are immense. In addition to understanding how brains generate and manage information, neuroscientists may be able to control neurons in individuals with epilepsy and Parkinson’s disease or restore lost function following a brain injury. Researchers may also be able to supply artificial brain signals that provide tactile sensation to amputees wearing a prosthetic device.
Stanley’s paper highlighted a major challenge neuroscientists face: selecting a viable code for conveying information through neural pathways. A longstanding debate exists in the neuroscience community over whether the neural code is a “rate code,” where neurons simply spike faster than their background spiking rate when they are coding for something, or a “timing code,” where the pattern of the spikes matters. Stanley expanded the debate by suggesting the neural code is a “synchrony code,” where the synchronization of spiking across neurons is important.
A synchrony code argues the need for precise millisecond timing coordination across groups of neighboring neurons to truly control the circuit. When a neuron receives an incoming stimulus, an electric pulse travels the neuron’s length and triggers the cell to dump neurotransmitters that can spark a new impulse in a neighboring neuron. In this way, the signal gets passed around the brain and then the body, enabling individuals to see, touch, and hear things in the environment. Depending on the signals it receives, a neuron can spike with hundreds of these impulses every second.
“Eavesdropping on neurons in the brain is like listening to a bunch of people talk—a lot of the noise is just filler, but you still have to determine what the important messages are,” explained Stanley. “My perspective is that information is relevant only if it is going to propagate downstream, a process that requires the synchronization of neurons.”
Neuronal synchrony is naturally modulated by the brain. In a study published in Nature Neuroscience in 2010, Stanley reported finding that a change in the degree of synchronous firing of neurons in the thalamus altered the nature of information as it traveled through the pathway and enhanced the brain’s ability to discriminate between different sensations. The thalamus serves as a relay station between the outside world and the brain’s cortex.
Synchrony induced through artificial stimulation poses a real challenge for creating a wide range of neural representations. Recent technological advances have provided researchers with new methods of activating and silencing neurons via artificial means. Electrical microstimulation had been used for decades to activate neurons, but the technique activated a large volume of neurons at a time and could not be used to silence them or separately activate excitatory and inhibitory neurons. Stanley compared the technique with driving a car that has the gas and brake pedals welded together.
New research methods, such as optogenetics, enable activation and silencing of neurons in close proximity and provide control unavailable with electrical microstimulation. Through genetic expression or viral transfection, different cell types can be targeted to express specific proteins that can be activated with light.
“Moving forward, new technologies need to be used to stimulate neural activity in more realistic and natural scenarios and their effects on the synchronization of neurons need to be thoroughly examined,” said Stanley. “Further work also needs to be completed to determine whether synchrony is crucial in different contexts and across brain regions.”

Neural “Synchrony” May be Key to Understanding How the Human Brain Perceives

Despite many remarkable discoveries in the field of neuroscience during the past several decades, researchers have not been able to fully crack the brain’s “neural code.” The neural code details how the brain’s roughly 100 billion neurons turn raw sensory inputs into information we can use to see, hear and feel things in our environment.

In a perspective article published in the journal Nature Neuroscience on Feb. 25, 2013, biomedical engineering professor Garrett Stanley detailed research progress toward “reading and writing the neural code.” This encompasses the ability to observe the spiking activity of neurons in response to outside stimuli and make clear predictions about what is being seen, heard, or felt, and the ability to artificially introduce activity within the brain that enables someone to see, hear, or feel something that is not experienced naturally through sensory organs.

Stanley also described challenges that remain to read and write the neural code and asserted that the specific timing of electrical pulses is crucial to interpreting the code. He wrote the article with support from the National Science Foundation (NSF) and the National Institutes of Health (NIH). Stanley has been developing approaches to better understand and control the neural code since 1997 and has published about 40 journal articles in this area.

“Neuroscientists have made great progress toward reading the neural code since the 1990s, but the recent development of improved tools for measuring and activating neuronal circuits has finally put us in a position to start writing the neural code and controlling neuronal circuits in a physiological and meaningful way,” said Stanley, a professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University.

With recent reports that the Obama administration is planning a decade-long scientific effort to examine the workings of the human brain and build a comprehensive map of its activity, progress toward breaking the neural code could begin to accelerate.

The potential rewards for cracking the neural code are immense. In addition to understanding how brains generate and manage information, neuroscientists may be able to control neurons in individuals with epilepsy and Parkinson’s disease or restore lost function following a brain injury. Researchers may also be able to supply artificial brain signals that provide tactile sensation to amputees wearing a prosthetic device.

Stanley’s paper highlighted a major challenge neuroscientists face: selecting a viable code for conveying information through neural pathways. A longstanding debate exists in the neuroscience community over whether the neural code is a “rate code,” where neurons simply spike faster than their background spiking rate when they are coding for something, or a “timing code,” where the pattern of the spikes matters. Stanley expanded the debate by suggesting the neural code is a “synchrony code,” where the synchronization of spiking across neurons is important.

A synchrony code argues the need for precise millisecond timing coordination across groups of neighboring neurons to truly control the circuit. When a neuron receives an incoming stimulus, an electric pulse travels the neuron’s length and triggers the cell to dump neurotransmitters that can spark a new impulse in a neighboring neuron. In this way, the signal gets passed around the brain and then the body, enabling individuals to see, touch, and hear things in the environment. Depending on the signals it receives, a neuron can spike with hundreds of these impulses every second.

“Eavesdropping on neurons in the brain is like listening to a bunch of people talk—a lot of the noise is just filler, but you still have to determine what the important messages are,” explained Stanley. “My perspective is that information is relevant only if it is going to propagate downstream, a process that requires the synchronization of neurons.”

Neuronal synchrony is naturally modulated by the brain. In a study published in Nature Neuroscience in 2010, Stanley reported finding that a change in the degree of synchronous firing of neurons in the thalamus altered the nature of information as it traveled through the pathway and enhanced the brain’s ability to discriminate between different sensations. The thalamus serves as a relay station between the outside world and the brain’s cortex.

Synchrony induced through artificial stimulation poses a real challenge for creating a wide range of neural representations. Recent technological advances have provided researchers with new methods of activating and silencing neurons via artificial means. Electrical microstimulation had been used for decades to activate neurons, but the technique activated a large volume of neurons at a time and could not be used to silence them or separately activate excitatory and inhibitory neurons. Stanley compared the technique with driving a car that has the gas and brake pedals welded together.

New research methods, such as optogenetics, enable activation and silencing of neurons in close proximity and provide control unavailable with electrical microstimulation. Through genetic expression or viral transfection, different cell types can be targeted to express specific proteins that can be activated with light.

“Moving forward, new technologies need to be used to stimulate neural activity in more realistic and natural scenarios and their effects on the synchronization of neurons need to be thoroughly examined,” said Stanley. “Further work also needs to be completed to determine whether synchrony is crucial in different contexts and across brain regions.”

Filed under brain neurons neuronal circuits brain activity electrical pulses neuroscience science

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