Scientists discover response to anxiety linked to movement control areas in brain

Researchers have discovered that the response to anxiety in teenagers may include not only the parts of the brain which deal with emotions (the limbic system), as has been long understood, but also movement control centres in the brain, which may be associated with movement inhibition when stressed (“freezing”). This is a small longitudinal study, presented at the ECNP conference in Vienna.

A group of Italian and Canadian researchers have followed a selection of socially anxious and control group children from childhood to adolescence.  The researchers tested 150 children at the ages of 8/9, for signs of social inhibition. Some of these were shown to have early signs of social anxiety, and showed an increased tendency to withdraw from social situations. They also had more difficulty in recognising emotions, and particularly angry faces.

The anxious children, plus controls, were then followed into adolescence. At the ages of 14-15 they were tested again to see if signs of social anxiety had developed. The researchers also used fMRI brain scans to test how the teenage brains responded to angry facial expressions.

As lead researcher, Laura Muzzarelli said:

“We found that when presented with an angry face the brain of socially anxious adolescents showed increased activity in the amygdala, which is the brain area concerned with emotions, memory and how we respond to threats. Surprisingly, we also found this produced inhibition of some motor areas of the brain, the premotor cortex. This is an area which ‘prepares the body for action’, and for specific movements. This is the first hard proof that strong emotions produce a response in brain areas concerned with movement. Adolescents who don’t show social anxiety tend not to show the inhibition in the movement centres. We don’t yet know how this inhibition feeds into movement – it may be that this has something to do with why we sometimes ‘freeze’ when we are frightened or under strong emotional stress, this still has to be tested. What it does give us is a possible explanation for some motor inhibition associated with emotional stress.

We need to acknowledge that there are some limitations to this work. We started this 6-year study with 150 children, but by the time we reached adolescence we had narrowed down the field to just 5 children with social anxiety, and 5 with less severe (subthreshold) social anxiety, so it’s a small sample”.

Social Anxiety is a mental health condition characterised by excessive fear and avoidance of the judgement of others. It is the most common anxiety disorder, affecting around 6% to 8% people during their life*, meaning around 50m** Europeans are affected by the condition. It can occur at any age, but most commonly the onset is in adolescence, with early signs already visible during infancy. In early stages, social anxiety can be mistaken for shyness. 

The world's most valuable brain research prize goes to inventors and developers of revolutionary microscopic technique‏

The world’s most valuable (€1m) neuroscience prize, The Brain Prize has been awarded, to four scientists, Winfried Denk and Arthur Konnerth (Germany), and Karel Svoboda and David Tank (USA),  for the invention and development of two-photon microscopy, a transformative tool in brain research.

Two-photon microscopy is one of a handful of techniques which over the last 15 years have dramatically changed the way we study the brain. It combines advanced techniques from physics and biology, to allow scientists to examine the finest structures of the brain, in real time. 

Using this revolutionary technology, researchers are now able to examine the function of individual nerve cells with high precision, especially how nerve cells communicate with each other in networks.  This is a huge step forward in the understanding of the physical mechanisms of the human brain and in the understanding of how the brain’s networks process information. Furthermore, researchers have been able to follow how connections between nerve cells are established in the developing brain.

It has led to identification of signaling pathways that control communication between nerve cells and provide the basis for memory, and it has enabled the study of nerve cell activity in those networks that controls vision, hearing and movement.  

Professor Povl Krogsgaard-Larsen, Chair of Grete Lundbeck European Brain Research Foundation, which awards The Brain Prize, said:

"Thanks to these four scientists we’re now able to study the normal brain's development and attempt to understand what goes wrong when we're affected by destructive diseases such as Alzheimer’s and other types of dementia. More than that, we are able to visualise how adaptive behavioural changes affect the nerve cells of living animals”.

Winfried Denk was the driving force behind the invention of two-photon microscopy. With David Tank and Karel Svoboda he used the technique as an innovative tool to visualise activity at the level of the neurons' fundamental signalling units, the "dendritic spines”.  Arthur Konnerth built on this invention to simultaneously monitor the activity in thousands of synaptic connections in living animals, and Karel Svoboda went on to use two-photon microscopy to map the changes that occur in the brain's network when animals learn new skills.

Since its invention in 1990, two-photon microscopy has formed the basis of more than 10,000 research papers, not only in brain research but also in other areas of physiology, embryology and tissue engineering.

Professor Maiken Nedergaard, of the University of Rochester Medical School, New York, said:

"Traditionally, brain research made use of electrical measurements to study the activity of neurons. Two-photon microscopy has revolutionised the study of the brain, since it is now possible to map the function of the individual parts of a neuron as well as communication between several thousand neurons in live, behaving animals”.

About two-photon microscopy

Two-photon microscopy uses an advanced form of fluorescence microscopy. In fluorescence microscopy, cell components are labelled with special molecules, which glow (fluoresce) when illuminated by light of a particular wavelength, usually UV-light. The microscope then picks up the emitted fluorescent light. However, the short wavelength, high energy UV-light tends to spread through, the tissue making more areas fluoresce and making it difficult to focus upon a specific cell or cell part. Furthermore, UV-light cannot penetrate deep into the tissue, and because of its high energy quickly exhausts the fluorescent molecules.

Two-photon microscopy uses pulsed infrared lasers to focus the illumination only on the target area, which is the only area which then emits light. “It’s like the difference between looking at a movie in daylight, and looking at a movie in a dark hall: if you take away the unwanted light you can see what you want to see much better”, said Maiken Nedergaard.

The two-photon principle allows the use of long wavelength (low energy) infrared light. Under normal circumstances, one photon of infrared light is not enough to elicit fluorescence. However, the pulsed laser can deliver a large amount of light to a specific point. Intermittently two photons will hit a fluorescent molecule, which is sufficient to make it glow.  The infrared light does not exhaust the fluorescent molecules, as happens in conventional fluorescence microscopy. Furthermore, infrared light can go much deeper down into the tissue: this gives the technique its main advantage, for the first time we can see real changes inside a living, active brain, even down to hundreds of micrometres below the brain surface (a human hair is around 90 micrometres thick).

The four researchers will share the one million Euro prize, which will be presented at a ceremony on 7 May in Copenhagen by His Royal Highness Crown Prince Frederik of Denmark.

World's most valuable neuroscience prize to be announced 9th March‏

Grete Lundbeck European Brain Research Prize – ‘The Brain Prize’- is awarded to one or more scientists who have distinguished themselves by an outstanding contribution to European neuroscience and who are still active in research. 

The Brain Prize recognises highly original and influential advances in any area of neuroscience, including fundamental research on molecular, cellular, physiological and pharmacological mechanisms, studies of behaviour and cognition, advances in technology for monitoring the nervous system, translational research on the application of basic knowledge to clinical and other problems of humankind, and clinical research on the causes, treatment and prevention of neurological and psychiatric disorders.

If several researchers have contributed significantly to this achievement, more than one individual may be nominated. Nominees can be of any nationality, but the research for which they are nominated must have been in Europe or in collaboration with researchers in Europe.

Only nominated candidates will be considered by the Selection Committee. Nominations are valid for three years.

The € 1 million prize is a personal prize. 

This year's winners.

Latest brain research unveiled at Science Festival

The latest in neuroscience research and development will be revealed at the 21^st Cambridge Science Festival (9-22 March), including how new technologies are helping researchers to understand the workings of the brain, experimental studies of drug addiction, and the outcomes from the public MEG and ME brain experiments, which are currently being conducted.

Building something as complicated as the brain is a challenging exercise. On Saturday 14 March, during the event Looking into how the brain is built, Professor Bill Harris and Professor Christine Holt demonstrate some of the steps to build a brain and discuss how new technologies help us investigate the underlying molecular and cellular mechanisms.

On Friday 20 March, during the Cambridge Neuroscience public lecture, Brain mechanisms of drug addiction: are abstinence and prevention of relapse realistic treatment goals? Professor of Behavioural Neuroscience, Barry Everitt, will discuss experimental studies of addiction that have identified pro-abstinence and relapse prevention treatments. He will discuss the psychological and neural mechanisms of the compulsion to seek and take drugs. Those addicted find it extremely difficult to abstain and, if they do, have a high propensity to relapse.  

Speaking ahead of the event, Professor Everitt said: “Many people use addictive drugs recreationally; some lose control over use and compulsively seek and take drugs.  I will summarise advances in understanding the neural and psychological basis of addictive behaviour, especially the importance of the learning mechanisms by which otherwise neutral environmental stimuli become associated with drug use. 

“These drug cues exert a major influence on addiction; they can elicit cravings, drug seeking and taking habits through involuntary processes, and they can precipitate relapse even long into abstinence. Increasingly, we are beginning to understand the nature of vulnerability to lose control over drug use, for example the trait of high impulsivity predisposes individuals to compulsive cocaine use and to relapse during abstinence. 

“Despite these advances in understanding the neural mechanisms underlying addiction there are few, if any, treatments in development or in clinical use that promote abstinence or prevent relapse, even though the potential targets for such treatments have been identified. I will discuss how diminishing the impact of drug associations on craving and relapse offers a novel and potentially effective treatment approach, in particular the possibility of reducing the impact of drug memories elicited by those associations.”

On Sunday 22 March, the Cambridge Science Festival will also present the results from the public MEG and Me experiments, which look at what happens to the brain when we lie, feel stressed and learn.

Dr Timothy Rittman, a Clinical Research Fellow at Cambridge, said: “The MEG and Me project was developed from a public challenge and uses the latest brain imaging technology. At the Science Festival, we will be revealing the results of experiments suggested by members of the public to understand our dynamic brains as we ask people to lie to their bosses, listen to crying babies, watch visual illusions and more.

“As people perform these tasks, we have recorded changes in the magnetic fields produced by their brains using a magnetoencephalography (MEG) scanner. We will give people a taste of neuroscience research and share our successes and frustrations along the way. We will be joined by active researchers from the University of Cambridge's department of Clinical Neurosciences and a visual artist to discuss what it all means.”

In addition, on Monday 16 March, a new performance by Laura Jane Dean, supported by the Wellcome Trust, will draw on personal experience of living with OCD and reveals the actualities and artefacts of a therapeutic process. In collaboration with Professor Trevor Robbins, Director of the Behavioural and Clinical Neuroscience Institute, and a Cognitive Behavioural Therapist, Laura attempts to understand what it means to be ill and what it might mean to get better during the theatrical performance,This Room.

Other events related to the brain and neurosciences include:

• Tuesday 10 – Sunday 15 March – the MindSong project is an exciting fusion of science and art that will allow visitors the chance to get inside the mind of Patient h69 – a woman who was suddenly and unexpectedly left paralysed and completely blind.
• Saturday 14 March – The multiple faces of the brain. Test how your brain works with our psychological illusions and investigate the relationship between your body and your brain.
• Tuesday 17 March – Dementia research in Cambridge: from bench to bedside. Sponsored by Alzheimer’s Research UK. Short talks from researchers using different techniques from stem cells to brain scans to understand what happens in the brain in dementia and what progress is being made to help.
• Wednesday 18 March – Exploring mind and brain. An evening exploring research in psychology and neuroscience through hands-on activities, practical demonstrations and talks.
• Thursday 19 March – Stem cells: unravelling brain disease. Dr Thóra Káradóttir will explore the brain’s superhighways and how they might be repaired when diseased.
• Sunday 22 March – Shining light on the newborn brain. Brain injury is a major problem facing premature infants. Using light, Dr Topun Austin will show how 3D images of blood flow in newborns are reconstructed.

Pathological gambling is associated with altered opioid system in the brain, and a reduced feeling of euphoria when compared to healthy volunteers.

All humans have a natural opioid system in the brain. Now new research, presented at the ECNP Congress in Berlin, has found that the opioid system of pathological gamblers responds differently to those of normal healthy volunteers. The work was carried out by a group of UK researchers from London and Cambridge, and was funded by the Medical Research Council. This work is being presented at the European College of Neuropsychopharmacology congress in Berlin.

Gambling is a widespread behaviour with about 70% of the British population gambling occasionally. However In some individuals, gambling spirals out of control and takes on the features of an addiction − pathological gambling, also known as problem gambling. The 2007 British Gambling Prevalence Survey estimated that 0.6% of UK adults have a problem with gambling, equivalent to approximately 300,000 people, which is around the total population of a town like Swansea. This condition has an estimated prevalence of 0.5−3% in Europe.

The researchers took 14 pathological gamblers and 15 healthy volunteers, and used PET scans (Positron Emission Tomography scans) to measure opioid receptor levels in the brains of the two groups. These receptors allow cell to cell communication – they are like a lock with the neurotransmitter or chemical, such as endogenous opioids called endorphins, acting like a key. The researchers found that there were no differences between the receptor levels in pathological gamblers and non-gamblers. This is different to addiction to alcohol, heroin or cocaine where increases are seen in opioid receptor levels.

All subjects were then given an amphetamine tablet which releases endorphins, which are natural opiates, in the brain and repeated the PET scan. Such a release – called an ‘endorphin rush’- is also thought to happen with alcohol or with exercise.  The PET scan showed that the pathological gamblers released less endorphins than non-gambling volunteers and also that this was associated with the amphetamine inducing less euphoria as reported by the volunteers (using a self-rating questionnaire called the ‘Simplified version of the amphetamine interview rating scale’, or SAIRS).

As lead researcher Dr Inge Mick said:

““From our work, we can say two things. Firstly, the brains of pathological gamblers respond differently to this stimulation than the brains of healthy volunteers. And secondly, it seems that pathological gamblers just don’t get the same feeling of euphoria as do healthy volunteers. This may go some way to explaining why the gambling becomes an addiction”.

“This is the first PET imaging study to look at the involvement of the opioid system in pathological gambling, which is a behavioural addiction. Looking at previous work on other addictions, such as alcoholism, we anticipated that pathological gamblers would have increased opiate receptors which we did not find, but we did find the expected blunted change in endogenous opioids from an amphetamine challenge. These findings suggest the involvement of the opioid system in pathological gambling and that it may differ from addiction to substances such as alcohol. We hope that in the long run this can help us to develop new approaches to treat pathological gambling”

Speaking on behalf of the ECNP, Professor Wim van den Brink (Amsterdam), Chair of the Scientific Committee for the Berlin Congress, said:

“At the moment, we find that treatment with opioid antagonists such as naltrexone and nalmefene seem to have a positive effect in the treatment of pathological gambling, and that the best results of these medications are obtained in those problem gamblers with a family history of alcohol dependence. But this report from Dr Mick and colleagues is interesting work, and if confirmed it could open doors to new treatment methods for pathological gamblers”.

Reducing brain activity improves memory after cognitive decline

A study led by a Johns Hopkins neuroscientist and published in the May 10 issue of the journal Neuron suggests a potential new therapeutic approach for improving memory and interrupting disease progression in patients with a form of cognitive impairment that often leads to full-blown Alzheimer's disease. The focus of the study was "excess brain activity" commonly associated with conditions that cause mild cognitive decline and memory loss, and are linked to an increased risk of Alzheimer's. Previously, it had been thought that this neural hyperactivity in the hippocampus was the brain's attempt to compensate for a weakness in forming new memories. Instead, the team found that this excess activity is contributing to conditions such as amnestic mild cognitive impairment (aMCI), in which patients' memories are worse than would be expected in healthy people the same age.

"In the case of aMCI, it has been suggested that the increased hippocampal activation may serve a beneficial function by recruiting additional neural 'resources' to compensate for those that are lost," explains lead author Michela Gallagher, the Krieger-Eisenhower Professor of Psychological and Brain Sciences in the Johns Hopkins University's Krieger School of Arts and Sciences. "However, animal studies have raised the alternative view that this excess activation may be contributing to memory impairment."

To test how a reduction in that hippocampal activity would affect human patients with aMCI, Gallagher's team administered a low dose of a drug clinically used to treat epilepsy. The goal was to reduce the test subjects' activity to levels that were similar to those of healthy, age-matched subjects in a control group. They used functional magnetic resonance imaging both to determine the levels of excess activity, and the reduction of it by way of the drug.

Gallagher and her team found that those subjects who had been treated with an effective dose of the drug did better on a memory task, pointing to the therapeutic potential of reducing this excess activation of the hippocampus in patients with aMCI. These findings in human patients with aMCI are the first to clinically demonstrate that over activity in the hippocampus has no benefit for cognition, and are consistent with Gallagher's research in an animal model of memory loss: aged rodents.

The findings may have broad clinical implications because increased hippocampal activation occurs not only in patients with aMCI, but also in other conditions of risk, such as familial Alzheimer's disease (AD).

Research in mouse models of familial AD conducted at the Gladstone Institutes of San Francisco has identified mechanisms of the brain that contribute to abnormal excitatory brain activity, as reported in a paper published in the April 27 issue of the journal Cell. In addition, the results of other studies in mice using the same drug used in aMCI patients were presented at last year's International Congress on Alzheimer's disease in Paris, showing both improved memory performance and neuronal function in the hippocampus.

"From both a scientific and clinical perspective, I am thrilled about the consistency of findings obtained in aMCI patients and related animal models," said Lennart Mucke, director of the Gladstone Institute of Neurological Disease and professor of neurology and neuroscience at the University of California San Francisco.

According to Gallagher, the elevated hippocampal activity observed in conditions that precede AD may be one of the underlying mechanisms contributing to neurodegeneration and memory loss. Studies have found that if patients with aMCI are followed for a number of years, those with the greatest excess activation have the greatest further decline in memory, and are more likely to receive a diagnosis of Alzheimer's over the next four to six years.

"Apart from a direct role in memory impairment, there is concern that elevated activity in vulnerable neural networks could be causing additional damage and possibly promoting the widespread disease-related degeneration that underlies cognitive decline and the conversion to Alzheimer's disease," says Gallagher. "Therefore, reducing the elevated activity in the hippocampus may help to restore memory and protect the brain. It will require a carefully monitored, lengthier clinical trial to determine if that is the case."

The team that conducted the Johns Hopkins study included Arnold Bakker, Greg Krauss, Marilyn Albert, Carolyn Speck, Lauren Jones, Michael Yassa, Amy Shelton and Susan Bassett. The team also included Craig Stark of the University of California at Irvine.

*Source: Johns Hopkins

Nanoparticles Home in On Brain Tumors, Boost Accuracy of Surgical Removal

Like special-forces troops laser-tagging targets for a bomber pilot, tiny particles that can be imaged three different ways at once have enabled Stanford University School of Medicine scientists to remove brain tumors from mice with unprecedented accuracy.

In a study published online April 15 in Nature Medicine, a team led by Sam Gambhir, MD, PhD, professor and chair of radiology, showed that the minuscule nanoparticles engineered in his lab homed in on and highlighted brain tumors, precisely delineating their boundaries and greatly easing their complete removal. The new technique could someday help improve the prognosis of patients with deadly brain cancers.
About 14,000 people are diagnosed annually with brain cancer in the United States. Of those cases, about 3,000 are glioblastomas, the most aggressive form of brain tumor. The prognosis for glioblastoma is bleak: the median survival time without treatment is three months. Surgical removal of such tumors -- a virtual imperative whenever possible -- prolongs the typical patient's survival by less than a year. One big reason for this is that it is almost impossible for even the most skilled neurosurgeon to remove the entire tumor while sparing normal brain.
"With brain tumors, surgeons don't have the luxury of removing large amounts of surrounding normal brain tissue to be sure no cancer cells are left," said Gambhir, who is the Virginia and D.K. Ludwig Professor for Clinical Investigation in Cancer Research and director of the Molecular Imaging Program at Stanford. "You clearly have to leave as much of the healthy brain intact as you possibly can."
This is a real problem for glioblastomas, which are particularly rough-edged tumors. In these tumors, tiny fingerlike projections commonly infiltrate healthy tissues, following the paths of blood vessels and nerve tracts. An additional challenge is posed by micrometastases: minuscule tumor patches caused by the migration and replication of cells from the primary tumor. Micrometastases dotting otherwise healthy nearby tissue but invisible to the surgeon's naked eye can burgeon into new tumors.
Although brain surgery today tends to be guided by the surgeon's naked eye, new molecular imaging methods could change that, and this study demonstrates the potential of using high-technology nanoparticles to highlight tumor tissue before and during brain surgery.
The nanoparticles used in the study are essentially tiny gold balls coated with imaging reagents. Each nanoparticle measures less than five one-millionths of an inch in diameter -- about one-sixtieth that of a human red blood cell.
"We hypothesized that these particles, injected intravenously, would preferentially home in on tumors but not healthy brain tissue," said Gambhir, who is also a member of the Stanford Cancer Institute. "The tiny blood vessels that feed a brain tumor are leaky, so we hoped that the spheres would bleed out of these vessels and lodge in nearby tumor material." The particles' gold cores, enhanced as they are by specialized coatings, would then render the particles simultaneously visible to three distinct methods of imaging, each contributing uniquely to an improved surgical outcome.
One of those methods, magnetic resonance imaging, is already frequently used to give surgeons an idea of where in the brain the tumor resides before they operate. MRI is well-equipped to determine a tumor's boundaries, but when used preoperatively it can't perfectly describe an aggressively growing tumor's position within a subtly dynamic brain at the time the operation itself takes place.

**Published in "SCIENCE DAILY"

Distinct Brain Cells Recognize Novel Sights

The brain's ability to learn to recognize objects plays out in the inferior temporal cortex. A new study offers a possible explanation of how two classes of neurons play distinct roles to help that happen.

No matter what novel objects we come to behold, our brains effortlessly take us from an initial "What's that?" to "Oh, that old thing" after a few casual encounters. In research that helps shed light on the malleability of this recognition process, Brown University neuroscientists have teased apart the potentially different roles that two distinct cell types may play.
In a study published online in advance in the journal Neuron, the researchers document that this kind of learning is based in the inferior temporal cortex (ITC), a brain area buried deep in the skull. Scientists already knew the area was important for visual recognition of familiar items, but they hadn't figured out the steps required to move from novelty to familiarity, a process they refer to as "plasticity."
"We know little about that because of the level at which this plasticity is taking place," said senior author David Sheinberg, professor of neuroscience and a member of the Brown Institute for Brain Science. "The inner workings made up of individual neurons make it very hard to actually track what's going on at that level."
Working with two monkeys, in whom they monitored single neuron activity using tiny microelectrodes, Sheinberg and graduate student Luke Woloszyn tracked the firing patterns of individual neurons in the ITC while monkeys viewed 125 objects they had been trained to recognize and 125 others that they had never seen before.
The scientists found that the two major classes of cells found in the brain, excitatory and inhibitory, responded differently depending on what the monkeys saw. Excitatory neurons were especially active when the monkeys saw a preferred familiar object -- the familiar image, out of the 125 such images, that the cell "liked" best. Although the particular preferred familiar image varied across the sample of neurons, almost every excitatory cell had at least one familiar image to which it responded more robustly than its preferred novel image, Sheinberg said. Inhibitory neurons, meanwhile, were much more active when the monkeys saw any novel image, independent of the object's actual identity.
Woloszyn and Sheinberg were able to distinguish between the neuron classes by the shapes of the voltage changes picked up by the microelectrodes. Excitatory neurons had characteristically broad spikes, while inhibitory neurons had narrower spikes.
Not only did the researchers see differences in what made the neurons respond, but also in when they did so. Excitatory neurons peaked in activity within 100 milliseconds to their preferred familiar objects, for example, while inhibitory neurons responded to a broad set of novel objects over a wider timeframe of up to 325 milliseconds.
Sheinberg speculated that the different roles of the cells and the specific timing of their responses might be explained by the following interplay: When the monkey sees something familiar (banana!), excitatory neurons fire to signal recognition, sending that signal to other parts of the brain to drive the appropriate behavioral response. But when the monkey sees something unfamiliar (stapler?), the excitatory response is more diffuse, permitting the inhibitory neurons to maintain their elevated activity, which in turn signals a learning event.
"When a familiar object has been recognized, that's a positive signal and that can cause the system to move on," Sheinberg said. "In the absence of that signal, that means the object isn't familiar. What we think is going on is that the ongoing inhibitory activity actually promotes a learning process. It can be a signal to learn."
Another finding is the possible manifestation of that learning. Sheinberg and Woloszyn found considerable significance in their observation that individual excitatory neurons would modulate their firing rate only in response to a few of the images the monkeys saw. This "sparseness" of firing is a measure of the neuron's specialized attention to just a few images.
"What really drove me and Luke along the way was this question of whether ... through repeated exposure, neurons really do specialize in a marked way," Sheinberg said. "The effect of the learning was surprising to me."
They further speculate that the specialization is originally driven by the inhibitory cells.
"We thus propose that the increased activity of our putative inhibitory cells is the neurochemical trigger for the robust selectivity changes within the excitatory population," Sheinberg and Woloszyn wrote in the journal.
The study ties into a separate effort at Brown, Stanford, and other institutions in which a team of scientists is striving to lay the basic science groundwork for ultimately treating people who have suffered traumatic brain injury.
"There is a huge diversity [of neurons] and this diversity could be very important because in the case where you need to repair circuits -- say you've had a stroke, and you want to retrain that area -- it may be that certain cell classes need to be functional in order to support that plasticity," he said. "We're only beginning to appreciate the interplay between these cell types that might support learning and reorganization."
The study was supported by the National Institutes of Health and the National Science Foundation.

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David Sheinberg. Scientists already knew the inferior temporal cortex was important for visual recognition of familiar items, but they hadn’t figured out the steps required to move from novelty to familiarity — “plasticity.” (Credit: Mike Cohea/Brown University)

**Published in "SCIENCE DAILY"

Brain-Injury Data Used to Map Intelligence in the Brain

Scientists report that they have mapped the physical architecture of intelligence in the brain. Theirs is one of the largest and most comprehensive analyses so far of the brain structures vital to general intelligence and to specific aspects of intellectual functioning, such as verbal comprehension and working memory.

Their study, published in Brain: A Journal of Neurology, is unique in that it enlisted an extraordinary pool of volunteer participants: 182 Vietnam veterans with highly localized brain damage from penetrating head injuries.
"It's a significant challenge to find patients (for research) who have brain damage, and even further, it's very hard to find patients who have focal brain damage," said University of Illinois neuroscience professor Aron Barbey, who led the study. Brain damage -- from stroke, for example -- often impairs multiple brain areas, he said, complicating the task of identifying the cognitive contributions of specific brain structures.
But the very focal brain injuries analyzed in the study allowed the researchers "to draw inferences about how specific brain structures are necessary for performance," Barbey said. "By studying how damage to particular brain regions produces specific forms of cognitive impairment, we can map the architecture of the mind, identifying brain structures that are critically important for specific intellectual abilities."
The researchers took CT scans of the participants' brains and administered an extensive battery of cognitive tests. They pooled the CT data to produce a collective map of the cortex, which they divided into more than 3,000 three-dimensional units called voxels. By analyzing multiple patients with damage to a particular voxel or cluster of voxels and comparing their cognitive abilities with those of patients in whom the same structures were intact, the researchers were able to identify brain regions essential to specific cognitive functions, and those structures that contribute significantly to intelligence.
"We found that general intelligence depends on a remarkably circumscribed neural system," Barbey said. "Several brain regions, and the connections between them, were most important for general intelligence."
These structures are located primarily within the left prefrontal cortex (behind the forehead), left temporal cortex (behind the ear) and left parietal cortex (at the top rear of the head) and in "white matter association tracts" that connect them.
The researchers also found that brain regions for planning, self-control and other aspects of executive function overlap to a significant extent with regions vital to general intelligence.
The study provides new evidence that intelligence relies not on one brain region or even the brain as a whole, Barbey said, but involves specific brain areas working together in a coordinated fashion.
"In fact, the particular regions and connections we found support an emerging body of neuroscience evidence indicating that intelligence depends on the brain's ability to integrate information from verbal, visual, spatial and executive processes," he said.
The findings will "open the door to further investigations into the biological basis of intelligence, exploring how the brain, genes, nutrition and the environment together interact to shape the development and continued evolution of the remarkable intellectual abilities that make us human," Barbey said.
The research team also included scientists from Universidad Autónoma de Madrid; Medical Numerics, in Germantown, Md.; George Mason University; the University of Delaware; and the Kessler Foundation, in West Orange, N.J.
The U.S. National Institute of Neurological Disorders and Stroke at the National Institutes of Health provided funding for this research.

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A new study found that specific structures, primarily on the left side of the brain, are vital to general intelligence and executive function (the ability to regulate and control behavior). Brain regions that are associated with general intelligence and executive function are shown in color, with red indicating common areas, orange indicating regions specific to general intelligence, and yellow indicating areas specific to executive function. (Credit: Photo courtesy Aron Barbey)

**Published in "SCIENCE DAILY"