Posts tagged science

April 3, 2012

Approximately 6 million Americans have brain aneurysms, a condition that occurs when a weak or thin spot develops on a blood vessel in the brain causing it to balloon. Often, these do not cause symptoms and go undetected, but every year an estimated 30,000 Americans experience a ruptured aneurysm that bleeds into the brain causing a life threatening injury. Immediate medical treatment is necessary to prevent stroke, nerve damage or death, and includes surgery or coiling. Coiling is an approach that blocks blood flow to the aneurysm by filling it with platinum coils. While less invasive than surgery, the likelihood of future aneurysm recurrence and subsequent treatment is higher with coiling. In an effort to lower the risk for repeat aneurysm treatment after coiling, Northwestern Medicine researchers are examining a new type of gel-coated coil to determine if it is more effective than the standard bare coils in preventing aneurysm recurrence.

Aneurysms can be a very serious health threat, according to Bernard R. Bendok, MD, a neurosurgeon at Northwestern Memorial Hospital, who is the principal investigator for the new generation Hydrogel Endovascular Aneurysm Treatment Trial (HEAT). “When an aneurysm needs treatment, it is important to perform the safest, most effective and most durable treatment. This clinical research trial, called HEAT, will help us determine whether bare platinum coils, which have been used for years, or the newer gel-coated coils are more effective long-term,” said Bendok, who is also an associate professor of neurological surgery and radiology at Northwestern University Feinberg School of Medicine.

Coiling involves inserting a catheter into an artery and threading it through the body using live x-rays as a guide to the site of the aneurysm. Coils are passed through the catheter and released into the aneurysm filling it to block blood from entering. Blood clots then form around the coil preventing the vessels from rupturing or leaking and destroying the aneurysm.

"Coils are not always able to fill the aneurysm completely, which leaves dead space in the aneurysm. This space has been associated with a higher rate of aneurysm recurrence," explained Bendok. "The new coils are made with platinum and a hydrogel that expands over time to eliminate the space between the coils, potentially limiting the need for future treatment."

HEAT is an international randomized study that seeks to determine how the gel packed coils measure up to the standard option in preventing future aneurysm recurrence. Northwestern is the lead site for the trial. Patients may be eligible for the trial if they are between the ages of 18 and 75 years with aneurysms 3 to 14mm in size, amenable to coiling. An estimated 30 sites around the world are expected to join the trial which has an enrollment goal of 600 participants. 

On average aneurysms impact about one percent of the adult population. Understanding symptoms and risk factors can be potentially lifesaving. Small aneurysms may not be associated with symptoms, but a larger, growing aneurysm may cause pressure on tissues and nerves, leading to symptoms including headache, pain above and behind the eye, a dilated pupil, double vision, and weakness, numbness or paralysis on one side of face or body.

"In many cases, brain aneurysms remain silent until there’s a major problem," said Bendok. "Most are not found until they rupture or are found incidentally on brain images taken to assess another condition. The number one sign to look for is a sudden and extremely severe headache. If this occurs, one should seek immediate medical attention."

Other indicators that a person may have a ruptured aneurysm include double vision, nausea, vomiting, stroke-like symptoms, stiff neck, loss of consciousness and in some cases, seizure and changes in memory. Risk factors include hypertension, alcohol and drug abuse, and smoking. Aneurysms can be influenced by genetic factors and family history may be an indication for screening. People with certain hereditary diseases including connective tissue disorders or polycystic kidney disease can have a higher occurrence. Other associations include arteriovenous malformation (AVM) and blockage of certain blood vessels in the brain. Women are more likely than men to have brain aneurysms. It’s estimated about 10 in every 100,000 people will experience a ruptured aneurysm each year.

"Brain aneurysm rupture can be very devastating," said H. Hunt Batjer, MD, chairman of the department of neurological surgery at Northwestern Memorial and Michael J. Marchese Professor of neurological surgery at the Feinberg School. "It’s important to know what to look for and who might be at increased risk for aneurysm disease. While current treatments are effective, trials like HEAT have the potential to advance the art and science of brain aneurysm treatment and lead to even better treatment options in the future."

Provided by Northwestern Memorial Hospital

Source: medicalxpress.com

April 3, 2012 By Miles O’ Brien and Jon Baime

(Medical Xpress) — It’s a chilling thought—losing the sense of sight because of severe injury or damage to the brain’s visual cortex. But, is it possible to train a damaged or injured brain to “see” again after such a catastrophic injury? Yes, according to Tony Ro, a neuroscientist at the City College of New York, who is artificially recreating a condition called blindsight in his lab.

"Blindsight is a condition that some patients experience after having damage to the primary visual cortex in the back of their brains. What happens in these patients is they go cortically blind, yet they can still discriminate visual information, albeit without any awareness." explains Ro.

[Video]

While no one is ever going to say blindsight is 20/20, Ro says it holds tantalizing clues to the architecture of the brain. “There are a lot of areas in the brain that are involved with processing visual information, but without any visual awareness.” he points out. “These other parts of the brain receive input from the eyes, but they’re not allowing us to access it consciously.”

With support from the National Science Foundation’s (NSF) Directorate for Social, Behavioral and Economic Sciences, Ro is developing a clearer picture of how other parts of the brain, besides the visual cortex, respond to visual stimuli.

In order to recreate blindsight, Ro must find a volunteer who is willing to temporarily be blinded by having a powerful magnetic pulse shot right into their visual cortex. The magnetic blast disables the visual cortex and blinds the person for a split second. “That blindness occurs very shortly and very rapidly—on the order of one twentieth of a second or so,” says Ro.

On the day of Science Nation’s visit to Ro’s lab in the Hamilton Heights section of Manhattan, volunteer Lei Ai is seated in a small booth in front of a computer with instructions to keep his eyes on the screen. A round device is placed on the back of Ai’s head. Then, the booth is filled with the sound of consistent clicks, about two seconds apart. Each click is a magnetic pulse disrupting the activity in his visual cortex, blinding him. Just as the pulse blinds him, a shape, such as a diamond or a square, flashes onto a computer screen in front of him.

Ro says that 60 to nearly 100 percent of the time, test subjects report back the shape correctly. “They’ll be significantly above chance levels at discriminating those shapes, even though they’re unaware of them. Sometimes they’re nearly perfect at it,” he adds.

Ro observes what happens to other areas of Ai’s brain during the instant he is blinded and a shape is flashed on the screen. While the blindness wears off immediately with no lasting effects, according to Ro, the findings are telling. “There are likely to be a lot of alternative visual pathways that go into the brain from our eyes that process information at unconscious levels,” he says.

Ro believes understanding and mapping those alternative pathways might be the key to new rehabilitative therapies. “We have a lot of soldiers returning home who have a lot of brain damage to visual areas of the brain. We might be able to rehabilitate these patients,” he says. And that’s something worth looking into.

Provided by National Science Foundation

Source: medicalxpress.com

April 3, 2012

The brains of people with anorexia and obesity are wired differently, according to new research. Neuroscientists for the first time have found that how our brains respond to food differs across a spectrum of eating behaviors – from extreme overeating to food deprivation. This study is one of several new approaches to help better understand and ultimately treat eating disorders and obesity.

Eating disorders have the highest mortality rate of any mental illness. And more than two-thirds of the U.S. population are overweight or obese – a health factor associated with cardiovascular issues, diabetes, and cancer. “This body of work not only increases our understanding of the relationship between food and brain function but can also inform weight loss programs,” says Laura Martin of Hoglund Brain Imaging Center at the University of Kansas Medical Center, one of several researchers whose work being presented today at a meeting of cognitive neuroscientists in Chicago.

"One of the most intriguing aspects of these studies of the brain on food," Martin says, is that they show "consistent activations of reward areas of the brain that are also implicated in studies of addiction." However, how those reward areas respond to food differs between people depending on their eating behaviors, according to the new brain imaging study by Laura Holsen of Harvard Medical School and Brigham and Women’s Hospital and colleagues.

Holsen’s team conducted fMRI brain scans of individuals with one of three eating conditions – anorexia nervosa, simple obesity, and Prader-Willi syndrome (extreme obesity) – as well as healthy control subjects. When hungry, those with anorexia, who severely restrict their food intake, showed substantially decreased responses to various pictures of food in regions of their brains associated with reward and pleasure. For those who chronically overeat, there were significantly increased responses in those same brain regions.

"Our findings provide evidence of an overall continuum relating food intake behavior and weight outcomes to food reward circuitry activity," Holsen says. Her work also has implications, she says, for everyday eating decisions in healthy individuals. "Even in individuals who do not have eating disorders, there are areas of the brain that assist in evaluating the reward value of different foods, which in turn plays a role in the decisions we make about which foods to eat."

Kyle Simmons of the Laureate Institute studies the neural mechanisms that govern such everyday eating decisions. His work with fMRI scans has found that as soon as people see food, their brains automatically gather information about how they think it will taste and how that will make them feel. The brain scans showed an apparent overlap in the region on the insula that responds to seeing food pictures and the region of the insula that processes taste, the “primary gustatory cortex.”

Simmons is currently expanding this work to better understand the differences in taste preferences between lean, healthy individuals and obese ones. “We simply don’t know yet if differences exist between lean and obese participants,” he says. “And knowing which brain regions underlie inferences about food taste and reward is critical if we are going to develop efficacious interventions for obesity and certain eating disorders, both of which are associated with enormous personal and public health costs.”

Provided by Cognitive Neuroscience Society

Source: medicalxpress.com

April 3rd, 2012

For children with autism, being born several weeks early or several weeks late tends to increase the severity of their symptoms, according to new research out of Michigan State University.

Additionally, autistic children who were born either preterm or post-term are more likely to self-injure themselves compared with autistic children born on time, revealed the study by Tammy Movsas of MSU’s Department of Epidemiology.

Though the study did not uncover why there is an increase in autistic symptoms, the reasons may be tied to some of the underlying causes of why a child is born preterm (prior to 37 weeks) or post-term (after 42 weeks) in the first place.

The research appears online in the Journal of Autism and Development Disorders.

Movsas, a postdoctoral epidemiology fellow in MSU’s College of Human Medicine, said the study reveals there are many different manifestations of autism spectrum disorder, a collection of developmental disorders including both autism and Asperger syndrome. It also shows the length of the mother’s pregnancy is one factor affecting the severity of the disorder.

While previous research has linked premature birth to higher rates of autism, this is one of the first studies to look at the severity of the disease among autistic children who had been born early, on time and late.

“We think about autism being caused by a combination of genetic and environmental factors,” she said. “With preterm and post-term babies, there is something underlying that is altering the genetic expression of autism.

“The outside environment in which a preterm baby continues to mature is very different than the environment that the baby would have experienced in utero. This change in environment may be part of the reason why there is a difference in autistic severity in this set of infants.”

Movsas added that for post-term babies, the longer exposure to hormones while a baby is in utero, the higher chance of placental malfunction and the increased rate of C-section and instrument-assisted births may play a role.

The study also found that babies born outside of normal gestational age (40 weeks) – specifically very preterm babies – showed an increase in stereotypical autistic mannerisms.

“Normal gestation age of birth seems to mitigate the severity of autism spectrum disorder symptoms, and the types of autistic traits tend to be different depending on age at birth,” she said.

The study analyzed an online database compiled by Kennedy Krieger Institute at Johns Hopkins University of nearly 4,200 mothers – with autistic children ages 4-21 – between 2006 and 2010. It divided the data on births into four categories: very preterm (born prior to 34 weeks); preterm (34 to 37 weeks); standard (37 to 42 weeks); and post-term (born after 42 weeks)

The mothers filled out a pair of questionnaires regarding the symptoms of their autistic children, and the results revealed very preterm, preterm and post-term autistic children had significantly higher screening scores for autism spectrum disorder than autistic children born full term.

“The findings point to the fact that although autism has a strong genetic component, something about pregnancy or the perinatal period may affect how autism manifests,” said Nigel Paneth, an MSU epidemiologist who worked with Movsas on the paper. “This adds to our earlier finding that prematurity is a major risk factor for autism spectrum disorder and may help us understand if anything can be done during early life to prevent or alleviate autism spectrum disorder.”

Source: Neuroscience News

April 2, 2012

New research confirms that childhood onset temporal lobe epilepsy has a significant impact on brain aging. Study findings published in Epilepsia, a peer-reviewed journal of the International League Against Epilepsy (ILAE), show age-accelerated ventricular expansion outside the normal range in this patient population.

According to the Centers for Disease Control and Prevention (CDC), epilepsy affects nearly 2 million Americans. Temporal lobe epilepsy is the most common form of partial epilepsy, with 60% of all patients having this form of the disease. Previous evidence suggests that patients with childhood onset epilepsy have significant cognitive and developmental deficiencies, which continue into adulthood, particularly in those resistant to antiepileptic drugs.

Prior imaging studies of patients with temporal lobe epilepsy have shown abnormalities in brain structure in hippocampus, in thalamus and other subcortical structures, and also in cortical and white matter volume. However, there is limited knowledge of the effects of aging on these structural changes.

To characterize differences in brain structure and patterns of age-related change, Dr. Bruce Hermann and colleagues from the University of Wisconsin-Madison recruited 55 patients with chronic temporal lobe epilepsy and 53 healthy controls for their study. Participants were between the ages of 14 and 60, with patients having mean age of onset of epilepsy in childhood/adolescence. Magnetic resonance imaging (MRI) was used to measure cortical thickness, area and volume in the brains of all subjects.

In participants with epilepsy, there were extensive abnormalities in brain structure, involving subcortical regions, cerebellum and cortical gray matter thickness and volume in the temporal and extratemporal lobes. Furthermore, researchers found that increasing chronological age was associated with progressive changes in cortical, subcortical and cerebellar regions for both epilepsy subjects and healthy controls. The pattern of change was similar for both groups, but epilepsy patients always showed more extensive abnormalities. In particular, epilepsy patients displayed age-accelerated expansion of the lateral and third ventricles. “The anatomic abnormalities in patients with epilepsy indicate a significant neurodevelopmental impact,” said Dr. Hermann.

"Patients with epilepsy are burdened with significant neurodevelopmental challenges due to these cumulative brain abnormalities," concludes Dr. Hermann. "The consequences of these anatomical changes for epilepsy patients as they progress into elder years remain unknown and further study of the adverse effects in those of older chronological age is needed."

Provided by Wiley

Source: medicalxpress.com

April 2, 2012

One of the most frustrating challenges for some stroke patients can be the inability to find and speak words even if they know what they want to say. Speech therapy is laborious and can take months. New research is seeking to cut that time significantly, with the help of non-invasive brain stimulation.

"Non-invasive brain stimulation can allow painless, inexpensive, and apparently safe method for cognitive improvement with with potential long term efficacy," says Roi Cohen Kadosh of the University of Oxford. Recent results, presented this week at a meeting of cognitive neuroscientists in Chicago, offer exciting possibilities for improving variety of abilities – from speech to memory to numerical proficiency.

A focus of many of these studies is tDCS – transcranial direct current stimulation. In tDCS, researchers apply weak electrical currents to the head via electrodes for a short period of time, for example 20 minutes. The currents pass through the skull and alter spontaneous neural activity. Some types of stimulation excite the neurons, while others suppress them. Subjects usually feel only a slight tingling for less than 30 seconds. The effects of tDCS can last for up to 12 months, Cohen Kadosh says, “most likely due to molecular and cellular changes that are important mechanisms implementing learning and memory.”

Stimulating speech recovery

For Jenny Crinion of University College London, who is both a neuroscientist and clinical speech and language therapist, the interest in tDCS sprang from a desire to help stroke patients through their long recovery. While speech therapy works well at improving speech following aphasic stroke, it can be frustratingly slow. She hopes to pair brain-stimulation interventions with proven language-rehabilitation methods, Crinion says, “such that the same maximum recovery is ultimately achieved as with therapy alone but with fewer hours of rehab.”

Crinion’s current work focuses on understanding how tDCS affects the areas of the brain involved in speech production. She paired an fMRI picture-naming study with a 6-week-long tDCS and word-finding treatment study to see if brain stimulation could improve stroke patients’ speech both immediately after treatment and three months later. In the picture-naming task, people were presented with pictures of simple, everyday words such as car and asked to name them as quickly and accurately as possible.

Read more …

April 2, 2012

Sleep plays a powerful role in preserving our memories. But while recent research shows that wakefulness may cloud memories of negative or traumatic events, a new study has found that wakefulness also degrades positive memories. Sleep, it seems, protects positive memories just as it does negative ones, and that has important implications for the treatment of post-traumatic stress disorder.

"The study of how sleep helps us remember and process emotional information is still young," says Alexis Chambers of the University of Notre Dame. Past work has focused on the role of negative memories for sleep, in particular how insomnia is a healthy biological response for people to reduce negative memories and emotions associated with a traumatic event.

Two new studies presented this week at a meeting of cognitive neuroscientists in Chicago are exploring the flip side: how sleep treats the positive. “Only if we investigate all the possibilities within this field will we ever fully understand the processes underlying our sleep, memory, and emotions,” Chambers says.

Protecting the positive

To test how sleep affects positive memories, Rebecca Spencer of the University of Massachusetts, Amherst, and her colleagues split 70 young adults into two groups, one that got to sleep overnight and one that had to stay awake. Both groups viewed images of positive items, such as puppies and flowers, and neutral items, such as furniture or dinner plates. The researchers then tested the participants’ memories of and emotional reactions to the images 12 hours later, after either the period of sleep or wake.

They found that “sleep enhances our emotionally positive memories while these memories decay over wake,” Spencer says. “Positive memories may even be prioritized for processing during sleep.” But while people remembered the positive images more than the neutral ones, their emotional response to the positive images did not change over sleep versus wake. “It doesn’t matter if you went to sleep or stayed awake – what you thought was a ‘9’ – really great – you still think is a ‘9’,” she says. 

Read more …

April 2, 2012

(Medical Xpress) — A research team including University of Wyoming neurobiologist Jeff Woodbury has discovered a new technique to determine how the touch sensory system is organized in hairy skin, providing a new understanding of the sense of touch.

The journal Cell’s cover story features research findings by University of Wyoming neurobiologist Jeff Woodbury. He was part of a research team that is providing a new understanding of the sense of touch.

Their findings were selected to appear as the feature and cover article in Cell, one of the pre-eminent international journals in the biological sciences.

The research provides the first picture of how nerve cells that carry signals from hair on the skin are organized. Unlike all other senses, the skin is least amenable to study and has remained the most poorly understood.

"We have described the system that is in place to help explain how sensory information is processed to perceive the sense of touch," says Woodbury, an associate professor in the UW Department of Zoology and Physiology. He was part of a multidisciplinary research team led by David Ginty from Johns Hopkins University. Colleen Cassidy, a doctoral student in Woodbury’s lab, was a co-author of the study, which also included colleagues from the Howard Hughes Medical Institute at Rockefeller University, University of Pennsylvania and University of Pittsburgh.

"We have also been able to identify how combinations of nerve cells respond to fine-tactile stimuli, so we can now really begin to tease apart the circuitry of touch sensation," Woodbury adds. "One of the real breakthroughs is that, for the first time in more than 200 years of study, we now know the specific functions of some of the many different kinds of nerve endings in the skin. This is truly exciting and a major advance."

Mice have several different types of hair follicles in their coat, each of which is linked to the central nervous system by low-threshold wire-like nerve cells that stretch all the way to the spinal cord. There, the myriad signals carried from the skin are integrated, processed and sent to the brain.

This network of nerve endings in the skin of most hairy mammals, including humans, allows them to perceive fine tactile sensations, such as a drop of rain or an insect landing on their skin. The researchers now have a better understanding of how this complex system is organized. Before this discovery, Woodbury says there was no way to see how all of these different nerve cells were arranged — both in the skin and at the top of the spinal cord, where they end up.

The study, Woodbury says, opens doors to understanding not only touch, but skin senses such as temperature detection and pain.

"Touch is ultimately felt in the brain; it alerts us that something is going on," he says. "We have identified the logic of how this system is organized. We now know that each individual hair is a distinct sensory organ, and each one will detect different forces. A broad spectrum of frequencies within a given stimulus are ultimately recombined and analyzed until we become aware that something has happened, like a drop of rain or a light breeze."

Once the different sensory neurons are identified, researchers could test hypotheses about the role of these cells in the process of sensation.

"For example, researchers could study the animal, in the presence or absence of each of the different types of sensory cells, to determine differences in the animal’s behavior," Woodbury says. "It will be possible to shut them off, take them out of the picture, to see how the animal responds to different types of stimulation. The key to understanding any system is first to gain a marker to identify all the different components, and we have made a major step in that direction."

Provided by University of Wyoming

Source: medicalxpress.com

April 2, 2012

New research published in the April issue of The Journal of Nuclear Medicine reveals that systemic inflammation causes an increase in depressive symptoms and metabolic changes in the parts of the brain responsible for mood and motivation. With this finding, researchers can begin to test potential treatments for depression for patients that experience symptoms that are related to inflammation in the body or within the brain.

Multiple studies in rodents have shown that inflammation in the body has effects on the brain. This has also been shown in a few human studies—both through measurements of behavioral changes and brain imaging—when subjects were engaged in various computer tasks. The study “Glucose Metabolism in the Insula and Cingulate Is Affected by Systemic Inflammation in Humans,” however, for the first time measured brain activity when subjects were at rest.

"In the study we used F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET), which can accurately measure glucose metabolism in the brain, to determine which brain regions responded to systemic inflammation. Since the subjects were at rest, the changes we observed in the brain can only attributed to systemic inflammation," noted Jonas Hannestad, MD, PhD, lead author of the article.

In the study, nine healthy individuals received a double-blind endotoxin (which elicits systemic inflammation and mild depressive symptoms such as fatigue and reduced social interest) and placebo on different days. After administration, F-18 FDG PET was used to measure the differences in the cerebral metabolic rate of glucose in the insula, cingulate and amygdala regions of the brain. Behavior changes were also primarily assessed on the Montgomery-Asberg Depression Rating Scale (MADRS).

A statistical analysis of the results showed that endotoxin administration was associated with a higher normalized glucose metabolism (NMG) in the insula and lower NMG in the cingulate compared to the placebo; there was no significant difference in the NMG in the amygdala. Seven of nine subjects had an increase in NMG in the insula and a decrease in NMG in the cingulate, and all nine subjects had a decrease in NMG in the right anterior cingulate, suggesting that systemic inflammation induces fundamental physiologic changes in regional brain glucose metabolism. In addition, the MADRS increased for each subject after endotoxin administration, whereas no significant change was noted with the placebo.

Most researchers agree that depression is not a homogeneous disease, but rather that there are multiple mechanisms that can lead to similar symptoms. “If we can show that a subtype of depression is caused in part by inflammation,” said Hannestad, “we can test the ability of treatments that reduce inflammation in only patients in whom we believe inflammation plays a role. In the future, I expect that researchers in this field will be able to develop more precise PET measures that can be used to distinguish between, for instance, a person with ‘inflammatory depression’ and a person with another kind of depression. PET could then be used as diagnostic biomarker to separate subtypes of depression and as a therapeutic biomarker to detect the response to treatment.”

Nearly 17 percent of adults experience depression at some point over their lifetime, with 30.4 percent of cases classified as severe, according to the U.S. National Institute of Mental Health. Fifty-seven percent of adults with depression report receiving treatment in the past 12 months, although 37.8 percent receive minimally adequate treatment.

Provided by Society of Nuclear Medicine

Source: medicalxpress.com

April 2, 2012

A team of University of Pittsburgh mathematicians is using computational models to better understand how the structure of neural variability relates to such functions as short-term memory and decision making. In a paper published online April 2 in Proceedings of the National Academy of Sciences (PNAS), the Pitt team examines how fluctuations in brain activity can impact the dynamics of cognitive tasks.

Previous recordings of neural activity during simple cognitive tasks show a tremendous amount of trial-to-trial variability. For example, when a person was instructed to hold the same stimulus in working, or short-term, memory during two separate trials, the brain cells involved in the task showed very different activity during the two trials.

"A big challenge in neuroscience is translating variability expressed at the cellular and brain-circuit level with that in cognitive behaviors," said Brent Doiron, assistant professor of mathematics in Pitt’s Kenneth P. Dietrich School of Arts and Sciences and the project’s principal investigator. "It’s a fact that short-term memory degrades over time. If you try to recall a stored memory, there likely will be errors, and these cognitive imperfections increase the longer that short-term memory is engaged."

Doiron explains that brain cells increase activity during short-term memory functions. But this activity randomly drifts over time as a result of stochastic (or chance) forces in the brain. This drifting is what Doiron’s team is trying to better understand.

"As mathematicians, what we’re really trying to do is relate the structure and dynamics of this stochastic variability of brain activity to the variability in cognitive performance," said Doiron. "Linking the variability at these two levels will give important clues about the neural mechanisms that support cognition."

Using a combination of statistical mechanics and nonlinear system theory, the Pitt team examined the responses of a model of a simplified memory network proposed to be operative in the prefrontal cortex. When sources of neural variability were distributed over the entire network, as opposed to only over subsections, the performance of the memory network was enhanced. This helped the Pitt team make the prediction published in PNAS, that brain wiring affects how neural networks contend with—and ultimately express—variability in memory and decision making.

Recently, experimental neurosciencists are getting a better understanding of how the brain is wired, and theories like those published in PNAS by Doiron’s group give a context for their findings within a cognitive framework. The Doiron group plans to apply the general principle of linking brain circuitry to neural variability in a variety of sensory, motor, and memory/decision-making frameworks.

Provided by University of Pittsburgh

Source: medicalxpress.com