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Sleep Patterns Uncovered Using Smartphone Application
By Jason von Stietz, M.A.
May 31, 2016
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What is the powerful influencer of our sleep patterns? Circadian rhythms? The needs and demands of society? Why is jet lag so difficult to overcome? Researchers from University of Michigan studied sleep patterns by employing a free app. The findings were discussed in a recent article in Medical Xpress:  

 

A pioneering study of worldwide sleep patterns combines math modeling, mobile apps and big data to parse the roles society and biology each play in setting sleep schedules.

 

The study, led by University of Michigan mathematicians, used a free smartphone app that reduces jetlag to gather robust sleep data from thousands of people in 100 nations. The researchers examined how age, gender, amount of light and home country affect the amount of shut-eye people around the globe get, when they go to bed, and when they wake up.

 

Among their findings is that cultural pressures can override natural circadian rhythms, with the effects showing up most markedly at bedtime. While morning responsibilities like work, kids and school play a role in wake-time, the researchers say they're not the only factor. Population-level trends agree with what they would expect from current knowledge of the circadian clock.

 

"Across the board, it appears that society governs bedtime and one's internal clock governs wake time, and a later bedtime is linked to a loss of sleep," said Daniel Forger, who holds faculty positions in mathematics at the U-M College of Literature, Science, and the Arts, and in the U-M Medical School's Department of Computational Medicine and Bioinformatics. "At the same time, we found a strong wake-time effect from users' biological clocks—not just their alarm clocks. These findings help to quantify the tug-of-war between solar and social timekeeping."

 

When Forger talks about internal or biological clocks, he's referring to circadian rhythms—fluctuations in bodily functions and behaviors that are tied to the planet's 24-hour day. These rhythms are set by a grain-of-rice-sized cluster of 20,000 neurons behind the eyes. They're regulated by the amount of light, particularly sunlight, our eyes take in.

 

Circadian rhythms have long been thought to be the primary driver of sleep schedules, even since the advent of artificial light and 9-to-5 work schedules. The new research helps to quantify the role that society plays.

 

Here's how Forger and colleague Olivia Walch arrived at their findings. Several years ago, they released an app called Entrain that helps travelers adjust to new time zones. It recommends custom schedules of light and darkness. To use the app, you have to plug in your typical hours of sleep and light exposure, and are given the option of submitting your information anonymously to U-M.

 

The quality of the app's recommendations depended on the accuracy of the users' information, and the researchers say this motivated users to be particularly careful in reporting their lighting history and sleep habits.

 

With information from thousands of people in hand, they then analyzed it for patterns. Any correlations that bubbled up, they put to the test in what amounts to a circadian rhythm simulator. The simulator—a mathematical model—is based on the field's deep knowledge of how light affects the brain's suprachiasmatic nucleus (that's the cluster of neurons behind the eyes that regulates our internal clocks). With the model, the researchers could dial the sun up and down at will to see if the correlations still held in extreme conditions.

 

"In the real world, bedtime doesn't behave how it does in our model universe," Walch said. "What the model is missing is how society affects that."

 

The spread of national averages of sleep duration ranged from a minimum of around 7 hours, 24 minutes of sleep for residents of Singapore and Japan to a maximum of 8 hours, 12 minutes for those in the Netherlands. That's not a huge window, but the researchers say every half hour of sleep makes a big difference in terms of cognitive function and long-term health.

 

The findings, the researchers say, point to an important lever for the sleep-deprived—a set that the Centers for Disease Control and Prevention is concerned about. A recent CDC study found that across the U.S., one in three adults aren't getting the recommended minimum of seven hours. Sleep deprivation, the CDC says, increases the risk of obesity, diabetes, high blood pressure, heart disease, stroke and stress.

 

The U-M researchers also found that:

 

  • Middle-aged men get the least sleep, often getting less than the recommended 7 to 8 hours.
  • Women schedule more sleep than men, about 30 minutes more on average. They go to bed a bit earlier and wake up later. This is most pronounced in ages between 30 and 60.
  • People who spend some time in the sunlight each day tend to go to bed earlier and get more sleep than those who spend most of their time in indoor light.
  • Habits converge as we age. Sleep schedules were more similar among the older-than-55 set than those younger than 30, which could be related to a narrowing window in which older individuals can fall and stay asleep.

 

Sleep is more important than a lot of people realize, the researchers say. Even if you get six hours a night, you're still building up a sleep debt, says Walch, doctoral student in the mathematics department and a co-author on the paper.

 

"It doesn't take that many days of not getting enough sleep before you're functionally drunk," she said. "Researchers have figured out that being overly tired can have that effect. And what's terrifying at the same time is that people think they're performing tasks way better than they are. Your performance drops off but your perception of your performance doesn't."

 

Aside from the findings themselves, the researchers say the work demonstrates that mobile technology can be a reliable way to gather massive data sets at very low cost.

 

"This is a cool triumph of citizen science," Forger said.

 

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Role of Frontal Cortex in Perceptual Decision-Making
By Jason von Stietz, M.A.
May 22, 2016
 

 

Why do we sometimes not see what is directly in front of us? Researchers at the Georgia Institute of Technology and University of California Berkeley studied the role of the frontal cortex in perceptual decision-making by utilizing transcranial magnetic stimulation. The study was published in the peer-reviewed journal Proceedings of the National Academy of the Sciences of the United States and later discussed in a recent article in Medical Xpress:  

 

A sportscaster lunges forward. "Interception! Drew Brees threw the ball right into the opposing linebacker's hands! Like he didn't even see him!"

 

The quarterback likely actually did not see the defender standing right in front of him, said Dobromir Rahnev, a psychologist at the Georgia Institute of Technology. Rahnev leads a research team making new discoveries about how the brain organizes visual perception, including how it leaves things out even when they're plainly in sight.

 

Rahnev and researchers from the University of California, Berkeley have come up with a rough map of the frontal cortex's role in controlling vision. They published their findings on Monday, May 9, 2016 in the journal of theProceedings of the National Academy of Sciences.

 

Thinking cap

 

The frontal cortex is often seen as our "thinking cap," the part of the brain scientists associate with thinking and making decisions. But it's not commonly connected with vision. "Some people believe that the frontal cortex is not involved," said Rahnev, an assistant professor at the School of Psychology. The new research adds to previous evidence that it is, he said.

 

The lack of association with that part of the brain may have to do with the fact it's other parts that transform information coming from the eyes into sight and others still that make sense of it by doing things like identifying objects in it.

 

But the thinking cap of the brain controls and oversees this whole process, making it as essential to how we see as those other areas, Rahnev said. How that works also accounts for why we sometimes miss things right in front of us.

 

A camera it's not

 

"We feel that our vision is like a camera, but that is utterly wrong," Rahnev said. "Our brains aren't just seeing, they're actively constructing the visual scene and making decisions about it." Sometimes the frontal cortex isn't expecting to see something, so although it's in plain sight, it blots it out of consciousness.

 

To test out the fontal cortex's involvement in vision, the researchers ran a two-part experiment.

 

First, they observed which regions of the brain—in particular the frontal cortex—lit up with activity while healthy volunteers completed visual tasks corresponding to three basic stages of conscious visual perception.

 

Second, they inhibited those same regions using magnetic stimulation to confirm their involvement in each visual stage.

 

Believing is part of seeing

 

The first stage of the visual perception the researchers tested for was selection, Rahnev said. That's when the brain picks out part of the vast array of available visual stimuli to actually pay attention to.

 

In the case of the football quarterback, this might mean focusing on the route the receiver takes.

 

The second stage is combination, he said. The brain merges the visual information it processed with other material. "The quarterback's brain is putting what he actually sees together with expectations based on the play he called," Rahnev said.

 

Then comes evaluation. The quarterback needs to decide whether to release the ball given everything he has processed.

 

Expecting a blocker to stop the defending player (which didn't happen), he may have blotted him out of perception and thrown the ball right at him. Interception.

 

"The frontal cortex sends a signal to move your attention onto the object you select," Rahnev said. "It does some of the combining with other information, and then it's probably the primary evaluator of what you think you saw."

 

Simple vision brain map

 

In experiments, during a functional MRI scan, different parts of the frontal cortex of the participants lit up, corresponding to each vision function.

 

The back of the frontal cortex activated during selection; its midsection lit up during combination, and the front, or anterior, part cranked up during evaluation.

 

That's how the researchers arrived at a kind of vision map of the frontal cortex. "It's a rudimentary map," Rahnev said. "A very simple one that just says, 'This is the back. This in the middle. This is the front.'"

 

The critical evidence

 

The critical evidence for this map came from the use of magnetic stimulation. When the researchers used it to inhibit the back and middle of the frontal cortex separately, subjects became less able to complete the corresponding functions of selection and combination.

 

When they stimulated the front, the opposite happened. Subjects were slightly but significantly better able to evaluate the accuracy of what they think they saw.

 

"This is a really clear demonstration of the role that the frontal cortex, which is usually seen as the seat of thought, plays in controlling vision."

 

Sorry officer!

 

And there is a practical takeaway for health and safety. Instead of the quarterback telling the coach, "I swear I didn't see that coming," often it's motorists telling police officers the same thing after a car accident.

 

Distraction is often the culprit, because it overtaxes the organization of perception, Rahnev said. These three functions are going on all the time in multiple scenarios in our brains while it processes the world around us.

 

But add too much to the pile, like texting behind the wheel, Rahnev said, and "you can run right into a parked car without ever seeing it."

 

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Do Mirror Neurons Influence Action Recognition?
By Jason von Stietz, M.A.
May 20, 2016
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Mirror neurons are thought to be the switching point between visual and motor centers in the brain. Mirror neurons help our brain to interpret the actions of others. When someone raises a fist toward us do they mean to give us a friendly greeting (fist bump) or do they mean to attack us? Researchers at the Max Plank Institute studied the role of mirror neurons in action recognition. The study was discussed in a recent article in Medical Xpress: 

 

It is suspected that mirror neurons enable us to empathize and put ourselves 'in other people's shoes'. When we see that someone has been injured, we also experience internal suffering: these special neurons cause what we see to be simulated in our brain in a way that makes us feel as though we are experiencing it in our own bodies.

 

In perception research, it is assumed that mirror neurons enable people go through a movement they have seen in their own motor system. This internal recreation of what we have seen probably enables us to infer the meaning of the observed action. The mirror neurons act as the switching point between the motor and visual areas of the brain. Conversely, when the motor system is supposed to be the determining factor in the classification of an action, it means that the perception can also be manipulated by our own implementation of an action.

 

Attack or greeting?

 

In their study, the researchers analyzed the mechanism by which the brain recognizes an action. To do this, they showed the test subjects two different movements: a punch and a greeting gesture known as the 'fist bump', practised by young men in particular. The researchers arranged the scenario as realistically as possible. A life-sized avatar was shown on a screen facing the test subjects. Using 3D glasses, the subjects were able to see their virtual partners in three dimensions – the avatar's movements appeared as though they were unfolding within the test subjects' reach.

 

All the test subjects were required to do was to decide whether they were being presented with an aggressive punch or well-intentioned greeting. However, the scientists made the conditions more difficult by combining the two gestures in a single movement. The avatar's intentions were thus a matter of interpretation.

 

The question behind the experiment then was whether people allow themselves to be influenced by their own motor system when interpreting the actions of others. The test subjects were manipulated in different ways in the experiment: they could observe a clearly identifiable action played in a continuous loop on a screen. They became active at the same time themselves by carrying out air punches, for example. They were then asked to assess how the indefinable movement of the avatar should be interpreted.

 

I only believe what I also see

 

When the two sensory stimuli were played out against each other – that is the test subjects saw a fist bump in front of them while carrying out a punch movement themselves – the visual impression was the clear winner. The subject's own movement did not have any influence on the perception. Contrary to what was previously assumed, the motor system had little or no influence on the participants' assessment of the movement. To the astonishment of the scientists, the mirror neurons associated with the motor system clearly did not have any major role to play in the action recognition process.

 

With their experiment set up, the team was able to study the contribution of the motor system to action recognition during social interaction for the first time and, thereby also the existing theory on the interaction between mirror neurons and stimulus processing. "Contrary to what was previously assumed, the mirror neurons do not have a particularly significant influence on the interpretation of an action. Visual perception is namely far more important for our brain – in social situations, we rely almost exclusively on what we see," says the head of the study, Stephan de la Rosa, summarizing the study findings.

 

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Memory Impairment Related To Brain Signal Between Seizures
By Jason von Stietz, M.A.
May 15, 2016
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Many patients with epilepsy suffer from cognitive deficits. Researchers at New York University Langone Medical Center conducted an animal model study in which the relationship between signals from the hippocampus to the cortex relate to impaired memory in seizure patients. The study was published in Nature Medicine and discussed in a recent article of NeuroScientistNews: 

 

Between seizures and continually, brain cells in epileptic patients send signals that make "empty memories," perhaps explaining the learning problems faced by up to 40 percent of patients. This is the finding of a study in rats and humans led by researchers at New York University (NYU) Langone Medical Center and published in Nature Medicine.

 

"Our study sheds the first light on the mechanisms by which epilepsy hijacks a normal brain process, disrupting the signals needed to form memories," says study lead author and NYU Langone pediatric neurologist Jennifer Gelinas, MD, PhD. "Many of my patients feel that cognitive problems have at least as much impact on their lives as seizures, but we have nothing to offer them beyond seizure control treatments. We hope to change that."

 

The study results revolve around two brain regions, the hippocampus and cortex, shown by past studies to exchange precise signals as each day's experiences are converted into permanent memories during sleep. The study authors found that epileptic signals come from the hippocampus, not as the part of normal memory consolidation, but instead as meaningless commands that the cortex must process like memories.

 

Study rats experiencing such abnormal signals had significant difficulties navigating to places where they had previously found water. Furthermore, the degree of abnormal hippocampal-cortical signaling in study animals tracked closely with the level of memory impairment.

 

The study also looked at data from epilepsy patients that had their brain signals monitored as part of surgery preparation. Researchers found that rats and humans with epilepsy experienced similar, abnormal hippocampal discharges between seizures that resembled but out-competed normal memory-forming communication between brain regions.

 

Given the tens of milliseconds delay observed between hippocampus signals and the response from the cortex, researchers see a time window during which an implanted device might interrupt disease-related signals, and have launched a related design effort.

 

Foundation Built over Decades

 

Senior author of the study and NYU Langone neuroscientist Gyorgy Buzsaki, PhD, had established, starting in 1989, the theory that memories form in two stages: one while awake and another where we replay the day's events during sleep.

 

As the latest step in that work, Buzsaki also led a study published in the journal Science last month that explained key mechanisms behind hippocampal-cortical memory consolidation.

 

Countering the idea most neurons contribute equally as memories form, his team found that a few strongly active "rigid" neurons perform the same way before and after experiences; while a second set of rarely contributing "plastic" neurons behave differently before and after opportunities for memory consolidation.

 

"We seem to have evolved with both a stable template of neurons that process what is the same about the things we encounter, and a second group that can learn with new experiences," says Buzsaki. "This new understanding of memory consolidation made possible our insights into epilepsy."

 

Buzsaki has shown that the hippocampus processes information in rhythmic cycles, with thousands of nerve signals sent regularly and within milliseconds of each other. By firing in synchrony, brain cells cooperate to achieve complex signals, but only if this wave is sculpted, with signals afforded proper strengths and placed in order. Unfortunately, the synchronous nature of hippocampal signaling creates risk, says Buzsaki, because without proper control it can convey powerful nonsense messages to the rest of the brain.

 

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Autism Biomarker for Boys Found
By Jason von Stietz, M.A.
April 29, 2016
Credit: George Washington University

 

Researchers at the George Washington University investigated the use of brain scans in measuring the progress of treatments for Autism Spectrum Disorder in boys.  Findings indicated that a biomarker related to brain circuitry involved in social perception may assist in more quickly diagnosing and treating difficult to diagnose patients. The study was discussed in a recent article in Medical Xpress: 

 

Researchers have developed a new method to map and track the function of brain circuits affected by autism spectrum disorder (ASD) in boys using brain imaging. The technique will provide clinicians and therapists with a physical measure of the progress patients are making with behavioral and/or drug treatments - a tool that has been elusive in autism treatment until this point.

 

For the first time, doctors would be able to quantify how that brain circuit is working in their patients and assess the effectiveness of an intervention. The research is outlined in a paper, "Quantified Social Perception Circuit Activity as a Neurobiological Marker of Autism Spectrum Disorder," published Wednesday in JAMA Psychiatry. The paper focuses on the use of biomarkers, measurable indicators of a biological condition, to measure the function of the social perception circuit of the brain.

 


"This is significant because biomarkers give us a 'why' for understanding autism in boys that we haven't had before," said Kevin Pelphrey, a co-author of the paper, who is the Carbonell Family Professor in Autism and Neurodevelopmental Disorders and director of the Autism and Neurodevelopmental Disorders Institute at the George Washington University. "We can now use functional biomarkers to identify what treatments will be effective for individual cases and measure progress."

 


Researchers analyzed a series of 164 images from each of 114 individuals and discovered the brain scans of the social perception circuits only indicated ASD in boys. This new research has the potential to improve treatment for ASD by measuring changes in the social perception brain circuit in response to different interventions. The researchers found the brain scan data can be an effective indicator of function of the circuit in younger children and older patients alike.

 

The research is particularly relevant for ASD patients who are difficult to diagnose and treat by providing a more definitive diagnosis and in developing a treatment program when it is not clear if behavioral, drug or a combination of the treatments will be most effective.

 

"The behavioral symptoms of ASD are so complex and varied it is difficult to determine whether a new treatment is effective, especially within a realistic time frame," said Malin Björnsdotter, assistant professor at the University of Gothenburg and lead author of the paper. "Brain function markers may provide the specific and objective measures required to bridge this gap."

 

A Path to Widespread use of Brain Scans?

 

In addition to helping to identify the most effective ASD treatment for an individual, this research provides evidence that brain imaging is an important intervention tool. Currently, functional MRI, the type of brain scan used in this study, is not a standard part of ASD treatment, as there is not enough evidence linking the scan to effective treatments. The Autism and Neurodevelopmental Disorders Institute at GW aims to make significant contributions toward the establishment of evidence-based therapies for ASD.

 

Credit: George Washington University

 

 

"This kind of imaging can help us answer the question, 'On day one of treatment, will this child benefit from a 16-week behavioral intervention?'" Dr. Pelphrey said. "Answering that question will help parents save time and money on diagnosis and treatments."

 

Following the study, Dr. Pelphrey and his colleagues will test their findings at the next level: studying a larger pool of people with autism and other neurological disorders in collaboration with Children's National Medical Center to see if the scan can successfully distinguish ASD from other disorders and track treatment progress.

 

The authors emphasized that this research is still in the earliest days, pointing out that doctors' offices and most hospitals do not have the specialized imaging equipment necessary to carry out the brain scans used by the team involved in this study.

 

"To really help patients we need to develop inexpensive, easy-to-use techniques that can be applied in any group, including infants and individuals with severe behavioral problems," said Dr. Björnsdotter. "This study is a first step toward that goal."

 

While this method currently only works for boys with autism, the researchers are leading a large-scale, nationwide study of girls with autism to identify equivalent techniques that will work for them. The group expects to have the initial results from that study later this year.

 

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Anticholinergics Linked to Changes in Brain and Cognitive Impairment
By Jason von Stietz, M.A.
April 26, 2016
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Are over the counter drugs completely safe? Researchers at Indiana University School of Medicine used positron emission tests (PET) to study the relationship between anticholinergic drugs and cognitive decline. Anticholinergics are commonly used as sleep aids as wells as treatments for hypertension and cardiovascular disease. Findings linked the use of anticholinergics to physical changes in the brain and cognitive impairment. The study was discussed in a recent article in Medical Xpress:  

 

Older adults might want to avoid a using class of drugs commonly used in over-the-counter products such as nighttime cold medicines due to their links to cognitive impairment, a research team led by scientists at Indiana University School of Medicine has recommended.

 

Using brain imaging techniques, the researchers found lower metabolism and reduced brain sizes among study participants taking the drugs known to have an anticholinergic effect, meaning they block acetylcholine, a nervous system neurotransmitter.

 

Previous research found a link between between the anticholinergic drugs and cognitive impairment and increased risk of dementia. The new paper published in the journal JAMA Neurology, is believed to be the first to study the potential underlying biology of those clinical links using neuroimaging measurements of brain metabolism and atrophy.

 

"These findings provide us with a much better understanding of how this class of drugs may act upon the brain in ways that might raise the risk of cognitive impairment and dementia," said Shannon Risacher, Ph.D., assistant professor of radiology and imaging sciences, first author of the paper, "Association Between Anticholinergic Medication Use and Cognition, Brain Metabolism, and Brain Atrophy in Cognitively Normal Older Adults."

 

"Given all the research evidence, physicians might want to consider alternatives to anticholinergic medications if available when working with their older patients," Dr. Risacher said.

 

Drugs with anticholinergic effects are sold over the counter and by prescription as sleep aids and for many chronic diseases including hypertension, cardiovascular disease, and chronic obstructive pulmonary disease.

 

A list of anticholinergic drugs and their potential impact is athttp://www.agingbraincare.org/uploads/products/ACB_scale_-_legal_size.pdf.

 

Scientists have linked anticholinergic drugs cognitive problems among older adults for at least 10 years. A 2013 study by scientists at the IU Center for Aging Research and the Regenstrief Institute found that drugs with a strong anticholinergic effect cause cognitive problems when taken continuously for as few as 60 days. Drugs with a weaker effect could cause impairment within 90 days.

 

The current research project involved 451 participants, 60 of whom were taking at least one medication with medium or high anticholinergic activity. The participants were drawn from a national Alzheimer's research project—the Alzheimer's Disease Neuroimaging Initiative—and the Indiana Memory and Aging Study.

 

To identify possible physical and physiological changes that could be associated with the reported effects, researchers assessed the results of memory and other cognitive tests, positron emission tests (PET) measuring brain metabolism, and magnetic resonance imaging (MRI) scans for brain structure.

 

The cognitive tests revealed that patients taking anticholinergic drugs performed worse than older adults not taking the drugs on short-term memory and some tests of executive function, which cover a range of activities such as verbal reasoning, planning, and problem solving.

 

Anticholinergic drug users also showed lower levels of glucose metabolism—a biomarker for brain activity—in both the overall brain and in the hippocampus, a region of the brain associated with memory and which has been identified as affected early by Alzheimer's disease.

 

The researchers also found significant links between brain structure revealed by the MRI scans and anticholinergic drug use, with the participants using anticholinergic drugs having reduced brain volume and larger ventricles, the cavities inside the brain.

 

"These findings might give us clues to the biological basis for the cognitive problems associated with anticholinergic drugs, but additional studies are needed if we are to truly understand the mechanisms involved," Dr. Risacher said.

 

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Study Links Affective Understanding to Attraction
By Jason von Stietz, M.A.
April 8, 2016
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What is it that leads to attraction? Researchers conducted an experiment utilizing fMRI scans of participants watching a video of a woman. It was found that participants found her more attractive, which was reflected in the reward center of the brain, when they perceived themselves to understand her emotional experience.  The findings were discussed in a recent article in Medical Xpress: 

 

(Medical Xpress)—A team of researchers with members from a large number of institutions in Germany has conducted a study that has revealed more about the way interpersonal attraction works in the brain. In their paper published in Proceedings of the National Academy of Sciences, the group describes two experiments they conducted with volunteers, their results and what they believe was revealed about the nature of the mechanism of attraction between people.

 

Most everyone has experienced near instant attraction to someone else, whether of a social or sexual nature, but few are able to pin down exactly why they felt that attraction. Based on two experiments they conducted with human volunteers, the researchers suggest it may have to do with matchingneural circuitry.

 

To learn more about attraction, the researchers ran two experiments, the first consisted of showing 19 male and 21 female volunteers, videos of six different women as they experienced fear or sadness. The volunteers were asked to choose which emotion was being shown, and then to mark down how confident they were in their choice. To gauge how much of an attraction they volunteers felt for the women in the videos, they were asked to enlarge a picture of the woman both before and after seeing her in the video—each was also asked to answer questions about each woman, such as how much they would like to meet her in real life, if she would understand them, etc.

The second experiment was run with a different set of volunteers who were also asked to watch the woman in the videos, but the second group did so while undergoing an fMRI imaging—the researchers were specifically looking for activity in the part of the brain known to be associated with rewards.

 

The final phase of the experiment involved combining data from both experiments to see if any patterns might emerge. The researchers report that most of the volunteers were able to identify the emotions being portrayed, and the more confident they felt they were able to identify the correct emotion, the more attracted to her they felt. This was confirmed in the fMRI scans—reward centers in the volunteers' brains lit up more when watching women they felt they could read their emotions better.

 

The researchers propose that their results suggest that in addition to physical attractiveness, people are attracted to other people due to their own feelings of similarity to another person, which gives them a feeling of understanding, or connectedness.

 

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Neuronal Feedback Changes Our Perception
By Jason von Stietz, M.A.
April 4, 2016
Photo Credit: Carnegie Mellon University

 

Have you ever thought you saw one thing, but when you looked again it was something else? Often times the brain notices the beginning of a visual pattern and will automatically connect the rest of the dots. How does this happen? Researchers at the Carnegie Mellon University studied top-down visual processing. Findings were discussed in a recent article in MedicalXpress: 

 

Understanding this feedback system could provide new insight into thevisual system's neuronal circuitry and could have further implications for understanding how the brain interprets and understands sensory stimuli.

 

Many optical illusions make you see something that's not there. Take the Kanizsa triangle: when you place three Pac-Man-like wedges in the right spot, you see a triangle, even though the edges of the triangle aren't drawn.

 

"We see with both our brain and our eyes. Your brain is making inferences that allow you to see the triangle. It's connecting the dots between the corners of the wedges," said Kuhlman, who is a member of Carnegie Mellon's BrainHub neuroscience initiative and the joint Carnegie Mellon/University of Pittsburgh Center for the Neural Basis of Cognition (CNBC). "Optical illusions illustrate some of the amazing things our visual system can do."

 

When we look at an object, information about what we see travels through circuits of neurons beginning in the retina, through the thalamus and into the brain's visual cortex. In the visual cortex, the information gets processed in multiple stages and is ultimately sent to the prefrontal cortex—the area of the brain that makes decisions, including how to respond to a given stimulus.

 

However, not all information stays on this forward moving path. At the secondary stage of processing in the visual cortex some neurons reverse course and send information back to the first stage of processing. Researchers at Carnegie Mellon wondered if this feedback could change how the neurons in the visual cortex respond to a stimulus and alter the messages being sent to the prefrontal cortex.

 

While there has been a good deal of research studying how information moves forward through the visual system, less has been done to study the impact of the information that moves backward. To find out if the information traveling from the secondary stage of processing back to the first stage impacted how information is encoded in the visual system, the researchers needed to quantify the magnitude of information that was being sent from the second stage back to the first stage. Using a mouse model, they recorded normal neuronal firing in the first stage of the visual cortex as the mouse looked at moving patterns that represented edges. They then silenced the neurons in the second stage using modified optogenetic technology. This halted the feedback of information from the second stage back to the first stage, and allowed the researchers to determine how much of the neuronal activity in the first stage of visual processing was the result of feedback.

 

Twenty percent of the neuronal activity in the visual cortex was the result of feedback, a concept Kuhlman calls reciprocal connectivity. This indicates that some of the information coming from the visual cortex is not a direct response to a visual stimuli, but is a response to how the stimuli was perceived by higher cortical areas.

 

The feedback, she says, might be what causes our brain to complete the undrawn lines in the Kanizsa triangle. But more importantly, it signifies that studying neuronal feedback is important to our understanding of how the brain works to process stimuli.

 

"This represents a new way to study visual perception and neural computation. If we want to truly understand the visual pathway, and cortical function in general, we have to understand these reciprocal connection," Kuhlman said.

 

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fMRI Utilized in Neurofeedback
By Jason von Stietz, M.A.
March 25, 2016
Credit: Jeff MacInnes, Duke University.

 

Although neurofeedback has traditionally relied on the use of EEG, researchers from Duke University have examined the use of fMRI data. Participants’ brain activity was monitored and feedback was provided to them in the form of a fluctuating thermometer. Both EEG and fMRI neurofeedback were discussed in a recent article in NeuroscienceNews:    

 

At our best, we motivate ourselves every day to get dressed and go to work or school. Although there are larger incentives at work, it’s our own volition that powers us through our innumerable daily tasks.

 

If we could learn to control the motivational centers of our brains that drive volition, would it lead us toward healthier, more productive lives? Using a new brain imaging strategy, Duke University scientists have now taken a first step in understanding how to manipulate specific neural circuits using thoughts and imagery.

 

The technique, which is described in the March 16 issue of the journal Neuron, is part of a larger approach called ‘neurofeedback,’ which gives participants a dynamic readout of brain activity, in this case from a brain area critical for motivation.

 

“These methods show a direct route for manipulating brain networks centrally involved in healthy brain function and daily behavior,” said the study’s senior investigator R. Alison Adcock, an assistant professor of psychiatry and behavioral sciences and associate director of the Center for Cognitive Neuroscience in the Duke University Institute for Brain Sciences.

 

Neurofeedback is a specialized form of biofeedback, a technique that allows people to monitor aspects of their own physiology, such as heart rate and skin temperature. It can help generate strategies to overcome anxiety and stress or to cope with other medical conditions.

 

Neurofeedback has historically relied on electroencephalography or EEG, in which patterns of electrical activity are monitored noninvasively by electrodes attached to the scalp. But these measures provide only rough estimates of where activity occurs in the brain.

 

In contrast, the new study employed functional magnetic resonance imaging (fMRI), which measures changes in blood oxygen levels, allowing more precisely localized measurements of brain activity.

 

Adcock’s team has been working on ways to use thoughts and behavior to tune brain function for the past eight years. In this time, they’ve developed tools allowing them to analyze complex brain imaging data in real time and to display it to participants as neurofeedback while they are in the fMRI scanner.

 

This study focused on the ventral tegmental area (VTA), a small area deep within the brain that is a major source of dopamine, a neurochemical well known for its role in motivation, experiencing rewards, learning, and memory.

 

According to Adcock’s previous research, when people are given incentives to remember specific images, an increase in VTA activation before the image appears predicts whether the participants are going to successfully remember the image.

 

External incentives like money work well to stimulate the VTA, but it was unclear whether people could exercise this area on their own, said co-author Jeff MacInnes, a postdoctoral researcher in Adcock’s lab.

 

In the new study, the team encouraged participants in the scanner to generate feelings of motivation – using their own personal strategies – during 20-second intervals. They weren’t able to raise their VTA activity consistently on their own.

 

But when the scientists provided participants with neurofeedback from the VTA, presented in the form of a fluctuating thermometer, participants were able to learn which strategies worked, and ultimately adopt more effective strategies. Compared to control groups, the neurofeedback-trained participants successfully elevated their VTA activity.

 

Participants reported using a variety of different motivational strategies, from imagining parents or coaches encouraging them, to playing out hypothetical scenarios in which their efforts were rewarded, said co-author Kathryn Dickerson, a postdoctoral researcher in Adcock’s group.

 

The self-generated boost in VTA activation worked even after the thermometer display was removed. Only the participants who had received accurate neurofeedback were able to consistently raise their VTA levels.

 

“Because this is the first demonstration of its kind, there is much still to be understood,” Adcock added. “But these tools could offer benefits for everyone, particularly those with depression or attention problems.”

 

The neurofeedback training also activated other regions involved in learning and experiencing rewards, confirming that, at least in the short term, the brain changes its activity more broadly as a result of neurofeedback, Dickerson said.

 

Adcock said one caveat of the study is that the team has not tested whether the neurofeedback drove changes in behavior. The group is working on those studies now and also plans to conduct the same study in participants with depression and attention deficit hyperactivity disorder (ADHD).

 

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Exercise Boosts Neurotransmitters
By Jason von Stietz, M.A.
March 18, 2016
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Why does exercise seem to improve our mood? Depression often results in the depletion of two key neurotransmitters: glutamate and GABA. However, recent findings suggest that vigorous exercise boosts the production of these neurotransmitters in the brain. Researchers at University of California Davis examined the effect of exercise on the brain using MRI scans. The study was discussed in a recent article in NeuroScientistNews: 

 

"Major depressive disorder is often characterized by depleted glutamate and GABA, which return to normal when mental health is restored," said study lead author Richard Maddock, professor in the Department of Psychiatry and Behavioral Sciences. "Our study shows that exercise activates the metabolic pathway that replenishes these neurotransmitters."

 

The research also helps solve a persistent question about the brain, an energy-intensive organ that consumes a lot of fuel in the form of glucose and other carbohydrates during exercise. What does it do with that extra fuel?

 

"From a metabolic standpoint, vigorous exercise is the most demanding activity the brain encounters, much more intense than calculus or chess, but nobody knows what happens with all that energy," Maddock said. "Apparently, one of the things it's doing is making more neurotransmitters."

 

The striking change in how the brain uses fuel during exercise has largely been overlooked in brain health research. While the new findings account for a small part of the brain's energy consumption during exercise, they are an important step toward understanding the complexity of brain metabolism. The research also hints at the negative impact sedentary lifestyles might have on brain function, along with the role the brain might play in athletic endurance.

 

"It is not clear what causes people to 'hit the wall' or get suddenly fatigued when exercising," Maddock said. "We often think of this point in terms of muscles being depleted of oxygen and energy molecules. But part of it may be that the brain has reached its limit."

 

To understand how exercise affects the brain, the team studied 38 healthy volunteers. Participants exercised on a stationary bicycle, reaching around 85 percent of their predicted maximum heart rate. To measure glutamate and GABA, the researchers conducted a series of imaging studies using a powerful 3-tesla MRI to detect nuclear magnetic resonance spectra, which can identify several compounds based on the magnetic behavior of hydrogen atoms in molecules.

 

The researchers measured GABA and glutamate levels in two different parts of the brain immediately before and after three vigorous exercise sessions lasting between eight and 20 minutes, and made similar measurements for a control group that did not exercise. Glutamate or GABA levels increased in the participants who exercised, but not among the non-exercisers. Significant increases were found in the visual cortex, which processes visual information, and the anterior cingulate cortex, which helps regulate heart rate, some cognitive functions and emotion. While these gains trailed off over time, there was some evidence of longer-lasting effects.

 

"There was a correlation between the resting levels of glutamate in the brain and how much people exercised during the preceding week," Maddock said. "It's preliminary information, but it's very encouraging."

 

These findings point to the possibility that exercise could be used as an alternative therapy for depression. This could be especially important for patients under age 25, who sometimes have more side effects from selective serotonin reuptake inhibitors (SSRIs), anti-depressant medications that adjust neurotransmitter levels.

 

For follow-up studies, Maddock and the team hope to test whether a less-intense activity, such as walking, offers similar brain benefits. They would also like to use their exercise-plus-imaging method on a study of patients with depression to determine the types of exercise that offer the greatest benefit.

 

"We are offering another view on why regular physical activity may be important to prevent or treat depression," Maddock said. "Not every depressed person who exercises will improve, but many will. It's possible that we can help identify the patients who would most benefit from an exercise prescription."

 

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