Mental picture of others can be seen using fMRI

It is possible to tell who a person is thinking about by analyzing images of his or her brain. Our mental models of people produce unique patterns of brain activation, which can be detected using advanced imaging techniques according to a study by Cornell University neuroscientist Nathan Spreng and his colleagues.

"When we looked at our data, we were shocked that we could successfully decode who our participants were thinking about based on their brain activity," said Spreng, assistant professor of human development in Cornell’s College of Human Ecology.

Understanding and predicting the behavior of others is a key to successfully navigating the social world, yet little is known about how the brain actually models the enduring personality traits that may drive others’ behavior, the authors say. Such ability allows us to anticipate how someone will act in a situation that may not have happened before.

To learn more, the researchers asked 19 young adults to learn about the personalities of four people who differed on key personality traits. Participants were given different scenarios (i.e. sitting on a bus when an elderly person gets on and there are no seats) and asked to imagine how a specified person would respond. During the task, their brains were scanned using functional magnetic resonance imaging (fMRI), which measures brain activity by detecting changes in blood flow.

They found that different patterns of brain activity in the medial prefrontal cortex (mPFC) were associated with each of the four different personalities. In other words, which person was being imagined could be accurately identified based solely on the brain activation pattern.

The results suggest that the brain codes the personality traits of others in distinct brain regions and this information is integrated in the medial prefrontal cortex (mPFC) to produce an overall personality model used to plan social interactions, the authors say.

"Prior research has implicated the anterior mPFC in social cognition disorders such as autism and our results suggest people with such disorders may have an inability to build accurate personality models," said Spreng. "If further research bears this out, we may ultimately be able to identify specific brain activation biomarkers not only for diagnosing such diseases, but for monitoring the effects of interventions."

Why your brain tires when exercising

A marathon runner approaches the finishing line, but suddenly the sweaty athlete collapses to the ground. Everyone probably assumes that this is because he has expended all energy in his muscles. What few people know is that it might also be a braking mechanism in the brain which swings into effect and makes us too tired to continue. What may be occurring is what is referred to as ‘central fatigue’.

"Our discovery is helping to shed light on the paradox which has long been the subject of discussion by researchers. We have always known that the neurotransmitter serotonin is released when you exercise, and indeed, it helps us to keep going. However, the answer to what role the substance plays in relation to the fact that we also feel so exhausted we have to stop has been eluding us for years. We can now see it is actually a surplus of serotonin that triggers a braking mechanism in the brain. In other words, serotonin functions as an accelerator but also as a brake when the strain becomes excessive," says Associate Professor Jean-François Perrier from the Department of Neuroscience and Pharmacology, who has spearheaded the new research.

Help in the battle against doping

Jean-François Perrier hopes that mapping the mechanism that prompts central fatigue will be useful in several ways. Central fatigue is a phenomenon which has been known for about 80 years; it is a sort of tiredness which, instead of affecting the muscles, hits the brain and nervous system. By conducting scientific experiments, it is possible to observe and measure that the brain sends insufficient signals to the muscles to keep going, which in turn means that we are unable to keep performing. This makes the mechanism behind central fatigue an interesting area in the battle against doping, and it is for this reason that Anti Doping Danmark has also helped fund the group’s research.

"In combating the use of doping, it is crucial to identify which methods athletes can use to prevent central fatigue and thereby continue to perform beyond what is naturally possible. And the best way of doing so is to understand the underlying mechanism," says Jean-François Perrier.

Developing better drugs

The brain communicates with our muscles using so-called motoneurons. In several diseases, motoneurons are hyperactive. This is true, for example, of people suffering from spasticity and cerebral palsy, who are unable to control their movements. Jean-François Perrier therefore hopes that, in the long term, this new knowledge can also be used to help develop drugs against these symptoms and to find out more about the effects of antidepressants.

"This new discovery brings us a step closer to finding ways of controlling serotonin. In other words, whether it will have an activating effect or trigger central fatigue. It is all about selectively activating the receptors which serotonin attaches to," explains Jean-François Perrier.

"For selective serotonin re-uptake inhibitor (SSRI) drugs which are used as antidepressants, we can possibly help explain why those who take the drugs often feel more tired and also become slightly clumsier than other people. What we now know can help us develop better drugs," concludes Jean-François Perrier.

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How the brain loses and regains consciousness

Study reveals brain patterns produced by a general anesthesia drug; work could help doctors better monitor patients.

Since the mid-1800s, doctors have used drugs to induce general anesthesia in patients undergoing surgery. Despite their widespread use, little is known about how these drugs create such a profound loss of consciousness.

In a new study that tracked brain activity in human volunteers over a two-hour period as they lost and regained consciousness, researchers from MIT and Massachusetts General Hospital (MGH) have identified distinctive brain patterns associated with different stages of general anesthesia. The findings shed light on how one commonly used anesthesia drug exerts its effects, and could help doctors better monitor patients during surgery and prevent rare cases of patients waking up during operations.

Anesthesiologists now rely on a monitoring system that takes electroencephalogram (EEG) information and combines it into a single number between zero and 100. However, that index actually obscures the information that would be most useful, according to the authors of the new study, which appears in the Proceedings of the National Academy of Sciences the week of March 4.

“When anesthesiologists are taking care of someone in the operating room, they can use the information in this article to make sure that someone is unconscious, and they can have a specific idea of when the person may be regaining consciousness,” says senior author Emery Brown, an MIT professor of brain and cognitive sciences and health sciences and technology and an anesthesiologist at MGH.

Research advances understanding of the human brain

Advanced neuroimaging techniques are giving researchers new insight into how the human brain plans and controls limb movements. This advance could one day lead to new understanding of disease and dysfunction in the brain and has important implications for movement-impaired patient populations, like those who suffer from spinal cord injuries.

Randy Flanagan (Psychology and Centre for Neuroscience Studies), working with colleagues at Western University, used functional magnetic resonance imaging (fMRI) to uncover what regions of the human brain are used to plan hand actions with the left and right arm. This study, spearheaded by Jason Gallivan, a Banting postdoctoral fellow at Queen’s found that by using the fMRI signals from several different brain regions, they could predict the limb to be used (left vs. right) and hand action to be performed (grasping vs. touching an object), moments before that movement is actually executed.

“We are trying to understand how the brain plans actions,” says Dr. Gallivan. “By using highly sensitive analysis techniques that enable the detection of subtle changes in brain activity patterns, we can reveal which of a series of actions a volunteer is merely intending to do, seconds later. Mapping and characterizing these predictive signals across the human brain allows us to pinpoint the key brain structures involved in generating normal, everyday behaviours.”

In another study, Dr. Flanagan and doctoral student Jonathan Diamond examined how the brain learns object mechanical properties, knowledge that is essential for skilled manipulation. They found that, through experience, humans use mismatches between predicted and actual fingertip forces and between predicted and actual object motions to build internal representations, or models, of the mechanical properties of the objects.

“The goal of this work is to understand the representations underlying skilled manipulation,” explains Dr. Flanagan. “This is important because it will enable us to better characterize deficits in manipulation tasks that often result from stroke and neurological diseases.”

Dr. Flanagan, Dr. Gallivan, and Ingrid Johnsrude (Psychology and Centre for Neuroscience Studies) have recently been awarded a CIHR operating grant to support ongoing neuroimaging work.

Both research papers were published in the Journal of Neuroscience. Read Dr. Flanagan’s paper here and read the joint paper here.

(Image: Getty Images)

A proposed link between aging, autism, and oxidation

Like any fac­tory, the body burns oxygen to get energy for its var­ious needs. As a result, detri­mental byprod­ucts are released and our cells try to clean up shop with antiox­i­dants. But as we age, this process becomes a losing battle.

“Oxi­da­tion inex­orably moves us along toward an oxi­dized state,” said phar­ma­ceu­tical sci­ences pro­fessor Richard Deth. “You have to deal with it progressively.”

One option is to slow down the syn­thesis of new pro­teins, a process that requires energy. Indeed, as we age, we pro­duce fewer new pro­teins, which explains why our capacity for learning and healing suffer as we grow old.

Since every pro­tein orig­i­nates from instruc­tions in the DNA, pro­tein syn­thesis can be slowed down by turning off par­tic­ular genes. A process called epi­ge­netic reg­u­la­tion accom­plishes the task by adding mol­e­c­ular tags on top of the genome. The pro­tein methio­nine syn­thase reg­u­lates this process. But what reg­u­lates methio­nine syn­thase? Oxidation.

“This enzyme is the most easily oxi­dized mol­e­cule in the body,” said Deth, whose research on the sub­ject was recently pub­lished in the journal PLOS ONE. The senior author for the study, Christina Mura­tore, received her doc­torate in phar­ma­ceu­tical sci­ences from North­eastern in 2010.

When­ever the body is under oxida­tive stress, Deth explained, methio­nine syn­thase, or MS, stops working. He and his team hypoth­e­sized that MS plays an impor­tant reg­u­la­tory role in aging and that it might be impaired in autism, which Deth has con­nected to unchecked oxida­tive stress in pre­vious research.

To examine their hypoth­esis, the researchers looked at post­mortem human brain sam­ples across the lifespan, with sub­jects as young as 28 weeks of fetal devel­op­ment to as old as 84 years. They mea­sured the levels of a mol­e­cule called MS mRNA, which tran­scribes the genetic code for methio­nine syn­thase into actual protein.

As the sub­jects aged, their brain tissue showed lower levels of MS mRNA. But, sur­pris­ingly, the levels of the pro­tein itself remained con­stant across the lifespan.

Deth and his col­leagues sus­pect that this observed decrease in MS mRNA over our lives may act as a check in the system to save energy that we no longer have in plen­tiful supply and to slow down oxida­tive stress. “One way that the system can guard against too much pro­tein syn­thesis is to restrict the amount of mRNA,” Deth said.

The team also com­pared MS pro­tein and mRNA levels between brain tissue sam­ples from autistic and nor­mally devel­oping sub­jects. Autistic brains had markedly less MS mRNA than the con­trol sam­ples but sim­ilar pro­tein levels. Addi­tion­ally, the age-​​dependent trend seen in nor­mally devel­oping brains was not mim­icked among the autistic sample.

If decreased MS mRNA does mean decreased pro­tein pro­duc­tion, it’s no big deal for adults who don’t need to make new pro­teins as often. But for the devel­oping brain, new pro­teins are crit­ical. “Your capacity for learning might be pre­ma­turely reduced because meta­bol­i­cally you can’t afford it,” Deth suggested.

While the results are pre­lim­i­nary and will ben­efit from repeated studies and more inves­ti­ga­tion, Deth’s find­ings add to a growing body of evi­dence linking both aging and autism to oxida­tive stress.

Split-Brain Patients Reveal Brain’s Flexibility

Study looks to distinguish cognitive functioning in centenarians

As life expectancy continues to increase, more and more people will reach and surpass the century mark in age. But even as greater numbers reach and surpass the 100-year milestone, little is known about what constitutes normal levels of cognitive function in the second century of life.

Led by Adam Davey, associate professor in Temple’s Department of Public Health, a group of researchers used a new method called factor mixture analysis — a statistical technique for identifying different groups within a population — to identify the prevalence of cognitive impairment in centenarians and try to understand the cognitive changes that are part of extreme aging. They published their findings, “Profiles of Cognitive Functioning in a Population-Based Sample of Centenarians Using Factor Mixture Analysis,” in the journal Experimental Aging Research.

“One of the motivations for studying centenarians is that they are very close to the upper limit of human life expectancy right now,” said Davey. “By looking at their cognitive functioning we can learn a lot in terms of how common or prevalent cognitive impairment is among that age group.”

Using voter registration lists and nursing home records in 44 counties in northern Georgia, the researchers identified 244 people between the ages of 98-108 — approximately 20 percent of all centenarians living in that region — who participated in the study. Participants were assessed based on a series of standard tests used to measure cognitive functioning.

“As people get into later life and the prevalence of cognitive impairment becomes relatively high, we need some way of distinguishing between those people who are aging normally and the people who have cognitive impairment, which could indicate dementia,” said Davey.

The researchers found that even though approximately two-thirds of centenarians were at or below the threshold for cognitive impairment by one commonly used measure, only one-third of centenarians were identified as cognitively impaired using their new approach.

“That’s consistent with the level of cognitive impairment found in another study that looked at people up to the age of 85-plus,” said Davey. “But even the normal folks have had cognitive declines to the point that they are functioning at a level that would indicate impairment at younger ages.”

The researchers found that characteristics such as age, race and educational attainment can help to distinguish those in the lower cognitive performance group.

“This is the first study that I’m aware of that allows us to distinguish between these two groups of centenarians, so that we can start to develop benchmarks for what is normal cognitive functioning among members of this age group,” said Davey. “These people have lived so long that even their normal cognitive function could be mistaken for a form of dementia if a physician were to treat them as they would someone who was merely old.”

(Image credit: Krissy_77)

Authors: Develop digital games to improve brain function and well-being

Neuroscientists should help to develop compelling digital games that boost brain function and improve well-being, say two professors specializing in the field in a commentary article published in the science journal Nature.

In the Feb. 28 issue, the two — Daphne Bavelier of the University of Rochester and Richard J. Davidson of the University of Wisconsin-Madison — urge game designers and brain scientists to work together to design new games that train the brain, producing positive effects on behavior, such as decreasing anxiety, sharpening attention and improving empathy. Already, some video games are designed to treat depression and to encourage cancer patients to stick with treatment, the authors note.

Davidson is founder and chair of the Center for Investigating Healthy Minds at the UW’s Waisman Center. Bavelier is a professor in the Department of Brain and Cognitive Sciences at Rochester.

Video game usage, which continues to rise among American children, has been associated with a number of negative outcomes, such as obesity, aggressiveness, antisocial behavior and, in extreme cases, addiction. “At the same time, evidence is mounting that playing games can have a beneficial effects on the brain,” the authors write.

Last year, Bavelier and Davidson presided over a meeting at the White House in which neuroscientists met with entertainment media experts to discuss ways of using interactive technology such as video games to further understanding of brain functions, as well as to provide new, engaging tools for boosting attention and well-being.

Bavelier’s work is focused on how humans learn and how the brain adapts to changes in experience, either by nature (as in deafness) or by training (such as playing video games). Her lab investigates how new media, including video games, can be leveraged to foster learning and brain plasticity.

Davidson, who studies emotion and the brain, is leading a project in collaboration with UW-Madison’s Games + Learning + Society to develop two video games designed to help middle school students develop social and emotional skills, such as empathy, cooperation, mental focus and self-regulation.

"Gradually, this work will begin to document the burning social question of how technology is having an impact on our brains and our lives, and enable us to make evidence-based choices about the technologies of the future, to produce a new set of tools to cultivate positive habits of mind," the authors conclude.

Ectopic Eyes Function Without Connection to Brain

For the first time, scientists have shown that transplanted eyes located far outside the head in a vertebrate animal model can confer vision without a direct neural connection to the brain.

Biologists at Tufts University School of Arts and Sciences used a frog model to shed new light – literally – on one of the major questions in regenerative medicine, bioengineering, and sensory augmentation research.

"One of the big challenges is to understand how the brain and body adapt to large changes in organization," says Douglas J. Blackiston, Ph.D., first author of the paper "Ectopic Eyes Outside the Head in Xenopus Tadpoles Provide Sensory Data For Light-Mediated Learning," in the February 27 issue of the Journal of Experimental Biology. “Here, our research reveals the brain’s remarkable ability, or plasticity, to process visual data coming from misplaced eyes, even when they are located far from the head.”

Blackiston is a post-doctoral associate in the laboratory of co-author Michael Levin, Ph.D., professor of biology and director of the Center for Regenerative and Developmental Biology at Tufts University.

Levin notes, “A primary goal in medicine is to one day be able to restore the function of damaged or missing sensory structures through the use of biological or artificial replacement components. There are many implications of this study, but the primary one from a medical standpoint is that we may not need to make specific connections to the brain when treating sensory disorders such as blindness.”

In this experiment, the team surgically removed donor embryo eye primordia, marked with fluorescent proteins, and grafted them into the posterior region of recipient embryos. This induced the growth of ectopic eyes. The recipients’ natural eyes were removed, leaving only the ectopic eyes.

Fluorescence microscopy revealed various innervation patterns but none of the animals developed nerves that connected the ectopic eyes to the brain or cranial region.

To determine if the ectopic eyes conveyed visual information, the team developed a computer-controlled visual training system in which quadrants of water were illuminated by either red or blue LED lights. The system could administer a mild electric shock to tadpoles swimming in a particular quadrant. A motion tracking system outfitted with a camera and a computer program allowed the scientists to monitor and record the tadpoles’ motion and speed.

Eyes See Without Wiring to Brain

The team made exciting discoveries: Just over 19 percent of the animals with optic nerves that connected to the spine demonstrated learned responses to the lights. They swam away from the red light while the blue light stimulated natural movement.

Their response to the lights elicited during the experiments was no different from that of a control group of tadpoles with natural eyes intact. Furthermore, this response was not demonstrated by eyeless tadpoles or tadpoles that did not receive any electrical shock.

"This has never been shown before," says Levin. "No one would have guessed that eyes on the flank of a tadpole could see, especially when wired only to the spinal cord and not the brain."
The findings suggest a remarkable plasticity in the brain’s ability to incorporate signals from various body regions into behavioral programs that had evolved with a specific and different body plan.

"Ectopic eyes performed visual function," says Blackiston. "The brain recognized visual data from eyes that impinged on the spinal cord. We still need to determine if this plasticity in vertebrate brains extends to different ectopic organs or organs appropriate in different species."

One of the most fascinating areas for future investigation, according to Blackiston and Levin, is the question of exactly how the brain recognizes that the electrical signals coming from tissue near the gut is to be interpreted as visual data.

In computer engineering, notes Levin, who majored in computer science and biology as a Tufts undergraduate, this problem is usually solved by a “header”—a piece of metadata attached to a packet of information that indicates its source and type. Whether electric signals from eyes impinging on the spinal cord carry such an identifier of their origin remains a hypothesis to be tested.