Reminiscing can help boost mental performance

To solve a mental puzzle, the brain’s executive control network for externally focused, goal-oriented thinking must activate, while the network for internally directed thinking like daydreaming must be turned down to avoid interference – or so we thought.

New research led by Cornell University neuroscientist Nathan Spreng shows for the first time that engaging brain areas linked to so-called “off-task” mental activities (such as mind-wandering and reminiscing) can actually boost performance on some challenging mental tasks. The results advance our understanding of how externally and internally focused neural networks interact to facilitate complex thought, the authors say.

“The prevailing view is that activating brain regions referred to as the default network impairs performance on attention-demanding tasks because this network is associated with behaviors such as mind-wandering,” said Spreng. “Our study is the first to demonstrate the opposite – that engaging the default network can also improve performance.”

There are plenty of neuroimaging studies showing that default network activation interferes with complex mental tasks – but in most, Spreng explained, the mental processes associated with default network conflict with task goals. If you start thinking about what you did last weekend while taking notes during a lecture, for example, your note-taking and ability to keep up will suffer.

Spreng and his team developed a new approach in which off-task processes such as reminiscing can support rather than conflict with the aims of the experimental task. Their novel task, “famous faces n-back,” tests whether accessing long-term memory about famous people, which typically engages default network brain regions, can support short-term memory performance, which typically engages executive control regions.

While undergoing brain scanning, 36 young adults viewed sets of famous and anonymous faces in sequence and were asked to identify whether the current face matched the one presented two faces back. The team found participants were faster and more accurate when matching famous faces than when matching anonymous faces and that this better short-term memory performance was associated with greater activity in the default network. The results show that activity in the default brain regions can support performance on goal-directed tasks when task demands align with processes supported by the default network, the authors say.

“Outside the laboratory, pursuing goals involves processing information filled with personal meaning – knowledge about past experiences, motivations, future plans and social context,” Spreng said. “Our study suggests that the default network and executive control networks dynamically interact to facilitate an ongoing dialogue between the pursuit of external goals and internal meaning.”

Working memory hinders learning in schizophrenia

A new study pinpoints working memory as a source of learning difficulties in people with schizophrenia.

Working memory is known to be affected in the millions of people — about 1 percent of the population — who have schizophrenia, but it has been unclear whether that has a specific role in making learning more difficult, said Anne Collins, a postdoctoral researcher at Brown University and lead author of the study.

“We really tend to think of learning as a unitary, single process, but really it is not,” said Collins, who in 2012 along with co-author Michael Frank, associate professor of cognitive, linguistic, and psychological sciences, developed an experimental task and a computational model of cognition that can distinguish the contributions of working memory and reinforcement in the learning process. “We thought we could try to disentangle that here and see if the impairment was in both aspects, or only one of them.”

In the new study in the Journal of Neuroscience, cognitive scientists Collins and Frank collaborated with schizophrenia experts James Waltz and James Gold of the University of Maryland to measure the effects of working memory and reinforcement in learning by applying these methods. They found that only working memory was a source of impairment.

Learning about learning’s components

To find that out, they marshaled 49 volunteers with schizophrenia and an otherwise comparable set of 36 people without the condition to participate in the specially designed learning task. In each round, participants were shown a set of images and then were asked to push one of three buttons when they saw each image. With each button push they were told whether they had hit the correct button for that image. Over time, through trial and error, participants could learn which picture called for which button. With perfect memory, one wouldn’t need to see an image more than three times to learn the right button to push when it appeared.

The task explicitly involves employing the brain’s systems for working memory (keeping each image–button association in mind) and for reinforcement learning (wanting to repeat an action that led to the feedback of “correct” and to avoid one that produced “incorrect”). But in different rounds while the degree of reinforcement remained the same, the experimenters varied the number of images in the sets the volunteers saw, from two to six. What varied, therefore, was the degree to which working memory was taxed.

What the researchers found was that for both people with schizophrenia and for controls, the larger the image set size, the more trials it took to learn to press the correct button consistently for each image and the longer it took to react to each stimulus. People with schizophrenia generally performed worse on the task than healthy controls.

Those results show that as the task involved more images, it became harder to do – a matter of working memory, since the capacity to maintain information explicitly in memory is limited – but that alone did not prove that working memory was a source of learning problems for people with schizophrenia. They could also be doing worse because of a slower use of the reinforcement.

To determine that, the researchers used their computational models of how learning occurs in the brain to fit the experimental data. They asked what parameters in the models needed to vary to accurately predict the behavior they measured in people with and without schizophrenia.

That analysis revealed that varying parameters of working memory, such as capacity, but not parameters of reinforcement learning, accounted best for differences in behavior between the groups.

“With model-fitting techniques, I can look quantitatively, trial-by-trial and see that the model predicts subject’s choices,” she said. “The same model explains both the healthy group and the patient group, but with differences in parameters.”

That confirmed that working memory uniquely affected learning in people with schizophrenia, while reinforcement learning mechanisms did not, Collins said.

The study suggests that working memory could be a more important target than reinforcement learning among researchers and clinicians hoping to help improve learning for people with schizophrenia, Collins said.

Among mentally healthy people as well, the study illustrates that the different components of learning can be understood individually, even as they all interact in the brain to make learning happen.

“More broadly, it brings attention to the fact that we need to consider learning as a multiactor kind of behavior that can’t be just summarized by a single system,” Collins said. “It’s important to design tasks that can separate them out so we can extract different sources of variance and correctly match them to different neural systems.”

(Image: Shutterstock)

Strong working memory put brakes on problematic drug use

Adolescents with strong working memory are better equipped to escape early drug experimentation without progressing into substance abuse issues, says a University of Oregon researcher.

Most important in the picture is executive attention, a component of working memory that involves a person’s ability to focus on a task and ignore distractions while processing relevant goal-oriented information, says Atika Khurana, a professor in the Department of Counseling Psychology and Human Services.

Khurana, also a member of the UO’s Prevention Science Institute, is lead author of a study online ahead of print in the quarterly journal Development and Psychopathology. The findings, drawn from a long-term study of 382 adolescents in a mostly at-risk urban population, provide a rare, early view of adolescents’ entry into the use of alcohol, tobacco and marijuana.

Khurana collaborated with researchers at the University of Pennsylvania and Children’s Hospital of Philadelphia. They focused on 11- to 13-year-old children as they began to explore risky and sensation-seeking experiences that often mark the road to independence and adulthood. Previous studies generally have relied on adult recall of when individuals began experimenting, with early drug use thought to be a marker of later substance abuse problems.

"Not all forms of early drug use are problematic," Khurana said. "There could be some individuals who start early, experiment and then stop. And there are some who could start early and go on into a progressive trajectory of continued drug use. We wanted to know what separates the two?"

During four assessments, participants provided self-reports of drug use in the previous 30 days. Four working memory tests also were conducted: Corsi block tapping, in which subjects viewed identical blocks that lit up randomly on a screen and tapped each box in reverse order of the lighting sequence; a digit-span test where numbers shown are to be repeated in reverse order; a letter two-back test, in which subjects identify specific letters in time-sensitive sequences; and a spatial working-memory task where hidden tokens must be found quickly within sets of four to eight randomly positioned boxes on a computer screen.

The pattern that emerged was that early drug experimentation more likely to lead into progressive drug use among young people whose impulsive tendencies aren’t kept in check by strong working memory ability. Later assessments of the participants, who have now reached late adolescence, are being analyzed, but it appears that the compulsive progression, not just the experimentation, of drug use is likely to lead to disorder, Khurana said.

"Prefrontal regions of the brain can apply the brakes or exert top-down control over impulsive, or reward seeking urges," Khurana said. "By its nature, greater executive attention enables one to be less impulsive in one’s decisions and actions because you are focused and able to control impulses generated by events around you. What we found is that if teens are performing poorly on working memory tasks that tap into executive attention, they are more likely to engage in impulsive drug-use behaviors."

The findings suggest new approaches for early intervention since weaknesses in executive functioning often underlie self-control issues in children as young as 3 years old, she said. A family environment strong in structured routines and cognitive-stimulation could strengthen working memory skills, she said.

For older children, interventions could be built around activities that encourage social competence and problem solving skills in combination with cognition-building efforts to increase self-control and working memory. The latter allows people to temporarily store, organize and manipulate mental information and is vital for evaluating consequences of decisions.

"We need to compensate for the weakness that exists, before drug experimentation starts to help prevent the negative spiral of drug abuse," Khurana said.

The interactive brain

Neuroscientist explores mechanism that can cause deficit in working memory

Amy Griffin, associate professor of psychological and brain sciences at the University of Delaware, has received a five-year, $1.78 million grant from the National Institute of Mental Health to support her research into the brain mechanisms of working memory.

A neuroscientist, Griffin has been interested for some time in the interaction between the prefrontal cortex, located at the front of the brain, and the hippocampus, a region in the temporal lobe of the brain. When the two areas fail to work together, that failure appears to be correlated with deficits in working memory, a condition that commonly occurs in schizophrenia, general anxiety and other psychiatric disorders.

The hippocampus is the portion of the brain responsible for memory, while the prefrontal cortex controls executive function, a term that includes such cognitive abilities as problem-solving, planning and abstract thinking.

“These are two areas of the brain that are far apart, but their oscillations [rhythmic activities] are synchronized,” Griffin said. “When one area is active, so is the other.”

Working memory, sometimes called short-term memory, is “the kind of memory that fails when you walk into a room and forget why you came there,” she said.

When the oscillations in the hippocampus and prefrontal cortex are out of sync, deficits of working memory occur. In those cases, Griffin said, “both regions are active, but they’re not talking to each other.” The mechanism that causes that lack of communication has not been well explored, and her research will seek to do that.

Griffin and her research team plan to conduct two types of experiments. One will inhibit activity in a brain region called the nucleus reuniens, a region that is hypothesized to synchronize the hippocampus and prefrontal cortex and is expected to cause impairments with working memory. In the other experiment, researchers will activate the nucleus reuniens to increase synchrony, hoping to learn if that improves working memory.

The research will employ a cutting-edge technique called optogenetics, a process that uses proteins to make neurons sensitive to light and then uses light to control them. 

“Optogenetics is becoming a common technique,” Griffin said. “It’s a way to study these processes on a millisecond timescale.” 

A 2013 article in the journal Nature Neuroscience said optogenetics “is transforming the field of neuroscience. For the first time, it is now possible to use light to both trigger and silence activity in genetically defined populations of neurons with millisecond precision.”

Griffin, using a rat model, will inject the light-sensitizing substance — a harmless virus — into the nucleus reuniens and then use a laser to inhibit or activate this brain region. The rats then perform tasks that assess their working memory. Synchronization between the hippocampus and prefrontal cortex will also be recorded, with the prediction that the degree of the working memory impairment will be correlated with reductions in synchrony.

“Our experiments will not be interfering with the activities of the hippocampus or the prefrontal cortex within themselves,” Griffin said. “We want to affect only the ability of the structures to talk to each other.”

Neural Anatomy of Primary Visual Cortex Limits Visual Working Memory

Despite the immense processing power of the human brain, working memory storage is severely limited, and the neuroanatomical basis of these limitations has remained elusive. Here, we show that the stable storage limits of visual working memory for over 9 s are bound by the precise gray matter volume of primary visual cortex (V1), defined by fMRI retinotopic mapping. Individuals with a bigger V1 tended to have greater visual working memory storage. This relationship was present independently for both surface size and thickness of V1 but absent in V2, V3 and for non-visual working memory measures. Additional whole-brain analyses confirmed the specificity of the relationship to V1. Our findings indicate that the size of primary visual cortex plays a critical role in limiting what we can hold in mind, acting like a gatekeeper in constraining the richness of working mental function.

Full Article

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Important advance in brain mapping and memory

“When a tiger starts to move towards you, you need to know whether it is something you are actually seeing or whether it’s just something that you remember or have imagined,” says Prof. Julio Martinez-Trujillo of McGill’s Department of Physiology. The researcher and his team have discovered that there is a clear frontier in the brain between the area that encodes information about what is immediately before the eyes and the area that encodes the abstract representations that are the product of our short-term memory or imagination. It is an important advance in brain mapping and opens the doors to further research in the area of short-term memory.

These finding, which are described in an article just published in Nature Neuroscience, resolve a question that has occupied neuroscientists for years. Namely that of how and where exactly in the brain the visual information coming from our eyes is first transformed into short-term memories. “We found that while one area in the brain processes information about what we are currently seeing, an area right beside it stores the information in short-term memory,” says McGill PhD student Diego Mendoza-Halliday, first author of the article.  “What is so exciting about this finding is that until now, no one knew the place where visual information first gets transformed into short-term memory.”

The researchers arrived at this conclusion by measuring the neuronal activity in these two areas in the brains of macaques as they first looked at, and then after a short time (1.2 - 2 seconds) remembered, a random sequence of dots moving across a computer screen like rainfall. What surprised Martinez-Trujillo and his team was how clearly demarcated the divide was between the activities and functions of the two brain areas, and this despite the fact that they lie side-by-side.

“It is rare to find this kind of sharp boundary in biological systems of any kind,” says Martinez-Trujillo. “Most of the time, when you look at the function of different brain areas, there is more of a transitional zone, more grey and not such a clear border between black and white. I think the evolutionary reason for this clear frontier is that it helped us to survive in dangerous situations.”

The discovery comes after five years spent by Martinez-Trujillo and his team doing research in the area. Despite this fact, he acknowledges that there was a certain amount of serendipity, and a lot of technological help involved in being able to capture a signal that travels for 3 milliseconds and fires synapses in neurons that lie right beside one another.

Martinez-Trujillo and his team continue to work on mapping the receptors and connectivity between these two areas of the brain. But what is most important for him is to try and relate this discovery to schizophrenia and other diseases that involve hallucinations, and in order to do so he is working with a psychiatrist at Montreal’s Douglas Hospital.

(Image: Bigstock)

Prenatal Alcohol Exposure Alters Development of Brain Function

In the first study of its kind, Prapti Gautam, PhD, and colleagues from The Saban Research Institute of Children’s Hospital Los Angeles found that children with fetal alcohol spectrum disorders (FASD) showed weaker brain activation during specific cognitive tasks than their unaffected counterparts. These novel findings suggest a possible neural mechanism for the persistent attention problems seen in individuals with FASD. The results of this study will be published in Cerebral Cortex on August 4.

“Functional magnetic resonance imaging (fMRI) has been used to observe brain activity during mental tasks in children with FASD, but we are the first to utilize these techniques to look at brain activation over time,” says Gautam. “We wanted to see if the differences in brain activation between children with FASD and their healthy peers were static, or if they changed as children got older.”

FASD encompasses the broad spectrum of symptoms that are linked to in utero alcohol exposure, including cognitive impairment, deficits in intelligence and attention and central nervous system abnormalities. These symptoms can lead to attention problems and higher societal and economic burdens common in individuals with FASD.

During the period of childhood and adolescence, brain function, working memory and attention performance all rapidly improve, suggesting that this is a crucial time for developing brain networks. To study how prenatal alcohol exposure may alter this development, researchers observed a group of unaffected children and a group of children with FASD over two years. They used fMRI to observe brain activation through mental tasks such as visuo-spatial attention—how we visually perceive the spatial relationships among objects in our environment —and working memory.

“We found that there were significant differences in development brain activation over time between the two groups, even though they did not differ in task performance,” notes Elizabeth Sowell, PhD, director of the Developmental Cognitive Neuroimaging Laboratory at The Saban Research Institute and senior author on the manuscript. “While the healthy control group showed an increase in signal intensity over time, the children with FASD showed a decrease in brain activation during visuo-spatial attention, especially in the frontal, temporal and parietal brain regions.”

These results demonstrate that prenatal alcohol exposure can change how brain signaling develops during childhood and adolescence, long after the damaging effects of alcohol exposure in utero. The atypical development of brain activation observed in children with FASD could explain the persistent problems in cognitive and behavioral function seen in this population as they mature.