Posts tagged brain
Articles and news from the latest research reports.
Research Reveals Exactly How the Human Brain Adapts to Injury
For the first time, scientists at Carnegie Mellon University’s Center for Cognitive Brain Imaging (CCBI) have used a new combination of neural imaging methods to discover exactly how the human brain adapts to injury. The research, published in Cerebral Cortex, shows that when one brain area loses functionality, a “back-up” team of secondary brain areas immediately activates, replacing not only the unavailable area but also its confederates.
“The human brain has a remarkable ability to adapt to various types of trauma, such as traumatic brain injury and stroke, making it possible for people to continue functioning after key brain areas have been damaged,” said Marcel Just, the D. O. Hebb Professor of Psychology at CMU and CCBI director. “It is now clear how the brain can naturally rebound from injuries and gives us indications of how individuals can train their brains to be prepared for easier recovery. The secret is to develop alternative thinking styles, the way a switch-hitter develops alternative batting styles. Then, if a muscle in one arm is injured, they can use the batting style that relies more on the uninjured arm.”
For the study, Just, Robert Mason, senior research psychologist at CMU, and Chantel Prat, assistant professor of psychology at the University of Washington, used functional magnetic resonance imaging (fMRI) to study precisely how the brains of 16 healthy adults adapted to the temporary incapacitation of the Wernicke area, the brain’s key region involved in language comprehension. They applied Transcranial Magnetic Stimulation (TMS) in the middle of the fMRI scan to temporarily disable the Wernicke area in the participants’ brains. The participants, while in the MRI scanner, were performing a sentence comprehension task before, during and after the TMS was applied. Normally, the Wernicke area is a major player in sentence comprehension.
The research team used the fMRI scans to measure how the brain activity changed immediately following stimulation to the Wernicke area. The results showed that as the brain function in the Wernicke area decreased following the application of TMS, a “back-up” team of secondary brain areas immediately became activated and coordinated, allowing the individual’s thought process to continue with no decrease in comprehension performance.
The brain’s back-up team consisted of three types of brain regions: (1) contralateral areas —areas that are in the mirror-image location of the brain; (2) areas that are right next to the impaired area; and (3) a frontal executive area.
“The first two types of back-up areas have similar brain capabilities as the impaired Wernicke area, although they are less efficient at the capability,” Just said. “The third area plays a strategic role as in responding to the initial impairment and recruiting back-up areas with similar capabilities.”
Additionally, the research showed that impairing the Wernicke area also negatively affected the cortical partners with which the Wernicke area had been working. “Thinking is a network function,” Just explained. “When a key node of a network is impaired, the network that is closely collaborating with the impaired node is also impaired. People do their thinking with groups of brain areas, not with single brain areas.”
Mason, the study’s lead author, noted that following the TMS, the impaired area and its partners gradually returned to their previous levels of coordinated activity, while the back-up team of brain areas was still in place. “This means, that for some period of time, there were two cortical teams operating simultaneously, explaining why performance is sometimes improved by TMS,” he said.
This research builds on Just’s previous research on brain resilience after stroke and brain training to remediate dyslexia. The studies are motivated by a computational theory, called 4CAPS, that provides an account of how autonomous brain systems dynamically self-organize themselves in response to changing circumstances, which the researchers believe to be the basis of fluid intelligence.
Transmission of Tangles in Alzheimer’s Mice Provides More Authentic Model of Tau Pathology
Brain diseases associated with the misformed protein tau, including Alzheimer’s disease and frontotemporal lobar degeneration with tau pathologies, are characterized by neurofibrillary tangles (NFTs) comprised of pathological tau filaments. Tau tangles are also found in progressive supranuclear palsy, cortical basal degeneration and other related tauopathies, including chronic traumatic encephalopathy due to repetitive traumatic brain injuries sustained in sports or on the battle field.
By using synthetic fibrils made from pure recombinant protein, Penn researchers provide the first direct and compelling evidence that tau fibrils alone are entirely sufficient to recruit and convert soluble tau within cells into pathological clumps in neurons, followed by transmission of tau pathology to other inter-connected brain regions from a single injection site in an animal model of tau brain disease.
The laboratory of senior author Virginia M.-Y. Lee, Ph.D., MBA, director of the Center for Neurodegenerative Disease Research and professor of Pathology and Laboratory Medicine at the Perelman School of Medicine, University of Pennsylvania, published their findings in the Journal of Neuroscience this week.
“Our new model of tau pathology spread provides an explanation to account for the stereotypical progression of Alzheimer’s and other related tauopathies by implicating the cell-to-cell transmission of pathological tau in this process,” says Lee.
Studies Provide New Insights into Brain-Behavior Relationships
Approximately half a million individuals suffer strokes in the US each year, and about one in five develops some form of post-stroke aphasia, the partial or total loss of the ability to communicate. By comparing different types of aphasia, investigators have been able to gain new insights into the normal cognitive processes underlying language, as well as the potential response to interventions. Their findings are published alongside papers on hemispatial neglect and related disorders in the January, 2013 issue of Behavioural Neurology.
The January issue of Behavioural Neurology, edited by the journal’s co-Editor in Chief, Argye E. Hillis, MD, of the Departments of Neurology, Physical Medicine and Rehabilitation, and Department of Cognitive Science, Johns Hopkins University, Baltimore, Maryland, features papers on two topics that have traditionally captured the interest of behavioral neurologists – aphasia and hemispatial neglect.
The first section on aphasia includes a number of papers that compare post-stroke aphasia with primary progressive aphasia (PPA), in which the predominant deficit is language (with or without apraxia).
Andreia V. Faria, MD, Department of Radiology, Johns Hopkins University School of Medicine, and colleagues from Johns Hopkins and University College, London, report patterns of dysgraphia (spelling impairment) in participants with primary progressive aphasia, and compare these patterns to those in participants with dysgraphia following stroke. They also report the areas of focal atrophy associated with the most common pattern of dysgraphia in PPA and suggest this can not only provide a better understanding of the neural substrates of spelling, but may also provide clues to more effective treatment approaches.
Matthew A. Lambon Ralph, FRSLT (hons), FBPsS, and colleagues from the School of Psychological Sciences, University of Manchester, UK; the Department of Psychology, University of York, UK; and the Stroke and Dementia Research Centre, St George’s University of London, UK, use a novel approach to explore nonverbal semantic processing to demonstrate the qualitative differences between semantic aphasia and semantic dementia. Their conclusions provide further support for the proposal that semantic cognition is underpinned by two principle components: semantic representations and regulatory control processes which regulate and shape activation within the semantic system.
Cynthia K. Thompson, PhD, and colleagues from the Department of Communication Sciences and Disorders, Department of Neurology, Cognitive Neurology and Alzheimer’s Disease Center, and Department of Psychiatry and Behavioral Sciences at Northwestern University, Evanston, Illinois, evaluate the distinct patterns of morphological and syntactic errors in the variants of PPA, and compare them with patterns of errors in post-stroke aphasia.
Other papers compare treatment results of spelling in one individual with logopenic variant PPA (lvPPA) with an individual with post-stroke dysgraphia, and results of a new method of assessment of verbal and nonverbal memory in PPA. The issue is completed by three Clinical Notes including a fascinating case of an unusual form of lvPPA that degenerated into jargon aphasia, a case of nonfluent agrammatic variant PPA due to Pick disease with (what is argued to be) concomitant incidental Alzheimer’s disease pathology, and a case of successful treatment of PPA.
“Together, these papers illustrate how investigating PPA and post-stroke aphasia can yield complementary insights about brain-behavior relationships as well as about potential response to interventions and the normal cognitive processes underlying language,” says Dr Hillis.
Hemispatial neglect is characterized by reduced awareness of stimuli on one side of space. It occurs only after relatively focal (or at least asymmetric) brain damage, most commonly stroke, but is occasionally observed in other syndromes. In this second group of seven papers, Jonathan T. Kleinman, MD, of Johns Hopkins University School of Medicine, and Stanford University School of Medicine, Stanford, California, and colleagues from Johns Hopkins University School of Medicine, report an investigation of perseveration versus hemispatial neglect, and the lesion sites associated with each in acute stroke. The issue also includes an important paper by Junichi Ishizaki, PhD, and co-workers at the Department of Geriatric Behavioral Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan, of impaired visual-spatial attention in Alzheimer’s disease, which shows how a symmetric neurodegenerative disease results in impaired shifting of visual spatial attention, but not hemispatial neglect.
“Hemispatial neglect remains one of the most remarkable syndromes investigated by behavioral neurologists,” comments Dr Hillis. “These novel studies of neglect and related disorders provide new insights into brain-behavior relationships on the basis of detailed analysis of patient performance – and in many cases, their lesion sites.“
(Source: iospress.nl)
Whether in society or nature, decisions are often the result of complex interactions between many factors. Because of this it is usually difficult to determine how much weight the different factors have in making a final decision. Neuroscientists face a similar problem since decisions made by the brain always involve many neurons. Working in collaboration, the University of Tübingen and the Max Planck Institute for Biological Cybernetics, supported within the framework of the Bernstein Network, researchers lead by CIN professor Matthias Bethge have now shown how the weight of individual neurons in the decision-making process can be reconstructed despite interdependencies between the neurons.
When we see a person on the other side of the street who looks like an old friend, the informational input enters the brain via many sensory neurons. But which of these neurons are crucial in passing on the relevant information to higher brain areas, which will decide who the person is and whether to wave and say ‘hello’? A research group lead by Matthias Bethge has now developed an equation that allows them to calculate to what degree a given individual sensory neuron is involved in the decision process.
To approach this question, researchers have so far considered the information about the final decision that an individual sensory neuron carries. Just as an individual is considered suspicious if he or she is found to have insider information about a crime, those sensory neurons whose activity contains information about the eventual decision are presumed to have played a role in reaching the final decision. The problem with this approach is that neurons – much like people – are constantly communicating with each other. A neuron which itself is not involved in the decision may simply have received this information from a neighboring neuron and “joined in” the conversation. Actually, the neighboring cell sends out the crucial signal transmitted to the higher decision areas in the brain.
The new formula that has been developed by scientists addresses this by accounting not just for the information in the activity of any one neuron but also for the communication that takes place between them. This formula will now be used to determine whether only a few neurons that carry a lot of information are involved in the brain’s decision process, or whether the information contained in very many neurons gets combined. In particular, it will be possible to address the more fundamental question: In which decisions does the brain use information in an optimal way, and for which decisions is its processing suboptimal?
New Discovery in Autism-Related Disorder Reveals Key Mechanism in Brain Development and Disease
A new finding in neuroscience for the first time points to a developmental mechanism linking the disease-causing mutation in an autism-related disorder, Timothy syndrome, and observed defects in brain wiring, according to a study led by scientist Ricardo Dolmetsch and published online yesterday in Nature Neuroscience. These findings may be at the heart of the mechanisms underlying intellectual disability and many other brain disorders.
The present study reveals that a mutation of the disease-causing gene throws a key process of neurodevelopment into reverse. That is, the mutation underlying Timothy syndrome causes shrinkage, rather than growth, of the wiring needed for the development of neural circuits that underlie cognition.
“In addition to the implications for autism, what’s really exciting is that we now have a way to get at the core mechanisms tying genes and environmental influences to development and disease processes in the brain,” said Dolmetsch, Senior Director of Molecular Networks at the Allen Institute for Brain Science.
“Imagine what we can learn if we do this hundreds and hundreds of times for many different human genetic variations in a large-scale, systematic way. That’s what we are doing now at the Allen Institute,” Dolmetsch continued.
In normal brain development, brain activity causes branches emanating from neural cells to stretch or expand. In cells with the mutation, these branched extensions, called dendrites, instead retract in response to neural activity, according to this study. This results in abnormal brain circuitry favoring connections with nearby neurons rather than farther-reaching connections. Further, the study identified a previously unknown mode of signaling to uncover the chemical pathway that causes the dendritic retraction.
This finding may have wide-reaching implications in neuroscience, as impaired dendrite formation is a common feature of many neurodevelopmental disorders. Further, the same gene has been implicated in other disorders including bipolar disorder and schizophrenia.
Under Dolmetsch’s leadership, the Molecular Networks program at the Allen Institute, one of three major new initiatives announced by the Institute last March, is using similar methods on a grand scale. The Institute is probing a large number of human genetic variations and many pathways in the brain to untangle the cellular mechanisms of neurodevelopment and disease. In addition to identifying the molecular and environmental rules that shape how the brain is built, the program will create new research tools and data sets that it will share publicly with the global research community.
Timothy syndrome is a neurodevelopmental disorder associated with autism spectrum disorders and caused by a mutation in a single gene. In addition to autism, it is also characterized by cardiac arrhythmias, webbed fingers and toes, and hypoglycemia, and often leads to death in early childhood.
(Image: iStock)
Big Picture: Inside the Brain
The Spring 2013 issue of Big Picture, Inside the Brain, is now available online. This issue, explores the technologies that are helping us to understand the brain, including magnetic resonance imaging (MRI) and computed tomography (CT).
About the cover:
This photograph, taken by Robert Ludlow, shows the surface (cortex) of a human brain belonging to an epileptic patient. The image displays the bright red arteries that supply the brain with nutrients and oxygen and the purple veins that remove deoxygenated blood. This photograph was taken before an intracranial electrode recording procedure for epilepsy, in which electrical activity is measured from the exposed surface of the brain. To find out more about Robert’s image and its creation, view this video on the UCL Institute of Neurology’s website. (Wellcome Image Awards 2012)
How The Memory Works In Learning
Teachers are the caretakers of the development of students’ highest brain during the years of its most extensive changes. As such, they have the privilege and opportunity to influence the quality and quantity of neuronal and connective pathways so all children leave school with their brains optimized for future success.
This introduction to the basics of the neuroscience of learning includes information that should be included in all teacher education programs. It is intentionally brief such that it can be taught in a single day of instruction. Ideally there would be additional opportunities for future teachers to pursue further inquiry into the science of how the brain learns, retrieves, and applies information.
Shakespeare and Wordsworth boost the brain, new research reveals
Scientists, psychologists and English academics at Liverpool University have found that reading the works of the Bard and other classical writers has a beneficial effect on the mind, catches the reader’s attention and triggers moments of self-reflection.
Using scanners, they monitored the brain activity of volunteers as they read works by William Shakespeare, William Wordsworth, T.S Eliot and others.
They then “translated” the texts into more “straightforward”, modern language and again monitored the readers’ brains as they read the words.
Scans showed that the more “challenging” prose and poetry set off far more electrical activity in the brain than the more pedestrian versions.
Scientists were able to study the brain activity as it responded to each word and record how it “lit up” as the readers encountered unusual words, surprising phrases or difficult sentence structure.
This “lighting up” of the mind lasts longer than the initial electrical spark, shifting the brain to a higher gear, encouraging further reading.
The research also found that reading poetry, in particular, increases activity in the right hemisphere of the brain, an area concerned with “autobiographical memory”, helping the reader to reflect on and reappraise their own experiences in light of what they have read. The academics said this meant the classics were more useful than self-help books.
Philip Davis, an English professor who has worked on the study with the university’s magnetic resonance centre, will tell a conference this week: “Serious literature acts like a rocket-booster to the brain.
"The research shows the power of literature to shift mental pathways, to create new thoughts, shapes and connections in the young and the staid alike."
New understanding of brain’s early spatial development
Researchers at the University of Bath have uncovered a new understanding of how the brain develops its sense of space by working with blind people.
The researchers from the University’s Department of Psychology found that people who lose their sight later in life use a different method of following directions to those who are born without sight. This means that the brain needs to have a visual experience early on in life in order to build a visual perspective, or frame of reference, to know what is where.
The researchers carried out a study with participants including those who were congenitally blind; those who became blind later in life; and others who were sighted, to learn which methods the different groups used to remember where things are.
The study revealed that people who have been sighted and then become blind use a ‘allocentric’ reference frame, meaning they remember locations as they are positioned relative to one another, and this is the same as sighted people who do this task, even when blindfolded.
In contrast congenitally blind participants preferred an ‘egocentric’ reference frame meaning they first remember a starting point at home and then store a memory of the locations from the home location. Dr Michael Proulx who led the study said the results help us to understand more about the role of a critical period for developmental vision on spatial cognition and brain organisation.
He said: “In our study we were curious as to whether having visual experience during child development was key to creating the structures in the brain to support such an allocentric reference frame. First we found an interesting difference between the congenitally blind and sighted people: although the sighted people preferred the allocentric, reference frame, the congenitally blind participants preferred the self-centred or egocentric reference frame for remembering locations.
“The important piece of the puzzle, however, was whether the late blind people would perform like the congenitally blind, showing that current visual experience matters, or like the sighted, showing the role of early visual experience. The results were clear: the late blind performed the same as the sighted participants. Therefore having the experience of vision early in life lays the groundwork in the brain for the representation of locations in a different reference frame than that found in people who never had visual experience.”
All of the participants of the study were blindfolded and then walked to the locations of objects in a large room. They were later tested on a computer with a virtual pointing task that asked them to remember objects in the room relative to the other object locations.
Dr Proulx and his colleagues are following up this finding with additional research to investigate how additional information, such as the texture or sound of the environment, might influence the frame of reference used.
This would allow for improved maps rendered in Braille or sound to be produced for visually impaired persons to use in public places, such as rail stations, or in new cities.
They are also examining the impact of visual experience on the neural basis for spatial learning and memory by examining how the congenitally blind and late blind brains represent spatial information in the absence of vision.
My mistake or yours? How the brain decides
Humans and other animals learn by making mistakes. They can also learn from observing the mistakes of others. The brain processes self-generated errors in a region called the medial frontal cortex (MFC) but little is known about how it processes the observed errors of others. A Japanese research team led by Masaki Isoda and Atsushi Iriki of the RIKEN Brain Science Institute has now demonstrated that the MFC is also involved in processing observed errors.
The team studied the brains of monkeys while the animals performed the same task. Two monkeys sat opposite each other and took turns to choose between a yellow and green button, one of which resulted in a liquid reward for both. Each monkey’s turn consisted of two choices.
After blocks of between 5 and 17 choices, the button that resulted in reward was switched unpredictably, usually causing an error on the next choice. The choices made by each monkey immediately after such errors, or errors that were random, showed that they used both their own errors and their partner’s to guide their subsequent choices. While the monkeys performed this task, the researchers recorded activity of single neurons in their brains.
In this way they were able to determine which behavioural aspect was most closely associated with each neuron’s activity, explains Isoda. “We found that many neurons in the medial frontal cortex were not activated when the monkey made an error itself, but they became active when their partner made an error.” This brain activity shows that it is the MFC which processes observations of another’s error, and the corresponding behavior shows that observing and processing such errors guides subsequent actions.
“Such error identification and subsequent error correction are of crucial importance for developing and maintaining successful social communities,” says Isoda. “Humans are tuned into other people’s mistakes not only for competitive success, but also for cooperative group living. If non-invasive techniques become available in humans, then we should be able to identify medial frontal neurons that behave similarly.”
Having identified the MFC as being involved, Isoda now wants to delve deeper into the process. “The next steps will be to clarify whether the inactivation of medial frontal cortex neurons reduces the ability to identify others’ errors, and to determine whether other brain regions are also involved in the processing of others’ errors.”