Posts tagged neuroscience
Articles and news from the latest research reports.
Brain scans could predict response to antipsychotic medication
Researchers from King’s College London and the University of Nottingham have identified neuroimaging markers in the brain which could help predict whether people with psychosis respond to antipsychotic medications or not.
In approximately half of young people experiencing their first episode of a psychosis (FEP), the symptoms do not improve considerably with the initial medication prescribed, increasing the risk of subsequent episodes and worse outcome. Identifying individuals at greatest risk of not responding to existing medications could help in the search for improved medications, and may eventually help clinicians personalize treatment plans.
In a study published today in JAMA Psychiatry, researchers used structural Magnetic Resonance Imaging (MRI) to scan the brains of 126 individuals – 80 presenting with FEP, and 46 healthy controls. Participants had an MRI scan shortly after their FEP, and another assessment 12 weeks later, to establish whether symptoms had improved following the first treatment with antipsychotic medications.
The researchers examined a particular feature of the brain called “cortical gyrification” - the extent of folding of the cerebral cortex and a marker of how it has developed. They found that the individuals who did not respond to treatment already had a significant reduction in gyrification across multiple brain regions, compared to patients who did respond and to individuals without psychosis. This reduced gyrification was particularly present in brain areas considered important in psychosis, such as the temporal and frontal lobes. Those who responded to treatment were virtually indistinguishable from the healthy controls.
The researchers also investigated whether the differences could be explained by the type of diagnosis of psychosis (eg. with or without affective symptoms, such as depression or elated mood). They found that reduced gyrification predicted non-response to treatment independently of the diagnosis.
Dr Paola Dazzan from the Department of Psychosis Studies at King’s College London’s Institute of Psychiatry, and senior author of the paper, says: “Our study provides crucial evidence of a neuroimaging marker that, if validated, could be used early in psychosis to help identify those people less likely to respond to medications. It is possible that the alterations we observed are due to differences in the way the brain has developed early on in people who do not respond to medication compared to those who do.”
She continues:”There have been few advances in developing novel anti-psychotic drugs over the past 50 years and we still face the same problems with a sub-group of people who do not respond to the drugs we currently use. We could envisage using a marker like this one to identify people who are least likely to respond to existing medications and focus our efforts on developing new medication specifically adapted to this group. In the longer term, if we were able to identify poor responders at the outset, we may be able to formulate personalized treatment plans for that individual patient.”
Dr Lena Palaniyappan from the University of Nottingham adds: “All of us have complex and varying patterns of folding in our brains. For the first time we are showing that the measurement of these variations could potentially guide us in treating psychosis. It is possible that people with specific patterns of brain structure respond better to treatments other than antipsychotics that are currently in use. Clearly, the time is ripe for us to focus on utilising neuroimaging to guide treatment decisions.”
Psychosis is a term used to indicate mental health disorders that present with symptoms like hallucinations (such as hearing voices) or delusions (unshakeable beliefs based on the person’s altered perception of reality, which may not correspond to the way others see the world). Psychotic episodes are present in conditions such as schizophrenia and bipolar disorder.
Approximately 1 in 100 people in England have at least one episode of psychosis throughout their lives. In most cases, psychosis develops during late adolescence (15 or above) or adulthood. Treatment involves a combination of antipsychotic medication, psychological therapies and social support. Many people with psychosis go on to lead ordinary lives and for about 60% of people, the symptoms disappear within 12 months from onset. However, for others, treatment is less straightforward and many do not respond to the initial antipsychotic treatment prescribed by their doctor. Early response to antipsychotic medication is known to be associated with better outcome and fewer subsequent episodes, and intervening early with effective treatments is therefore important.
(Source: kcl.ac.uk)
Two left feet? Study looks to demystify why we lose our balance
It’s always in front of a million people and feels like eternity. You’re strolling along when suddenly you’ve stumbled—the brain realizes you’re falling, but your muscles aren’t doing anything to stop it.
For a young person, a fall is usually just embarrassing. However, for the elderly, falling can be life threatening. Among the elderly who break a hip, 80 percent die within a year.
University of Michigan researchers believe that the critical window of time between when the brain senses a fall and the muscles respond may help explain why so many older people suffer these serious falls. A better understanding of what happens in the brain and muscles during this lag could go a long way toward prevention.
To that end, researchers at the U-M School of Kinesiology developed a novel way of looking at the electrical response in the brain before and during a fall by using an electroencephalogram.
Findings showed that many areas of the brain sense and respond to a fall, but that happens well before the muscles react. Lead researcher Daniel Ferris likened the study method to recording an orchestra with many microphones and then teasing out the sounds of specific instruments. In the study, researchers measured electrical activity in different regions of the brain.
"We’re using an EEG in a way others don’t, to look at what’s going on inside the brain," said Ferris, a professor in kinesiology. "We were able to determine what parts of the brain first identify when you are losing your balance during walking."
During the study, healthy young subjects with electrodes attached to their scalps walked on a balance beam mounted to a treadmill. When participants lost their balance and went off the beam, they simply continued walking on the moving treadmill, thus avoiding injury.
Ferris and colleagues then used a method called independent components analysis to separate and visualize the electrical activity in different parts of the brain. They found that people sense the start of a fall much better with both feet on the ground. Two grounded feet make it easier to determine where the ground is relative to the body, but people aren’t as sure of their stability on one foot.
The researchers were surprised that so many different parts of the brain activate during a fall, and they didn’t expect the brain to recognize a loss of balance as early as it does.
Future studies comparing the elderly with younger subjects could determine if the elderly sense falls too late, in which case, pharmaceuticals might help them regain their balance. If it’s a simple motor problem such as muscles not responding properly, strengthening exercises could help.
Other experiments under the same grant in the Ferris lab look to separate sensory and motor contributions to brain activity during walking.
The study, “Loss of balance during balance beam walking elicits a broadly distributed theta band electrocortical response,” was published in advance online in the Journal of Neurophysiology.
Researchers Building a Computer Chip Based on the Human Brain
Today’s computing chips are incredibly complex and contain billions of nano-scale transistors, allowing for fast, high-performance computers, pocket-sized smartphones that far outpace early desktop computers, and an explosion in handheld tablets.
Despite their ability to perform thousands of tasks in the blink of an eye, none of these devices even come close to rivaling the computing capabilities of the human brain. At least not yet. But a Boise State University research team could soon change that.
Electrical and computer engineering faculty Elisa Barney Smith, Kris Campbell and Vishal Saxena are joining forces on a project titled “CIF: Small: Realizing Chip-scale Bio-inspired Spiking Neural Networks with Monolithically Integrated Nano-scale Memristors.”
Team members are experts in machine learning (artificial intelligence), integrated circuit design and memristor devices. Funded by a three-year, $500,000 National Science Foundation grant, they have taken on the challenge of developing a new kind of computing architecture that works more like a brain than a traditional digital computer.
“By mimicking the brain’s billions of interconnections and pattern recognition capabilities, we may ultimately introduce a new paradigm in speed and power, and potentially enable systems that include the ability to learn, adapt and respond to their environment,” said Barney Smith, who is the principal investigator on the grant.
The project’s success rests on a memristor – a resistor that can be programmed to a new resistance by application of electrical pulses and remembers its new resistance value once the power is removed. Memristors were first hypothesized to exist in 1972 (in conjunction with resistors, capacitors and inductors) but were fully realized as nano-scale devices only in the last decade.
One of the first memristors was built in Campbell’s Boise State lab, which has the distinction of being one of only five or six labs worldwide that are up to the task.
The team’s research builds on recent work from scientists who have derived mathematical algorithms to explain the electrical interaction between brain synapses and neurons.
“By employing these models in combination with a new device technology that exhibits similar electrical response to the neural synapses, we will design entirely new computing chips that mimic how the brain processes information,” said Barney Smith.
Even better, these new chips will consume power at an order of magnitude lower than current computing processors, despite the fact that they match existing chips in physical dimensions. This will open the door for ultra low-power electronics intended for applications with scarce energy resources, such as in space, environmental sensors or biomedical implants.
Once the team has successfully built an artificial neural network, they will look to engage neurobiologists in parallel to what they are doing now. A proposal for that could be written in the coming year.
Barney Smith said they hope to send the first of the new neuron chips out for fabrication within weeks.
Two different versions of the same signaling protein tell a nerve cell which end is which, UA researchers have discovered. The findings could help improve therapies for spinal injuries and neurodegenerative diseases.
University of Arizona scientists have discovered an unknown mechanism that establishes polarity in developing nerve cells. Understanding how nerve cells make connections is an important step in developing cures for nerve damage resulting from spinal cord injuries or neurodegenerative diseases such as Alzheimer’s.
In a study published on Aug. 12 in the journal Proceedings of the National Academy of Sciences, UA doctoral student Sara Parker and her adviser, assistant professor of cellular and molecular medicine Sourav Ghosh, report that the decision which will be the “plus” and the “minus” end in a newborn nerve cell is made by a long and a short version of the same signaling molecule.
Nerve cells – or neurons – differ from many other cells by their highly asymmetric shape: Vaguely resembling a tree, a neuron has one long, trunk-like extension ending in a tuft of root-like bristles. This is called the axon. From the opposite end of the cell body sprout branch-like structures known as dendrites. By connecting the “branches” of their dendrites to the “root tips” of other neurons’ axons, nerve cells form networks, which can be as simple as the few connections involved in the knee-jerk reflex or as complex as those in the human brain.
Parker and her team found that embryonic nerve cells manufacture a well-known signaling enzyme called Atypical Protein Kinase C (aPKC) in two varieties: a full-length one and a truncated one. Both varieties compete to bind the same molecular partner, a protein called Par3. If the short form of aPKC pairs up with Par3, it tells the cell to grow a dendrite, and if the long one pairs up with Par3, it will make an axon instead.
When the researchers blocked the production of the short form, the nerve cell grew multiple axons and no dendrites. When they created an artificial abundance of the short form, dendrites formed at the expense of axons. UA undergraduate student Sophie Hapak performed many of the experiments revealing how the two isoforms compete for Par3.
"We show that wiring a neuronal circuit is much more complex than previously thought," said Ghosh. "The process has a built-in robustness that explicitly defines which part of the cell is ‘positive’ and which is ‘negative.’"
"In order to have a functioning neuronal circuit, you have to have receiving and sending ends," Parker said. "Initially, when a neuron is formed, it lacks the polarity it needs once it develops into a part of a circuit. The mechanism we discovered establishes that polarity."
"How the various brain regions are wired is the basis of emotion, memory and all cognitive functions," said Ghosh, who is a member of the UA’s BIO5 Institute. "Establishing neuronal polarity in single neurons is absolutely essential for neuronal circuits to form."
"If we understand this mechanism, we could think about methods to spur new axons after the original ones were severed in a traumatic spinal cord injury, for example," Ghosh said.
The findings defy conventional wisdom, which maintains that a developing neuron will make dendrites by default unless instructed by the long form of aPKC to make an axon instead. By cultivating and studying neurons just after they formed, Parker and her group found that both forms of aPKC, long and short, are initially distributed equally throughout the cell. These forms subsequently segregate into different parts of the cell as the neuron matures and establishes polarity.
Because the cells were isolated from rat brains and kept in culture, the researchers could demonstrate that no external clues from other cells are needed to instruct a developing neuron. Whether the establishment of polarity is a random process or whether other signals yet to be identified play a role in regulating the abundance of the two aPKC varieties is not known.
Researchers Debunk Myth of “Right-brain” and “Left-brain”Personality Traits
Newly released research findings from University of Utah neuroscientists assert that there is no evidence within brain imaging that indicates some people are right-brained or left-brained.
Chances are, you’ve heard the label of being a “right-brained” or “left-brained” thinker. Logical, detail-oriented and analytical? That’s left-brained behavior. Creative, thoughtful and subjective? Your brain’s right side functions stronger —or so long-held assumptions suggest.
But newly released research findings from University of Utah neuroscientists assert that there is no evidence within brain imaging that indicates some people are right-brained or left-brained.
For years in popular culture, the terms left-brained and right-brained have come to refer to personality types, with an assumption that some people use the right side of their brain more, while some use the left side more.
Following a two-year study, University of Utah researchers have debunked that myth through identifying specific networks in the left and right brain that process lateralized functions. Lateralization of brain function means that there are certain mental processes that are mainly specialized to one of the brain’s left or right hemispheres. During the course of the study, researchers analyzed resting brain scans of 1,011 people between the ages of seven and 29. In each person, they studied functional lateralization of the brain measured for thousands of brain regions —finding no relationship that individuals preferentially use their left -brain network or right- brain network more often.
“It’s absolutely true that some brain functions occur in one or the other side of the brain. Language tends to be on the left, attention more on the right. But people don’t tend to have a stronger left- or right-sided brain network. It seems to be determined more connection by connection, ” said Jeff Anderson, M.D., Ph.D., lead author of the study, which is formally titled “An Evaluation of the Left-Brain vs. Right-Brain Hypothesis with Resting State Functional Connectivity Magnetic Resonance Imaging.” It is published in the journal PLOS ONE this month.
Researchers obtained brain scans for the population they studied from a database called INDI, the International Neuroimaging Data-Sharing Initiative. The participants’ scans were taken during a functional connectivity MRI analysis, meaning a participant laid in a scanner for 5 to 10 minutes while their resting brain activity was analyzed.
By viewing brain activity, scientists can correlate brain activity in one region of the brain compared to another. In the study, researchers broke up the brain into 7,000 regions and examined which regions of the brain were more lateralized. They looked for connections — or all of the possible combinations of brain regions — and added up the number of connections for each brain region that was left- lateralized or right-lateralized. They discovered patterns in brain imaging for why a brain connection might be strongly left- or right-lateralized, said Jared Nielsen, a graduate student in neuroscience who carried out the study as part of his coursework.
“If you have a connection that is strongly left- lateralized, it relates to other strongly lateralized connection only if both sets of connections have a brain region in common,” said Nielsen.
Results of the study are groundbreaking, as they may change the way people think about the old right-brain versus left-brain theory, he said.
“Everyone should understand the personality types associated with the terminology ‘left-brained’ and ‘right-brained’ and how they relate to him or her personally; however, we just don’t see patterns where the whole left-brain network is more connected or the whole right-brain network is more connected in some people. It may be that personality types have nothing to do with one hemisphere being more active, stronger, or more connected,” said Nielsen.
Newly Discovered ‘Switch’ Plays Dual Role In Memory Formation
Researchers at Johns Hopkins have uncovered a protein switch that can either increase or decrease memory-building activity in brain cells, depending on the signals it detects. Its dual role means the protein is key to understanding the complex network of signals that shapes our brain’s circuitry, the researchers say. A description of their discovery appears in the July 31 issue of the Journal of Neuroscience.
“What’s interesting about this protein, AGAP3, is that it is effectively double-sided: One side beefs up synapses in response to brain activity, while the other side helps bring synapse-building back down to the brain’s resting state,” says Richard Huganir, Ph.D., a professor and director of the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins University School of Medicine and co-director of the Brain Science Institute at Johns Hopkins. “The fact that it links these two opposing activities indicates AGAP3 may turn out to be central to controlling the strength of synapses.”
Huganir has long studied how connections between brain cells, known as synapses, are strengthened and weakened to form or erase memories. The new discovery came about when he and postdoctoral fellow Yuko Oku, Ph.D., investigated the chain reaction of signals involved in one type of synaptic strengthening.
In a study of the proteins that interact with one of the known proteins from that chain reaction, the previously unknown AGAP3 turned up. It contained not only a site designed to bind another protein involved in the chain reaction that leads from brain stimulation to learning, but also a second site involved in bringing synapse-building activity down to normal levels after a burst of activity.
Although it might seem the two different functions are behaving at cross-purposes, Oku says, it also could be that nature’s bundling of these functions together in a single protein is an elegant way of enabling learning and memory while preventing dangerous overstimulation. More research is needed, Oku says, to figure out whether AGAP3’s two sites coordinate by affecting each other’s activity, or are effectively free agents.
A hypnotic suggestion can generate true and automatic hallucinations
A multidisciplinary group of researchers from Finland (University of Turku and University of Helsinki) and Sweden (University of Skövde) has now found evidence that hypnotic suggestion can modify processing of a targeted stimulus before it reaches consciousness. The experiments show that it is possible to hypnotically modulate even highly automatic features of perception, such as color experience. The results are presented in two articles published in PLoS ONE and International Journal of Clinical and Experimental Hypnosis. The Finnish part of the research is funded by the Academy of Finland.
The nature of hypnotically suggested changes in perception has been one of the main topics of controversy during the history of hypnosis. The major current theories of hypnosis hold that we always actively use our own imagination to bring about the effects of a suggestion. For example the occurrence of visual hallucinations always requires active use of goal directed imagery and can be experienced both with and without hypnosis.
The study published in PLoS ONE was done with two very highly hypnotizable participants who can be hypnotized and dehypnotized by just using a one-word cue.
The researchers measured brains oscillatory activity from the EEG in response to briefly displayed series of red or blue shapes (squares, triangles or circles). The participants were hypnotized and given a suggestion that certain shapes always have a certain color (e.g. all squares are always red). Participant TS-H reported constantly experiencing a change in color immediately when a suggested shape appeared on the screen (e.g. seeing a red square when the real color was blue). The researchers found that this experience was accompanied with enhanced high-frequency brain activity already 1/10 second after the stimulus appeared and it was only seen in response to the shapes mentioned in the suggestion. The second participant did not experience the color change or the enhanced activity. However, she reported a peculiar feeling when a suggestion-relevant shape was presented: “sometimes I saw a shape that was red but my brain told me it had a different color”.
This enhanced oscillatory brain activity is proposed to reflect automatic comparison of input to memory representations. In this case the hypnotic suggestion “all squares are red” led to a memory trace that was automatically activated when a square was presented. Furthermore, for the participant TS-H the effect was strong enough to override the real color of the square. The matching must have occurred preconsciously because of the early timing of the effect and the immediacy of the color change. Also, both participants reported having performed under posthypnotic amnesia without conscious memory of the suggestions.
In the article published in International Journal of Clinical and Experimental Hypnosis TS-H was tested in a similar type of setting, however, only behavioral data, including accuracy and response times in color recognition, were collected. These results further support that a hypnotic suggestion affects her color perception of targeted objects before she becomes conscious of them. Furthermore, TS-H was not capable of changing her experience of visually presented stable images without the use of hypnotic suggestions i.e. by using mere mental imagery.
Importantly, both of these experiments were done by using a posthypnotic suggestion. The effect was suggested during hypnosis but the experience was suggested to occur after hypnosis. Thus all the experiments were carried out while participants were in their normal state of consciousness.
This result indicates that all hypnotic responding can no longer be regarded merely as goal directed mental imagery. It shows that in hypnosis it is possible to create a memory trace that influences early and preconscious stages of visual processing already about 1/10 second after the appearance of a visual target. This result has important implications in psychology and cognitive neuroscience especially when studying visual perception, memory and consciousness.
Study identifies new culprit that may make aging brains susceptible to neurodegenerative diseases
The steady accumulation of a protein in healthy, aging brains may explain seniors’ vulnerability to neurodegenerative disorders, a new study by researchers at the Stanford University School of Medicine reports.
The study’s unexpected findings could fundamentally change the way scientists think about neurodegenerative disease.
The pharmaceutical industry has spent billions of dollars on futile clinical trials directed at treating Alzheimer’s disease by ridding brains of a substance called amyloid plaque. But the new findings have identified another mechanism, involving an entirely different substance, that may lie at the root not only of Alzheimer’s but of many other neurodegenerative disorders — and, perhaps, even the more subtle decline that accompanies normal aging.
The study, published Aug. 14 in the Journal of Neuroscience, reveals that with advancing age, a protein called C1q, well-known as a key initiator of immune response, increasingly lodges at contact points connecting nerve cells in the brain to one another. Elevated C1q concentrations at these contact points, or synapses, may render them prone to catastrophic destruction by brain-dwelling immune cells, triggered when a catalytic event such as brain injury, systemic infection or a series of small strokes unleashes a second set of substances on the synapses.
“No other protein has ever been shown to increase nearly so profoundly with normal brain aging,” said Ben Barres, MD, PhD, professor and chair of neurobiology and senior author of the study. Examinations of mouse and human brain tissue showed as much as a 300-fold age-related buildup of C1q.
The finding was made possible by the diligence and ingenuity of the study’s lead author, Alexander Stephan, PhD, a postdoctoral scholar in Barres’ lab. Stephan screened about 1,000 antibodies before finding one that binds to C1q and nothing else. (Antibodies are proteins, generated by the immune system, that adhere to specific “biochemical shapes,” such as surface features of invading pathogens.)
Comparing brain tissue from mice of varying ages, as well as postmortem samples from a 2-month-old infant and an older person, the researchers showed that these C1q deposits weren’t randomly distributed along nerve cells but, rather, were heavily concentrated at synapses. Analyses of brain slices from mice across a range of ages showed that as the animals age, the deposits spread throughout the brain.
“The first regions of the brain to show a dramatic increase in C1q are places like the hippocampus and substantia nigra, the precise brain regions most vulnerable to neurodegenerative diseases like Alzheimer’s and Parkinson’s disease, respectively,” said Barres. Another region affected early on, the piriform cortex, is associated with the sense of smell, whose loss often heralds the onset of neurodegenerative disease.
Other scientists have observed moderate, age-associated increases (on the order of three- or four-fold) in brain levels of the messenger-RNA molecule responsible for transmitting the genetic instructions for manufacturing C1q to the protein-making machinery in cells. Testing for messenger-RNA levels — typically considered reasonable proxies for how much of a particular protein is being produced — is fast, easy and cheap compared with analyzing proteins.
But in this study, Barres and his colleagues used biochemical measures of the protein itself. “The 300-fold rise in C1q levels we saw in 2-year-old mice — equivalent to 70- or 80-year-old humans — knocked my socks off,” Barres said. “I was not expecting that at all.”
C1q is the first batter on a 20-member team of immune-response-triggering proteins, collectively called the complement system. C1q is capable of clinging to the surface of foreign bodies such as bacteria or to bits of our own dead or dying cells. This initiates a molecular chain reaction known as the complement cascade. One by one, the system’s other proteins glom on, coating the offending cell or piece of debris. This in turn draws the attention of omnivorous immune cells that gobble up the target.
The brain has its own set of immune cells, called microglia, which can secrete C1q. Still other brain cells, called astrocytes, secrete all of C1q’s complement-system “teammates.” The two cell types work analogously to the two tubes of an Epoxy kit, in which one tube contains the resin, the other a catalyst.
Previous work in Barres’ lab has shown that the complement cascade plays a critical role in the developing brain. A young brain generates an excess of synapses, creating a huge range of options for the potential formation of new neural circuits. These synapses strengthen or weaken over time, in response to their heavy use or neglect. The presence of feckless connections contributes noise to the system, so the efficiency of the maturing brain’s architecture is improved if these underused synapses are pruned away.
In a 2007 paper in Cell, Barres’ group reported that the complement system is essential to synaptic pruning in normal, developing brains. Then in 2012, in Neuron, in a collaboration with the lab of Harvard neuroscientist Beth Stevens, PhD, they showed that it is specifically microglia — the brain’s in-house immune cells — that attack and ingest complement-coated synapses.
Barres now believes something similar is happening in the normal, aging brain. C1q, but not the other protein components of the complement system, gradually becomes highly prevalent at synapses. By itself, this C1q buildup doesn’t trigger wholesale synapse loss, the researchers found — although it does seem to impair their performance. Old mice whose capacity to produce C1q had been eliminated performed subtly better on memory and learning tests than normal older mice did.
Still, this leaves the aging brain’s synapses precariously perched on the brink of catastrophe. A subsequent event such as brain trauma, a bad case of pneumonia or perhaps a series of tiny strokes that some older people experience could incite astrocytes — the second tube in the Epoxy kit — to start secreting the other complement-system proteins required for synapse destruction.
Most cells in the body have their own complement-inhibiting agents. This prevents the wholesale loss of healthy tissue during an immune attack on invading pathogens or debris from dead tissue during wound healing. But nerve cells lack their own supply of complement inhibitors. So, when astrocytes get activated, their ensuing release of C1q’s teammates may set off a synapse-destroying rampage that spreads “like a fire burning through the brain,” Barres said.
“Our findings may well explain the long-mysterious vulnerability specifically of the aging brain to neurodegenerative disease,” he said. “Kids don’t get Alzheimer’s or Parkinson’s. Profound activation of the complement cascade, associated with massive synapse loss, is the cardinal feature of Alzheimer’s disease and many other neurodegenerative disorders. People have thought this was because synapse loss triggers inflammation. But our findings here suggest that activation of the complement cascade is driving synapse loss, not the other way around.”
(Source: med.stanford.edu)
Brain scans may help diagnose dyslexia
Differences in a key language structure can be seen even before children start learning to read.
About 10 percent of the U.S. population suffers from dyslexia, a condition that makes learning to read difficult. Dyslexia is usually diagnosed around second grade, but the results of a new study from MIT could help identify those children before they even begin reading, so they can be given extra help earlier.
The study, done with researchers at Boston Children’s Hospital, found a correlation between poor pre-reading skills in kindergartners and the size of a brain structure that connects two language-processing areas.
Previous studies have shown that in adults with poor reading skills, this structure, known as the arcuate fasciculus, is smaller and less organized than in adults who read normally. However, it was unknown if these differences cause reading difficulties or result from lack of reading experience.
“We were very interested in looking at children prior to reading instruction and whether you would see these kinds of differences,” says John Gabrieli, the Grover M. Hermann Professor of Health Sciences and Technology, professor of brain and cognitive sciences and a member of MIT’s McGovern Institute for Brain Research.
Gabrieli and Nadine Gaab, an assistant professor of pediatrics at Boston Children’s Hospital, are the senior authors of a paper describing the results in the Aug. 14 issue of the Journal of Neuroscience. Lead authors of the paper are MIT postdocs Zeynep Saygin and Elizabeth Norton.
The path to reading
The new study is part of a larger effort involving approximately 1,000 children at schools throughout Massachusetts and Rhode Island. At the beginning of kindergarten, children whose parents give permission to participate are assessed for pre-reading skills, such as being able to put words together from sounds.
“From that, we’re able to provide — at the beginning of kindergarten — a snapshot of how that child’s pre-reading abilities look relative to others in their classroom or other peers, which is a real benefit to the child’s parents and teachers,” Norton says.
The researchers then invite a subset of the children to come to MIT for brain imaging. The Journal of Neuroscience study included 40 children who had their brains scanned using a technique known as diffusion-weighted imaging, which is based on magnetic resonance imaging (MRI).
This type of imaging reveals the size and organization of the brain’s white matter — bundles of nerves that carry information between brain regions. The researchers focused on three white-matter tracts associated with reading skill, all located on the left side of the brain: the arcuate fasciculus, the inferior longitudinal fasciculus (ILF) and the superior longitudinal fasciculus (SLF).
When comparing the brain scans and the results of several different types of pre-reading tests, the researchers found a correlation between the size and organization of the arcuate fasciculus and performance on tests of phonological awareness — the ability to identify and manipulate the sounds of language.
Phonological awareness can be measured by testing how well children can segment sounds, identify them in isolation, and rearrange them to make new words. Strong phonological skills have previously been linked with ease of learning to read. “The first step in reading is to match the printed letters with the sounds of letters that you know exist in the world,” Norton says.
The researchers also tested the children on two other skills that have been shown to predict reading ability — rapid naming, which is the ability to name a series of familiar objects as quickly as you can, and the ability to name letters. They did not find any correlation between these skills and the size or organization of the white-matter structures scanned in this study.
Brian Wandell, director of Stanford University’s Center for Cognitive and Neurobiological Imaging, says the study is a valuable contribution to efforts to find biological markers that a child is likely to need extra help to learn to read.
“The work identifies a clear marker that predicts reading, and the marker is present at a very young age. Their results raise questions about the biological basis of the marker and provides scientists with excellent new targets for study,” says Wandell, who was not part of the research team.
Early intervention
The left arcuate fasciculus connects Broca’s area, which is involved in speech production, and Wernicke’s area, which is involved in understanding written and spoken language. A larger and more organized arcuate fasciculus could aid in communication between those two regions, the researchers say.
Gabrieli points out that the structural differences found in the study don’t necessarily reflect genetic differences; environmental influences could also be involved. “At the moment when the children arrive at kindergarten, which is approximately when we scan them, we don’t know what factors lead to these brain differences,” he says.
The researchers plan to follow three waves of children as they progress to second grade and evaluate whether the brain measures they have identified predict poor reading skills.
“We don’t know yet how it plays out over time, and that’s the big question: Can we, through a combination of behavioral and brain measures, get a lot more accurate at seeing who will become a dyslexic child, with the hope that that would motivate aggressive interventions that would help these children right from the start, instead of waiting for them to fail?” Gabrieli says.
For at least some dyslexic children, offering extra training in phonological skills can help them improve their reading skills later on, studies have shown.
Oprah’s and Einstein’s faces help spot dementia
New test designed for younger people reveals early-onset dementia
Simple tests that measure the ability to recognize and name famous people such as Albert Einstein, Bill Gates or Oprah Winfrey may help doctors identify early dementia in those 40 to 65 years of age, according to new Northwestern Medicine research.
The research appears in the August 13, 2013, print issue of Neurology, the medical journal of the American Academy of Neurology.
"These tests also differentiate between recognizing a face and actually naming it, which can help identify the specific type of cognitive impairment a person has," said study lead author Tamar Gefen, a doctoral candidate in neuropsychology at the Cognitive Neurology and Alzheimer’s Disease Center at Northwestern University Feinberg School of Medicine.
Gefen did the research in the lab of senior author Emily Rogalski, assistant research professor at Northwestern’s Cognitive Neurology and Alzheimer’s Disease Center.
Face recognition tests exist to help identify dementia, but they are outdated and more suitable for an older generation.
"The famous faces for this study were specifically chosen for their relevance to individuals under age 65, so that the test may be useful for diagnosing dementia in younger individuals," Rogalski said. An important component of the test is that it distinguishes deficits in remembering the name of a famous person from that of recognizing the same individual, she noted.
The study also used quantitative software to analyze MRI scans of the brains of the individuals who completed the test to understand the brain areas important for naming and recognition of famous faces.
For the study, 30 people with primary progressive aphasia, a type of early onset dementia that mainly affects language, and 27 people without dementia, all an average age of 62, were given a test. The test includes 20 famous faces printed in black and white, including John F. Kennedy, Lucille Ball, Princess Diana, Martin Luther King Jr. and Elvis Presley.
Participants were given points for each face they could name. If the subject could not name the face, he or she was asked to identify the famous person through description. Participants gained more points by providing at least two relevant details about the person. The two groups also underwent MRI brain scans.
Researchers found that the people who had primary progressive aphasia, a form of early onset dementia, performed significantly worse on the test, scoring an average of 79 percent in recognition of famous faces and 46 percent in naming the faces, compared to 97 percent in recognition and 93 percent on naming for those free of dementia.
The study also found that people who had trouble putting names to the faces were more likely to have a loss of brain tissue in the left temporal lobe of the brain, while those with trouble recognizing the faces had tissue loss on both the left and right temporal lobe.
"In addition to its practical value in helping us identify people with early dementia, this test also may help us understand how the brain works to remember and retrieve its knowledge of words and objects," Gefen said.