Posts tagged science
Posts tagged science
In a paper published in the prestigious journal Science Translational Medicine, Professor Colin Masters from the Florey Institute of Neuroscience and Mental Health and University of Melbourne – and colleagues in the UK and US – have found rapid neuronal damage begins 10 to 20 years before symptoms appear.
“As part of this research we have observed other changes in the brain that occur when symptoms begin to appear. There is actually a slowing of the neurodegeneration,” said Professor Masters.
Autosomal-dominant Alzheimer’s affects families with a genetic mutation, predisposing them to the crippling disease. These families provide crucial insight into the development of Alzheimer’s because they can be identified years before symptoms develop. The information gleaned from this group will also influence treatment offered to those living with the more common age-related version. Only about one per cent of those with Alzheimer’s have the genetic type of the disease.
The next part of the study involves a clinical trial. Using a range of imaging techniques (MRI and PET) and analysis of blood and cerebrospinal fluid, individuals from the US, UK and Australia will be observed as they trial new drugs to test their safety, side effects and changes within the brain.
“As part of an international study, family members are invited to be part of a trial in which two experimental drugs are offered many years before symptoms appear,” Prof Masters says. “It’s going to be very interesting to see how clinical intervention affects this group of patients in the decades before symptoms appear.”
The Florey is looking to recruit more participants in the Dominantly Inherited Alzheimer Network (DIAN) study. Those who either know they have a genetic mutation that causes autosomal-dominant Alzheimer’s or who don’t know their genetic status but have a parent or sibling with the mutation are invited to email: email@example.com
By examining the sense of touch in stroke patients, a University of Delaware cognitive psychologist has found evidence that the brains of these individuals may be highly plastic even years after being damaged.
The research is published in the March 6 edition of the journal Current Biology, in an article written by Jared Medina, assistant professor of psychology at UD, and Brenda Rapp of Johns Hopkins University’s Department of Cognitive Science. The findings, which are focused on patients who lost the sense of touch in their hands after a stroke, also have potential implications for other impairments caused by brain damage, Medina said.
“Our lab is interested in how the brain represents the body, not just in the sense of touch,” he said. “That involves a lot of different areas of the brain.”
For decades, scientists have been mapping the brain to determine which areas control certain functions, from movement to emotion to memory. In terms of representing the sense of touch, researchers know which specific parts of the brain are associated with representing specific parts of the body, Medina said.
Those scientists also know that, following the brain damage a stroke causes, patients often regain some of what they initially lost due to that damage.
“Even if every neuron has been killed in the part of the brain that represents touch on the hand, that doesn’t mean that you’re never going to feel anything on your hand again,” Medina said. “We’ve known that isn’t the case because the map can reorganize. The brain can change due to injury.”
But what the new research by Medina and Rapp found is that the brains of those stroke patients may change much more easily than the undamaged brains of healthy people — what they call “hyper-lability.”
The researchers worked with people who had had strokes in the past that affected their ability to localize touch. Each research participant, without being able to see his hand, was touched on the wrist and then on the fingertips. When asked to pinpoint the second touch, the stroke patients reported sensing the touch farther down their finger, toward the wrist, rather than in its actual location.
Medina says that likely occurs because the neural map in the brain is shifting based on the earlier wrist touch — a phenomenon termed “experience-dependent plasticity.”
“Now what’s interesting about this is that when you and I [who haven’t had a stroke] are touched on the wrist, then the fingertips, we don’t have these changes that the brain-damaged individuals do,” he said. “This provides the counterintuitive finding that the maps in brain-damaged individuals are actually much more plastic than in you and me.”
Hyper-plasticity has positive and negative implications, he said.
“On the positive side, this plasticity may potentially be harnessed in rehabilitation to improve function” after a stroke or various other types of brain injury, Medina said. But, he added, the brain may also be so plastic in those cases that changes aren’t stable, creating additional problems.
That’s what he expects additional research to address.
“Now that we’ve found that these maps are more plastic than we thought, can certain strategies help the map become more stable and more accurate again? That’s one of the next questions, and we can only answer it by continuing to learn more about how the mind works.”
A study conducted by local high school students and faculty from the Department of Computer and Information Science in the School of Science at Indiana University-Purdue University Indianapolis reveals new information about the motor circuits of the brain that may one day help those developing therapies to treat conditions such as stroke, schizophrenia, spinal cord injury or Alzheimer’s disease.
"MRI and CAT scans of the human brain can tell us many things about the structure of this most complicated of organs, formed of trillions of neurons and the synapses via which they communicate. But we are a long way away from having imaging techniques that can show single neurons in a complex brain like the human brain," said Gavriil Tsechpenakis, Ph.D., assistant professor of computer science in the School of Science at IUPUI.
"But using the tools of artificial intelligence, specifically computer vision and image processing, we are able to visualize and process actual neurons of model organisms. Our work in the brain of a model organism—the fruit fly—will help us and other researchers move forward to more complex organisms with the ultimate goal of reconstructing the human central nervous system to gain insight into what goes wrong at the cellular level when devastating disorders of the brain and spinal cord occur. This understanding may ultimately inform the treatment of these conditions," said Tsechpenakis.
In this study, which processed images and reconstructed neuronal motor circuitry in the brain, the researchers, who included two Indianapolis high school students—Rachel Stephens and Tiange (Tony) Qu—collected and analyzed data on minute structures over various developmental stages, efforts linking neuroscience and computer science.
"Both high school students who worked on this study performed neuroscience and computation efforts similar to that conducted elsewhere by graduate students. It was impressive to see what sophisticated and key work they could—with mentoring—do," said Tsechpenakis.
Qu said the work was initially rather scary and intimidating but that he rapidly grew to appreciate the opportunity to work in the School of Science lab. “Unlike high school, we were not told how to get from point A to point B. Dr. Tsechpenakis explained what point A and B were and taught us how to figure out how to get from A to B.”
Qu, a 17-year-old senior at Ben Davis High School, now sees neuroscience as a potential college major with biomedical research as an eventual career goal. He continues to work in the lab after school focusing on change over time in fruit fly larvae motor neurons.
Stephens, a senior at North Central High School, said she enjoyed the collaborative nature of the research, with computer scientists and life scientists working together on a problem.
"Dr. Tsechpenakis made it clear to us that different perspectives are necessary, and the ability to think about a problem is more valuable than the education and training you’ve had,” she said. “Before I joined the lab I hadn’t really thought about how computer science could help heal." The 17-year-old plans a pre-med major in college and a career as a physician.
Until recently, the answers to basic questions of how diseases affect the brain – much less the ways to treat them – were lost to the limitations on how scientists could study brain function under real-world conditions. Most technology immobilized subjects inside big, noisy machines or tethered them to computers that made it impossible to simulate what it’s really like to live and interact in a complex world.
But now UC San Francisco neuroscientist Adam Gazzaley, MD, PhD, is hoping to paint a fuller picture of what is happening in the minds and bodies of those suffering from brain disease with his new lab, Neuroscape, which bridges the worlds of neuroscience and high-tech.
In the Neuroscape lab, wireless and mobile technologies set research participants free to move around and interact inside 3-D environments, while scientists make functional recordings with an array of technologies. Gazzaley hopes this will bring his field closer to understanding how complex neurological and psychiatric diseases really work and help doctors like him repurpose technologies built for fitness or fun into targeted therapies for their patients.
“I want us to have a platform that enables us to be more creative and aggressive in thinking how software and hardware can be a new medicine to improve brain health,” said Gazzaley, an associate professor of neurology, physiology and psychiatry and director of the UCSF Neuroscience Imaging Center. “Often, high-tech innovations take a decade to move beyond the entertainment industry and reach science and medicine. That needs to change.”
As a demonstration of what Neuroscape can do, Gazzaley’s team created new imaging technology that he calls GlassBrain, in collaboration with the Swartz Center at UC San Diego and Nvidia, which makes high-end computational computer chips. GlassBrain creates vivid, color visualizations of the structures of the brain and the white matter that connects them, as they pulse with electrical activity in real time.
These brain waves are recorded through electroencephalography (EEG), which measures electrical potentials on the scalp. Ordinary EEG recordings look like wavy horizontal lines, but GlassBrain turns the data into bursts of rhythmic activity that speed along golden spaghetti-like connections threading through a glowing, multi-colored glass-like image of a brain. Gazzaley is now looking at how to feed this information back to his subjects, for example by using the data from real-time EEG to make video games that adapt as people play them to selectively challenge weak brain processes.
Gazzaley has already used the technology to image the brain of former Grateful Dead drummer Mickey Hart as he plays a hypnotic, electronic beat on a Roland digital percussion device with NeuroDrummer, a game the Gazzaley Lab is designing to enhance brain function through rhythmic training. Hart, whose brain is healthy, is collaborating with Gazzaley to develop the game and performed on NeuroDrummer while immersed in virtual reality on an Oculus Rift at the Neuroscape lab opening on March 5.
An international group led by Vanderbilt University researchers has found cannabinoid receptors, through which marijuana exerts its effects, in a key emotional hub in the brain involved in regulating anxiety and the flight-or-fight response.
This is the first time cannabinoid receptors have been identified in the central nucleus of the amygdala in a mouse model, they report in the current issue of the journal Neuron.
The discovery may help explain why marijuana users say they take the drug mainly to reduce anxiety, said Sachin Patel, M.D., Ph.D., the paper’s senior author and professor of Psychiatry and of Molecular Physiology and Biophysics.
Led by first author Teniel Ramikie, a graduate student in Patel’s lab, the researchers also showed for the first time how nerve cells in this part of the brain make and release their own natural “endocannabinoids.”
The study “could be highly important for understanding how cannabis exerts its behavioral effects,” Patel said. As the legalization of marijuana spreads across the country, more people — and especially young people whose brains are still developing — are being exposed to the drug.
Previous studies at Vanderbilt and elsewhere, Patel said, have suggested the following:
• The natural endocannabinoid system regulates anxiety and the response to stress by dampening excitatory signals that involve the neurotransmitter glutamate.
• Chronic stress or acute, severe emotional trauma can cause a reduction in both the production of endocannabinoids and the responsiveness of the receptors. Without their “buffering” effect, anxiety goes up.
• While marijuana’s “exogenous” cannabinoids also can reduce anxiety, chronic use of the drug down-regulates the receptors, paradoxically increasing anxiety. This can trigger “a vicious cycle” of increasing marijuana use that in some cases leads to addiction.
In the current study, the researchers used high-affinity antibodies to “label” the cannabinoid receptors so they could be seen using various microscopy techniques, including electron microscopy, which allowed very detailed visualization at individual synapses, or gaps between nerve cells.
“We know where the receptors are, we know their function, we know how these neurons make their own cannabinoids,” Patel said. “Now can we see how that system is affected by … stress and chronic (marijuana) use? It might fundamentally change our understanding of cellular communication in the amygdala.”
Researchers at The Scripps Research Institute (TSRI) and Vanderbilt University have created the most detailed 3-D picture yet of a membrane protein that is linked to learning, memory, anxiety, pain and brain disorders such as schizophrenia, Parkinson’s, Alzheimer’s and autism.
"This receptor family is an exciting new target for future medicines for treatment of brain disorders," said P. Jeffrey Conn, PhD, Lee E. Limbird Professor of Pharmacology and director of the Vanderbilt Center for Neuroscience Drug Discovery, who was a senior author of the study with Raymond Stevens, PhD, a professor in the Department of Integrative Structural and Computational Biology at TSRI. "This new understanding of how drug-like molecules engage the receptor at an atomic level promises to have a major impact on new drug discovery efforts."
The research—which focuses on the mGlu1 receptor—was reported in the March 6, 2014 issue of the journal Science.
A Family of Drug Targets
The mGlu1 receptor, which helps regulate the neurotransmitter glutamate, belongs to a superfamily of molecules known as G protein-coupled receptors (GPCRs).
GPCRs sit in the cell membrane and sense various molecules outside the cell, including odors, hormones, neurotransmitters and light. After binding these molecules, GPCRs trigger a specific response inside the cell. More than one-third of therapeutic drugs target GPCRs—including allergy and heart medications, drugs that target the central nervous system and anti-depressants.
The Stevens lab’s work has revolved around determining the structure and function of GPCRs. GPCRs are not well understood and many fundamental breakthroughs are now occurring due to the understanding of GPCRs as complex machines, carefully regulated by cholesterol and sodium.
When the Stevens group decided to pursue the structure of mGlu1 and other key members of the mGlu family, it was natural the scientists reached out to the researchers at Vanderbilt. “They are the best in the world at understanding mGlu receptors,” said Stevens. “By collaborating with experts in specific receptor subfamilies, we can reach our goal of understanding the human GPCR superfamily and how GPCRs control human cell signaling.”
Colleen Niswender, PhD, director of Molecular Pharmacology and research associate professor of Pharmacology at the Vanderbilt Center for Neuroscience Drug Discovery, also thought the collaboration made sense. “This work leveraged the unique strengths of the Vanderbilt and Scripps teams in applying structural biology, molecular modeling, allosteric modulator pharmacology and structure-activity relationships to validate the receptor structure,” she said.
The Challenge of the Unknown
mGlu1 was a particularly challenging research topic.
In general, GPCRs are exceedingly flimsy, fragile proteins when not anchored within their native cell membranes. Coaxing them to line up to form crystals, so that their structures can be determined through X-ray crystallography, has been a formidable challenge. And the mGlu1 receptor is particularly tricky as, in addition to the domain spanning the membrane, it has a large domain extending into the extracellular space. Moreover, two copies of this multidomain receptor associating in a dimer are needed to transmit glutamate’s signal across the membrane.
The task was made more difficult because there was no template for mGlu1 from closely related GPCR proteins to guide the researchers.
“mGlu1 belongs to class C GPCRs, of which no structure has been solved before,” said TSRI graduate student Chong Wang, a first author of the new study with TSRI graduate student Huixian Wu. “This made the project much harder. We could not use other GPCRs as a template to design constructs for expression and stabilization or to help interpret diffraction data. The structure was so different that old school methods in novel protein structure determination had to be used.”
The team decided to try to determine the structure of mGlu1 bound to novel “allosteric modulators” of mGlu1 contributed by the Vanderbilt group. Allosteric modulators bind to a site far away from the binding site of the natural activator (in this case, presumably the glutamate molecule), but change the shape of the molecule enough to affect receptor function. In the case of allosteric drug candidates, the hope is that the compounds affect the receptor function in a desirable, therapeutic way.
"Allosteric modulators are promising drug candidates as they can ‘fine-tune’ GPCR function,” said Karen Gregory, a former postdoctoral fellow at Vanderbilt University, now at Monash Institute of Pharmaceutical Sciences. “However, without a good idea of how drug-like compounds interact with the receptor to adjust the strength of the signal, discovery efforts are challenging."
The team proceeded to apply a combination of techniques, including X-ray crystallography, structure-activity relationships, mutagenesis and full-length dimer modeling. At the end of the study, they had achieved a high-resolution image of mGlu1 in complex with one of the drug candidates, as well as a deeper understanding of the receptor’s function and pharmacology.
The findings show that mGlu1 possesses structural features both similar to and distinct from those seen in other GPCR classes, but in ways that would have been impossible to predict in advance.
“Most surprising is that the entrance to a binding pocket in the transmembrane domain is almost completely covered by loops, restricting access for the binding of allosteric modulators,” said Vsevolod “Seva” Katritch, assistant professor of molecular biology at TSRI and a co-author of the paper. “This is very important for understanding action of the allosteric modulator drugs and may partially explain difficulties in screening for such drugs.
“The mGlu1 receptor structure now provides a solid platform for much more reliable modeling of closely related receptors,” he continued, “some of which are equally important in drug discovery.”
How do we “know” from the movements of speeding car in our field of view if it’s coming straight toward us or more likely to move to the right or left?
Scientists have long known that our perceptions of the outside world are processed in our cortex, the six-layered structure in the outer part of our brains. But how much of that processing actually happens in cortex? Do the eyes tell the brain a lot or a little about the content of the outside world and the objects moving within it?
In a detailed study of the neurons linking the eyes and brains of mice, biologists at UC San Diego discovered that the ability of our brains and those of other mammals to figure out and process in our brains directional movements is a result of the activation in the cortex of signals that originate from the direction-sensing cells in the retina of our eyes.
“Even though direction-sensing cells in the retina have been known about for half a century, what they actually do has been a mystery- mostly because no one knew how to follow their connections deep into the brain,” said Andrew Huberman, an assistant professor of neurobiology, neurosciences and ophthalmology at UC San Diego, who headed the research team, which also involved biologists at the Salk Institute for Biological Sciences. “Our study provides the first direct link between direction-sensing cells in the retina and the cortex and thereby raises the new idea that we ‘know’ which direction things are moving specifically because of the activation of these direction-selective retinal neurons.” The study, recently published online, will appear in the March 20 print issue of Nature.
The discovery of the link between direction-sensing cells in the retina and the cortex has a number of practical implications for neuroscientists who treat disabilities in motion processing, such as dysgraphia, a condition sometimes associated with dyslexia that affects direction-oriented skills.
“Understanding the cells and neural circuits involved in sensing directional motion may someday help us understand defects in motion processing, such as those involved dyslexia, and it may inform strategies to treat or even re-wire these circuits in response to injury or common neurodegenerative diseases, such as glaucoma or Alzheimer’s,” said Huberman.
He and his team discovered the link in mice by using new types of modified rabies viruses that were pioneered by Ed Callaway, a professor at the Salk Institute, and by imaging the activity of neurons deep in the brain during visual experience.
It may seem normal: As we age, we misplace car keys, or can’t remember a name we just learned or a meal we just ordered. But University of Florida researchers say memory trouble doesn’t have to be inevitable, and they’ve found a drug therapy that could potentially reverse this type of memory decline.
The drug can’t yet be used in humans, but the researchers are pursuing compounds that could someday help the population of aging adults who don’t have Alzheimer’s or other dementias but still have trouble remembering day-to-day items. Their findings will be published in today’s (March 5) issue of the Journal of Neuroscience.
The kind of memory responsible for holding information in the mind for short periods of time is called “working memory.” Working memory relies on a balance of chemicals in the brain. The UF study shows this chemical balance tips in older adults, and working memory declines. The reason? It could be because their brains are producing too much of a chemical that slows neural activity.
“Graduate student Cristina Banuelos’ work suggests that cells that normally provide the brake on neural activity are in overdrive in the aged prefrontal cortex,” said researcher Jennifer Bizon, Ph.D., an associate professor in the department of neuroscience and a member of UF’s Evelyn F. & William L. McKnight Brain Institute.
This chemical, an inhibitory brain neurotransmitter called GABA, is essential. Without it, brain cells can become too active, similar to what happens in the brains of people with schizophrenia and epilepsy. A normal level of GABA helps maintain the optimal levels of cell activation, said collaborator Barry Setlow, Ph.D., an associate professor in UF’s departments of psychiatry and neuroscience.
Working memory underlies many mental abilities and is sometimes referred to as the brain’s mental sketchpad, Bizon said. For example, Bizon said, you use your working memory in many everyday activities such as calculating your final bill at the end of dining at a restaurant. Most people can calculate a 15 percent tip and add it to the cost of their meal without pencil and paper. Central to this process is the ability to keep multiple pieces of information in mind for a short duration — such as remembering the cost of your dinner while calculating the amount needed for the tip.
“Almost all higher cognitive processes depend on this fundamental operation,” Bizon said.
To determine the culprit behind working memory decline, the researchers tested the memory of young and aged rats in a “Skinner box.” In the Skinner box, rats had to remember the location of a lever for short periods of up to 30 seconds. The scientists found that while both young and old rats could remember the location of the lever for brief periods of time, as those time periods lengthened, old rats had more difficulty remembering the location of the lever than young rats.
But not all older rats did poorly on the memory test, just as not all older adults have memory problems. The study shows the older brains of some people or rats with no memory problems might compensate for the overactive inhibitory system — they are able to produce fewer GABA receptors and therefore bind less of the inhibitory chemical.
Older rats with memory problems had more GABA receptors. The drug the researchers tested blocked GABA receptors, mimicking the lower number of those receptors that some older rats had naturally and restoring working memory in aged rats to the level of younger rats.
“Modern medicine has done a terrific job of keeping us alive for longer, and now we have to keep up and determine how to maximize the quality of life for seniors,” Bizon said. “A key aspect of that is going to be developing strategies and therapies that can maintain and improve cognitive health.”
When we drift into deep slow-wave sleep (SWS), waves of neuronal activity wash across our neocortex. Birds also engage in SWS, but they lack this particular brain structure. Researchers from the Max Planck Institute for Ornithology in Seewiesen, Germany together with colleagues from the Netherlands and Australia have gained deeper insight into the sleeping avian brain. They found complex 3D plumes of brain activity propagating through the brain that clearly differed from the two-dimensional activity found in mammals. These findings show that the layered neuronal organization of the neocortex is not required for waves to propagate, and raise the intriguing possibility that the 3D plumes of activity perform computations not found in mammals.
Mammals, including humans, depend upon the processing power of the neocortex to solve complex cognitive tasks. This part of the brain also plays an important role in sleep. During SWS, slow neuronal oscillations propagate across the neocortex as a traveling wave, much like sports fans performing the wave in a stadium. It is thought that this wave might be involved in coordinating the processing of information in distant brain regions. Birds have mammalian-like cognitive abilities, but yet different neuronal organization. They lack the elegant layered arrangement of neurons characteristic of the neocortex. Instead, homologous neurons are packaged in unlayered, seemingly poorly structured nuclear masses of neurons.
Researchers from the Max Planck Institute for Ornithology in Seewiesen together with colleagues from the Netherlands and Australia now investigated in female zebra finches how brain activity changed over space and time during sleep. “When we first looked at the recordings, it appeared that the slow waves were occurring simultaneously in all recording sites. However, when we visualized the data as a movie and slowed it down, a fascinating picture emerged!” says Gabriël Beckers from Utrecht University, who developed the high-resolution recording method at the Max Planck Institute for Ornithology in Seewiesen. The waves were moving across the two-dimensional recording array as rapidly changing arcs of activity. Rotating the orientation of the array by 90 degrees revealed similar patterns, and thereby established the 3D nature of the plumes propagating through the brain. The researchers found similar patterns in distant brain regions involved in processing different types of information, suggesting that this type of activity is a general feature of the sleeping avian brain.
In addition to revealing how neurons in the avian brain behave during sleep, this research also adds to our understanding of the sleeping neocortex. “Our findings demonstrate that the traveling nature of slow waves is not dependent upon the layered organization of neurons found in the neocortex, and is unlikely to be involved in functions unique to this pattern of neuronal organization,” says Niels Rattenborg, head of the Avian Sleep Group in Seewiesen. “In this respect, research on birds refines our understanding of what is and is not special about the neocortex.” Finally, the researchers wonder whether the 3D geometry of wave propagation in the avian brain reflects computational properties not found in the neocortex. While this idea is clearly speculative, the authors note that during the course of evolution, birds replaced the three-layered cortex present in their reptilian ancestors with nuclear brain structures. “Presumably, there are benefits to the seemingly disorganized, nuclear arrangement of neurons in the avian brain that we are far from understanding. Whether this relates to what we have observed in the sleeping bird brain is a wide open question,” says Rattenborg.
Veterans exposed to explosions who do not report symptoms of traumatic brain injury (TBI) may still have damage to the brain’s white matter comparable to veterans with TBI, according to researchers at Duke Medicine and the U.S. Department of Veterans Affairs.
The findings, published in the Journal of Head Trauma Rehabilitation on March 3, 2014, suggest that a lack of clear TBI symptoms following an explosion may not accurately reflect the extent of brain injury.
Veterans of recent military conflicts in Iraq and Afghanistan often have a history of exposure to explosive forces from bombs, grenades and other devices, although relatively little is known about whether this injures the brain. However, evidence is building – particularly among professional athletes – that subconcussive events have an effect on the brain.
"Similar to sports injuries, people near an explosion assume that if they don’t have clear symptoms – losing consciousness, blurred vision, headaches – they haven’t had injury to the brain,” said senior author Rajendra A. Morey, M.D., associate professor of psychiatry and behavioral sciences at Duke University School of Medicine and a psychiatrist at the Durham Veterans Affairs Medical Center. “Our findings are important because they’re showing that even if you don’t have symptoms, there may still be damage.”
Researchers in the Mid-Atlantic Mental Illness Research, Education and Clinical Center at the W.G. (Bill) Hefner Veterans Affairs Medical Center in Salisbury, N.C., evaluated 45 U.S. veterans who volunteered to participate in the study. The veterans, who served since September 2001, were split into three groups: veterans with a history of blast exposure with symptoms of TBI; veterans with a history of blast exposure without symptoms of TBI; and veterans without blast exposure. The study focused on veterans with primary blast exposure, or blast exposure without external injuries, and did not include those with brain injury from direct hits to the head.
To measure injury to the brain, the researchers used a type of MRI called Diffusion Tensor Imaging (DTI). DTI can detect injury to the brain’s white matter by measuring the flow of fluid in the brain. In healthy white matter, fluid moves in a directional manner, suggesting that the white matter fibers are intact. Injured fibers allow the fluid to diffuse.
White matter is the connective wiring that links different areas of the brain. Since most cognitive processes involve multiple parts of the brain working together, injury to white matter can impair the brain’s communication network and may result in cognitive problems.
Both groups of veterans who were near an explosion, regardless of whether they had TBI symptoms, showed a significant amount of injury compared to the veterans not exposed to a blast. The injury was not isolated to one area of the brain, and each individual had a different pattern of injury.
Using neuropsychological testing to assess cognitive performance, the researchers found a relationship between the amount of white matter injury and changes in reaction time and the ability to switch between mental tasks. However, brain injury was not linked to performance on other cognitive tests, including decision-making and organization.
“We expected the group that reported few symptoms at the time of primary blast exposure to be similar to the group without exposure. It was a surprise to find relatively similar DTI changes in both groups exposed to primary blast,” said Katherine H. Taber, Ph.D., a research health scientist at the W.G. (Bill) Hefner Veterans Affairs Medical Center and the study’s lead author. “We are not sure whether this indicates differences among individuals in symptoms-reporting or subconcussive effects of primary blast. It is clear there is more we need to know about the functional consequences of blast exposures.”
Given the study’s findings, the researchers said clinicians treating veterans should take into consideration a person’s exposure to explosive forces, even among those who did not initially show symptoms of TBI. In the future, they may use brain imaging to support clinical tests.
“Imaging could potentially augment the existing approaches that clinicians use to evaluate brain injury by looking below the surface for TBI pathology,” Morey said.
The researchers noted that the results are preliminary, and should be replicated in a larger study.