Posts tagged white matter
Articles and news from the latest research reports.
Quality of white matter in the brain is crucial for adding and multiplying
‘Grey’ cells process information in the brain and are connected via neural pathways, the tracts through which signals are transferred.
"Neural pathways are comparable to a bundle of cables. These cables are surrounded by an isolating sheath: myelin, or ‘white matter’. The thicker the isolating sheath and the more cables there are, the more white matter. And the more white matter, the faster the signals are transferred," explains educational neuroscientist Bert de Smedt.
While the correlation between arithmetic and white matter tracts linking certain brain regions is known, very little research has been done to test this correlation in normally-developing children. Nor has previous research teased out differences in neuroactivity when carrying out different arithmetic operations, e.g., adding, subtracting, multiplying and dividing.
In this study, the researchers had 25 children solve a series of different arithmetic operations while undergoing a brain scan. They then compared the quality of the children’s white matter tracts with their arithmetic test performance.
"We found that a better quality of the arcuate fasciculus anterior – a white matter tract that connects brain regions often used for arithmetic – corresponds to better performance in adding and multiplying, while there is no correlation for subtracting and dividing.”
“A possible explanation for this is that this white matter bundle is involved in rote memorization, whereas when we subtract and divide, such memorization plays less of a role. When subtracting and dividing we are more likely to use intermediary steps to calculate the solution, even as adults.”
Nursery rhymes
These findings also add insight into the link between reading and arithmetic, explains Professor De Smedt: “Reading proficiency and arithmetic proficiency often go hand-in-hand. The white matter tract that we studied also plays an important role in reading: when we learn to read, we have to memorize the correspondence between particular letters and the sound they represent. It is likely that a similar process occurs for addition and multiplication. Just think of the notorious times-table drills we all memorized as schoolchildren; it is almost like learning a nursery rhyme. Some of us can even auto-recall these sums.”
"This also might explain why we often see arithmetic problems in children with dyslexia. Likewise, children with dyscalculia often have trouble reading," says Professor De Smedt.
The researchers now aim to explore how these results relate to children with impairments such as dyscalculia or head trauma. In a next step, the team will also investigate how white matter tracts can be strengthened through extra arithmetic training.
For centuries, the brain was a mystery. Only in the last few decades have scientists begun to unravel its secrets. In recent years, using the latest technology and powerful computers further key discoveries have been made.
However, much remains to be understood about how the brain works. Here are five important areas of study attempting to unlock the last secrets of the brain.
How to fix it
When we think, move, speak, dream and even love - it all happens in the grey matter. But our brains are not simply one colour. White matter matters too.
Much of the research into dementia has focused on the tell-tale plaques of beta amyloid and tau protein tangles which occur in the grey matter.
But one British scientist, Dr Atticus Hainsworth says the white matter - and its blood supply - may be equally important.
The white colour results from fatty sheaths around the axons - which are extensions of the nerve cell bodies and help the cells to communicate.
He is using banks of donated brains, in Oxford and Sheffield, to analyse white matter for potential triggers such as leaking blood vessels.
"Some of the cases had an MRI or CT scan and that information can help give more clues about whether there was disease in the white matter - and what its basis might be," says Dr Hainsworth.
If leaking blood vessels in white matter do play a key role in the development of dementia then it may offer up a another potential route for new drug therapies.
How to make us all geniuses
For years caffeine was used to enhance alertness. But popping a pill to get straight-A’s may soon become the norm.
At Cambridge University neuroscientist Barbara Sahakian is investigating cognitive enhancers - drugs which make us smarter.
She studies how they can improve the performance of surgeons or pilots and asks if they could even be used to make us more entrepreneurial.
But she warns that there is no long-term safety information on these drugs and as a society we need to talk about their use.
She says the scientific and ethical challenges created by drugs which affect the production of brain chemicals like dopamine and noradrenaline - which induce pleasurable or “fight or flight” responses - need to be debated in order to decide whether drug-tests become routine before taking an exam.
Dr Sahakian adds: “I frequently talk to students about cognitive-enhancing drugs and a lot of students take them for studying and exams.
"But other students feel angry about this, they feel those students are cheating."
How can we harness our unconscious?
People need to be on top of their game when mastering skills like playing a musical instrument or detecting a bomb.
But research suggests that our unconscious can be harnessed to help us excel.
Repeatedly playing a tricky piece of music obviously helps develop a familiarity with the bits that are most difficult.
But cellist Tania Lisboa, who’s also a researcher in the Centre for Performance Science at London’s Royal College of Music, says it also helps to send the trickier parts of a piece from her conscious to the unconscious part of her brain.
After hours of practice, a fluent musician’s brain stores how to play the piece in an area at the back of the brain called the cerebellum - literally “the little brain”.
Neuroscientist Prof Anil Seth, of Sussex University, says: “It has more brain cells than the rest of the brain put together.
"It helps to promote fluid movements.. So the conscious effort of learning how to bow a cello is moved from the cortical areas which are involved when it’s new or difficult over to the cerebellum, which is very good at producing unconscious fluent behaviour on demand."
Music and defence may not appear to have much in common, but the unconscious can also help detect potential threats, whether it’s a suspicious person in a crowd or the presence of an improvised explosive device.
The unconscious brain is really good at spotting patterns - a skill which Paul Sajda at Colombia University in New York exploits - right at the boundary of the conscious/sub-conscious.
"I can flash 10 images a second and if one of those images has something out of the ordinary..that will essentially cause me to re-orient my brain to that image - but I’m not exactly aware of what that is."
Brain activity is monitored whilst the analyst looks at images so that researchers can later see which images triggered reactions.
What dreams are for
It’s just 60 years since scientists in Chicago first noted the tell-tale “rapid eye movement” or REM sleep which we now associate with dreaming.
But our fascination with dreams dates back at least 5,000 years to ancient Mesopotamia when people believed that the soul moved out of a sleeping body to visit the places they dreamed of.
REM sleep - which occurs every 90 minutes or so - begins with signals from the base of the brain which eventually reach the cerebral cortex - the outer layer of the brain which is responsible for learning and thought.
These nerve impulses are also directed to the spinal cord, inducing temporary paralysis of the limbs.
Prof Robert Stickgold, from the Beth Israel Deaconess Medical Center for Sleep and Cognition in Boston, believes that dreams are vital for processing memory associations.
He has asked the subjects of some of his sleep studies to play Tetris - and then noted their descriptions of how they floated amongst geometric shapes in their dreams.
He’s an admirer of Japanese scanning research where the scientists could “read” the dreams of subjects as they had MRI scans.
But he says it’s hard to get people to sleep in a noisy, expensive scanner.
And the future? “I would like to see research which reveals the rules for dream construction - and how it relates to the larger concept of memory processing during sleep.”
One even more elusive goal: how to dream just happy dreams and ditch the bad ones, especially nightmares.
Can we cure unreachable pain?
Excruciating chronic pain is one of medicine’s most difficult problems to solve.
Untouched by conventional treatments like painkilling drugs, surgeons are now testing their theory that deep brain stimulation could provide relief.
It is a brain surgery technique which involves electrodes being inserted to reach targets deep inside the brain.
The target areas are stimulated via the electrodes which are connected to a battery-powered pacemaker surgically placed under the patient’s collar bone.
One of the pioneers of this technique is Prof Tipu Aziz at the John Radcliffe Hospital in Oxford.
Deep brain stimulation has been used in the past for Parkinson’s disease and depression, and is now being trialled on obsessive compulsive disorder patients as well as those in chronic pain.
One of his patients, Clive, has suffered from terrible pain for nearly a decade after an operation to remove a disc in his neck.
"Sometimes I thought that if I had an axe, I’d chop my own arm off, if I thought it would get rid of the pain."
The doctors explained to him that his brain was getting signals from his arm to his brain confused and that the electrodes could help.
In Clive’s case this was an area of the brain called the anterior cingulate.
A week after his surgery he was one of the fortunate 70% of patients for whom the deep brain stimulation provides relief.
"It’s great to be out of that pain now. Since having the implant I can sit down for longer, I am able to walk further, everything is an improvement."
Prof Aziz is treating medical conditions. But he is aware of ethical dilemmas which could arise if the technique was applied to other areas.
"Putting electrodes in targets to improve memory.
"Or you could put electrodes into people to make them indifferent to danger and create the perfect soldier."
Brain connections may explain why girls mature faster
Newcastle University scientists have discovered that as the brain re-organises connections throughout our life, the process begins earlier in girls which may explain why they mature faster during the teenage years.
As we grow older, our brains undergo a major reorganisation reducing the connections in the brain. Studying people up to the age of 40, scientists led by Dr Marcus Kaiser and Ms Sol Lim at Newcastle University found that while overall connections in the brain get streamlined, long-distance connections that are crucial for integrating information are preserved.
The researchers suspect this newly-discovered selective process might explain why brain function does not deteriorate – and indeed improves –during this pruning of the network. Interestingly, they also found that these changes occurred earlier in females than in males.
Explaining the work which is being published in Cerebral Cortex, Dr Kaiser, Reader in Neuroinformatics at Newcastle University, says: “Long-distance connections are difficult to establish and maintain but are crucial for fast and efficient processing. If you think about a social network, nearby friends might give you very similar information – you might hear the same news from different people. People from different cities or countries are more likely to give you novel information. In the same way, some information flow within a brain module might be redundant whereas information from other modules, say integrating the optical information about a face with the acoustic information of a voice is vital in making sense of the outside world.”
Brain “pruned”
The researchers at Newcastle, Glasgow and Seoul Universities evaluated the scans of 121 healthy participants between the ages of 4 and 40 years as this is where the major connectivity changes can be seen during this period of maturation and improvement in the brain. The work is part of the EPSRC-funded Human Green Brain project which examines human brain development.
Using a non-invasive technique called diffusion tensor imaging – a special measurement protocol for Magnetic Resonance Imaging (MRI) scanners – they demonstrated that fibres are overall getting pruned that period.
However, they found that not all projections (long-range connections) between brain regions are affected to the same extent; changes were influenced differently depending on the types of connections.
Projections that are preserved were short-cuts that quickly link different processing modules, e.g. for vision and sound, and allow fast information transfer and synchronous processing. Changes in these connections have been found in many developmental brain disorders including autism, epilepsy and schizophrenia.
The researchers have demonstrated for the first time that the loss of white matter fibres between brain regions is a highly selective process – a phenomenon they call preferential detachment. They show that connections between distant brain regions, between brain hemispheres, and between processing modules lose fewer nerve fibres during brain maturation than expected. The researchers say this may explain how we retain a stable brain network during brain maturation.
Commenting on the fact that these changes occurred earlier in females than males, Ms Sol Lim explains: “The loss of connectivity during brain development can actually help to improve brain function by reorganizing the network more efficiently. Say instead of talking to many people at random, asking a couple of people who have lived in the area for a long time is the most efficient way to know your way. In a similar way, reducing some projections in the brain helps to focus on essential information.”
(Source: ncl.ac.uk)
Brain Chemical Ratios Help Predict Developmental Delays in Preterm Infants
Researchers have identified a potential biomarker for predicting whether a premature infant is at high risk for motor development problems, according to a study published online in the journal Radiology.
"We are living in an era in which survival of premature birth is more common," said Giles S. Kendall, Ph.D., consultant for the neonatal intensive care unit at University College London Hospitals NHS Foundation Trust and honorary senior lecturer of neonatal neuroimaging and neuroprotection at the University College London. "However, these infants continue to be at risk for neurodevelopmental problems."
Patients in the study included 43 infants (24 male) born at less than 32 weeks gestation and admitted to the neonatal intensive care unit (NICU) at the University College of London between 2007 and 2010. Dr. Kendall and his research team performed magnetic resonance imaging (MRI) and MR spectroscopy (MRS) exams on the infants at their approximate expected due dates (or term-equivalent age). MRS measures chemical levels in the brain.
The imaging studies were focused on the white matter of the brain, which is composed of nerve fibers that connect the functional centers of the brain.
"The white matter is especially fragile in the newborn and at risk for injury," Dr. Kendall explained.
One year later, 40 of the 43 infants were evaluated using the Bayley Scales of Infant and Toddler Development, which assess fine motor, gross motor and communication abilities. Of the 40 infants evaluated, 15 (38 percent) had abnormal composite motor scores and four (10 percent) showed cognitive impairment.
Statistical analysis of the MRS results and Bayley Scales scores revealed that the presence of two chemical ratios—increased choline/creatine (Cho/Cr) and decreased N-acetylaspartate/choline (NAA/Cho)—at birth were significantly correlated with developmental delays one year later.
"Low N-acetylaspartate/choline and rising choline/creatine observed during MRS at the baby’s expected due date predicted with 70 percent certainty which babies were at high risk for motor development problems at one year," Dr. Kendall said.
Dr. Kendall said a tool to predict the likelihood of a premature baby having neurodevelopmental problems would be useful in determining which infants should receive intensive interventions and in testing the effectiveness of those therapies.
"Physiotherapy interventions are available but are very expensive, and the vast majority of premature babies don’t need them," Dr. Kendall said. "Our hope is to find a robust biomarker that we can use as an outcome measure so that we don’t have to wait five or six years to see if an intervention has worked."
Dr. Kendall said severe disability associated with premature births has decreased over the past two decades as a result of improved care techniques in the NICU. However, many premature infants today have subtle abnormalities that are difficult to detect with conventional MRI.
"There’s a general shift away from simply ensuring the survival of these infants to how to give them the best quality of life," he said. "Our research is part of an effort to improve the outcomes for prematurely born infants and to identify earlier which babies are at greater risk."
Alzheimer’s risk gene may begin to affect brains as early as childhood
People who carry a high-risk gene for Alzheimer’s disease show changes in their brains beginning in childhood, decades before the illness appears, new research from the Centre for Addiction and Mental Health (CAMH) suggests.
The gene, called SORL1, is one of a number of genes linked to an increased risk of late-onset Alzheimer’s disease, the most common form of the illness. SORL1 carries the gene code for the sortilin-like receptor, which is involved in recycling some molecules in the brain before they develop into beta-amyloid a toxic Alzheimer protein. SORL1 is also involved in lipid metabolism, putting it at the heart of the vascular risk pathway for Alzheimer’s disease as well.
“We need to understand where, when and how these Alzheimer’s risk genes affect the brain, by studying the biological pathways through which they work,” says Dr. Aristotle Voineskos, head of the Kimel Family Translational Imaging-Genetics Laboratory at CAMH, who led the study. “Through this knowledge, we can begin to design interventions at the right time, for the right people.” The study was recently published online in Molecular Psychiatry with Dr. Voineskos’s graduate student, Daniel Felsky as first author, and was a collaborative effort with the Zucker Hillside Hospital/Feinstein Institute in New York and the Rush Alzheimer’s Disease Center in Chicago.
To understand SORL1’s effects across the lifespan, the researchers studied individuals both with and without Alzheimer’s disease. Their approach was to identify genetic differences in SORL1, and see if there was a link to Alzheimer’s-related changes in the brain, using imaging as well as post-mortem tissue analysis.
In each approach, a link was confirmed.
In the first group of healthy individuals, aged eight to 86, researchers used a brain imaging technique called diffusion tensor imaging (DTI). Even among the youngest participants in the study, those with a specific copy of SORL1 showed a reduction in white matter connections in the brain important for memory performance and executive function.
The second sample included post-mortem brain tissue from 189 individuals less than a year old to 92 years, without Alzheimer’s disease. Among those with that same copy of the SORL1 gene, the brain tissue showed a disruption in the process by which the gene translated its code to become the sortilin-like receptor.
Finally, the third set of post-mortem brains came from 710 individuals, aged 66 to 108, of whom the majority had mild cognitive impairment or Alzheimer’s. In this case, the SORL1 risk gene was linked with the presence of amyloid-beta, a protein found in Alzheimer’s disease.
Dr. Voineskos notes that risk for Alzheimer’s disease results from a combination of factors – unhealthy diet, lack of exercise, smoking, high blood pressure combined with a person’s genetic profile – which all contribute to the development of the illness. “The gene has a relatively small effect, but the changes are reliable, and may represent one ‘hit’, among a pathway of hits required to develop Alzheimer’s disease later in life”.
While it’s too early to provide interventions that may target these changes, “individuals can take measures in their own lifestyle to reduce the risk of late-onset Alzheimer’s disease.” Determining whether there is an interaction with this risk gene and lifestyle factors will be one important next step.
In order to develop genetically-based interventions to prevent Alzheimer’s disease, the biological pathways of other risk genes also need to be systematically analyzed, the researchers note.
This research does, however, build on a previous CAMH imaging-genetics study on another gene related to Alzheimer’s disease. That study showed that a genetic variation of brain-derived neurotrophic factor (BDNF) affected brain structures in Alzheimer’s.
“The interesting connection is that BDNF may have important therapeutic value. But there is data to suggest that the effects of BDNF won’t work unless SORL1 is present, so there is the possibility that if you boost the activity of one gene, the other will increase,” says Dr. Voineskos, adding that BDNF therapeutics are in development. A next stage in the research, he says, is to look at the interaction of BDNF and SORL1.
(Source: camh.ca)
MR Spectroscopy Shows Differences in Brains of Preterm Infants
Premature birth appears to trigger developmental processes in the white matter of the brain that could put children at higher risk of problems later in life, according to a study being presented next week at the annual meeting of the Radiological Society of North America (RSNA).
Preterm infants—generally those born 23 to 36 weeks after conception, as opposed to the normal 37- to 42-week gestation—face an increased risk of behavioral problems, ranging from impulsiveness and distractibility to more serious conditions like autism and attention deficit hyperactivity disorder (ADHD).
"In the United States, we have approximately 500,000 preterm births a year," said Stefan Blüml, Ph.D., director of the New Imaging Technology Lab at Children’s Hospital Los Angeles and associate professor of research radiology at the University of Southern California in Los Angeles. "About 60,000 of these babies are at high risk for significant long-term problems, which means that this is a significant problem with enormous costs."
Dr. Blüml and colleagues have been studying preterm infants to learn more about how premature birth might cause changes in brain structure that may be associated with clinical problems observed later in life. Much of the focus has been on the brain’s white matter, which transmits signals and enables communication between different parts of the brain. While some white matter damage is readily apparent on structural magnetic resonance imaging (MRI), Dr. Blüml’s group has been using magnetic resonance spectroscopy (MRS) to look at differences on a microscopic level.
In this study, the researchers compared the concentrations of certain chemicals associated with mature white matter and gray matter in 51 full-term and 30 preterm infants. The study group had normal structural MRI findings, but MRS results showed significant differences in the biochemical maturation of white matter between the term and preterm infants, suggesting a disruption in the timing and synchronization of white and gray matter maturation. Gray matter is the part of the brain that processes and sends out signals.
"The road map of brain development is disturbed in these premature kids," Dr. Blüml said. "White matter development had an early start and was ‘out of sync’ with gray matter development."
This false start in white matter development is triggered by events after birth, according to Dr. Blüml.
"This timeline of events might be disturbed in premature kids because there are significant physiological switches at birth, as well as stimulatory events, that happen irrespective of gestational maturity of the newborn," he said. "The most apparent change is the amount of oxygen that is carried by the blood."
Dr. Blüml said that the amount of oxygen delivered to the fetus’s developing brain in utero is quite low, and our brains have evolved to optimize development in that low oxygen environment. However, when infants are born, they are quickly exposed to a much more oxygen-rich environment.
"This change may be something premature brains are not ready for," he said.
While this change may cause irregularities in white matter development, Dr. Blüml noted that the newborn brain has a remarkable capacity to adapt or even “re-wire” itself—a concept known as plasticity. Plasticity not only allows the brain to govern new skills over the course of development, like learning to walk and read, but could also make the brains of preterm infants and young children more responsive to therapeutic interventions, particularly if any abnormalities are identified early.
"Our research points to the need to better understand the impact of prematurity on the timing of critical maturational processes and to develop therapies aimed at regulating brain development," Dr. Blüml said.
(Source: www2.rsna.org)
Navigational ability is visible in the brain
The brains of people who immediately know their way after travelling along as a passenger are different from the brains of people who always need a GPS system or a map to get from one place to another. This was demonstrated by Joost Wegman, who will defend his thesis at Radboud University Nijmegen, the Netherlands on the 27th of November.
Wegman demonstrates that good navigators store relevant landmarks automatically on their way. Bad navigators on the other hand, often follow a fixed procedure or route (such as: turn left twice, then turn right at the statue).
Anatomical differences
Wegman also found that there are detectable structural differences between the brains of good and bad navigators. ‘These anatomical differences are not huge, but we found them significant enough, because we had a lot of data’, the researcher explains. ‘The difference is in the hippocampus. We saw that good navigators had more so-called gray matter. In the brain’s gray matter information is processed. Bad navigators, on the other hand, have more white matter - which connects gray matter areas with each other - in a brain area called the caudate nucleus. This area stores spatial actions with respect to oneself. For example, to turn right at the record store’, Wegman describes.
Questionnaires
For his research, Wegman combined data from several studies done by the Radboud University research group Neural Correlates of Spatial Memory at the Donders Institute for Brain, Cognition and Behaviour.
Wegman: ‘We always give participants extensive questionnaires in our studies. This allows us to explain possible differences in behaviour afterwards. People generally have a good insight into their ability to find their way, so these questions provide a feasible way to assess these abilities. I have coupled the answers of these questionnaires with the brain scans we have collected over the years, which allowed us to detect these differences’.
Objects in space - the neural basis of landmark-based navigation and individual differences in navigational ability (PhD defence)
Wednesday 27 November 2013, promotors: prof. dr. L.T.W. Verhoeven, prof. dr. P. Hagoort,
copromotor: dr. G. Janzen
The papers to which this article refers are both included in Joost Wegman’s thesis:
1. Wegman, J. & Janzen, G. Neural encoding of objects relevant for navigation and resting state correlations with navigational ability. Journal of Cognitive Neuroscience 23, 3841-3854 (2011).
2. Wegman, J. et al. Gray and white matter correlates of navigational ability in humans. Human Brain Mapping (in press).
Blood Test Accurately Diagnoses Concussion and Predicts Long Term Cognitive Disability
A new blood biomarker correctly predicted which concussion victims went on to have white matter tract structural damage and persistent cognitive dysfunction following a mild traumatic brain injury (mTBI). Researchers in the Perelman School of Medicine at the University of Pennsylvania, in conjunction with colleagues at Baylor College of Medicine, found that the blood levels of a protein called calpain-cleaved αII-spectrin N-terminal fragment (SNTF) were twice as high in a subset of patients following a traumatic injury. If validated in larger studies, this blood test could identify concussion patients at increased risk for persistent cognitive dysfunction or further brain damage and disability if returning to sports or military activities.
More than 1.5 million children and adults suffer concussions each year in the United States, and hundreds of thousands of military personal endure these mild traumatic brain injuries worldwide. Current tests are not capable of determining the extent of the injury or whether the injured person will be among the 15-30 percent who experience significant, persistent cognitive deficits, such as processing speed, working memory and the ability to switch or balance multiple thoughts.
"New tests that are fast, simple, and reliable are badly needed to predict who may experience long-term effects from concussions, and as new treatments are developed in the future, to identify who should be eligible for clinical trials or early interventions," said lead author Robert Siman, PhD, research professor of Neurosurgery at Penn. "Measuring the blood levels of SNTF on the day of a brain injury may help to identify the subset of concussed patients who are at risk of persistent disability."
In a study published yesterday in Frontiers in Neurology, Penn and Baylor researchers evaluated blood samples and diffusion tensor images from a subgroup of 38 participants in a larger study of mTBI with ages ranging from 15 to 25 years old. 17 had sustained a head injury caused by blunt trauma, acceleration or deceleration forces, 13 had an orthopaedic injury, and 8 were healthy, uninjured, demographically matched controls.
In taking neuropsychological and cognitive tests over the course of three months, results within the mTBI group varied considerably, with some patients performing as well as the healthy controls throughout, while others showed impairment initially that resolved by three months, and a third group with cognitive dysfunction persisting through three months. The nine patients who had abnormally high levels of SNTF (7 mTBI and 2 orthopaedic patients) also had significant white matter damage apparent in radiological imaging.
"The blood test identified SNTF in some of the orthopaedic injury patients as well, suggesting that these injuries could also lead to abnormalities in the brain, such as a concussion, that may have been overlooked with existing tests," said Douglas Smith, MD, director of the Penn Center for Brain Injury and Repair and professor of Neurosurgery. "SNTF as a marker is consistent with our earlier research showing that calcium is dumped into neurons following a traumatic brain injury, as SNTF is a marker for neurodegeneration driven by calcium overload."
The blood test given on the day of the mild traumatic brain injury showed 100 percent sensitivity to predict concussions leading to persisting cognitive problems, and 75 percent specificity to correctly rule out those without functionally harmful concussions. If validated in larger studies, a blood test measuring levels of SNTF could be helpful in diagnosing and predicting risk of long term consequences of concussion. The Penn and Baylor researchers hope to determine the robustness of these findings with a second larger study, and determine the best time after concussion to measure SNTF in the blood in order to predict persistent brain dysfunction. The team also wants to evaluate their blood test for identifying when repetitive concussions begin to cause brain damage and persistent disability.
(Source: uphs.upenn.edu)
Study finds altered brain connections in epilepsy patients
Patients with the most common form of focal epilepsy have widespread, abnormal connections in their brains that could provide clues toward diagnosis and treatment, according to a new study published online in the journal Radiology.
(Image: MP-RAGE volumes are segmented into 83 ROIs, which are further parcellated into 1000 cortical and 15 subcortical ROIs. Whole-brain white matter tractography is performed after voxelwise tensor calculation, and the density of fibers that connect each pair of cortical ROIs is used to calculate structural connectivity. T1w = T1-weighted. Credit: Courtesy of Radiology and RSNA)
Temporal lobe epilepsy is characterized by seizures emanating from the temporal lobes, which sit on each side of the brain just above the ear. Previously, experts believed that the condition was related to isolated injuries of structures within the temporal lobe, like the hippocampus. But recent research has implicated the default mode network (DMN), the set of brain regions activated during task-free introspection and deactivated during goal-directed behavior. The DMN consists of several hubs that are more active during the resting state.
To learn more, researchers performed diffusion tensor imaging, a type of MRI that tracks the movement, or diffusion, of water in the brain’s white matter, the nerve fibers that transmit signals throughout the brain. The study group consisted of 24 patients with left temporal lobe epilepsy who were slated for surgery to remove the site from where their seizures emanated. The researchers compared them with 24 healthy controls using an MRI protocol dedicated to finding white matter tracts with diffusion imaging at high resolution. The data was analyzed with a new technique that identifies and quantifies structural connections in the brain.
Patients with left temporal lobe epilepsy exhibited a decrease in long-range connectivity of 22 percent to 45 percent among areas of the DMN when compared with the healthy controls.
"Using diffusion MRI, we found alterations in the structural connectivity beyond the medial temporal lobe, especially in the default mode network," said Steven M. Stufflebeam, M.D., from the Athinoula A. Martinos Center for Biomedical Imaging at Massachusetts General Hospital in Boston.
In addition to reduced long-range connectivity, the epileptic patients had an 85 percent to 270 percent increase in local connectivity within and beyond the DMN. The researchers believe this may be an adaptation to the loss of the long-range connections.
"The increase in local connections could represent a maladaptive mechanism by which overall neural connectivity is maintained despite the loss of connections through important hub areas," Dr. Stufflebeam said.
The results are supported by prior functional MRI studies that have shown decreased functional connectivity in DMN areas in temporal lobe epilepsy. Researchers are not certain if the structural changes cause the functional changes, or vice versa.
"It’s probably a breakdown of myelin, which is the insulation of neurons, causing a slowdown in the propagation of information, but we don’t know for sure," Dr. Stufflebeam said.
Dr. Stufflebeam and colleagues plan to continue their research, using structural and functional MRI with electroencephalography and magnetoencephalography to track diffusion changes and look at real-time brain activity.
"Our long-term goal is to see if we can we predict from diffusion studies who will respond to surgery and who will not," he said.
(Source: eurekalert.org)
Brain aging is conclusively linked to genes; a crucial first step in finding biological mechanisms of normal aging
For the first time in a large study sample, the decline in brain function in normal aging is conclusively shown to be influenced by genes, say researchers from the Texas Biomedical Research Institute and Yale University.
“Identification of genes associated with brain aging should improve our understanding of the biological processes that govern normal age-related decline,” said John Blangero, Ph.D., a Texas Biomed geneticist and the senior author of the paper. The study, funded by the National Institutes of Health (NIH), is published in the November 4, 2013 issue of the Proceedings of the National Academy of Sciences. David Glahn, Ph.D., an associate professor of psychiatry at the Yale University School of Medicine, is the first author on the paper.
In large pedigrees including 1,129 people aged 18 to 83, the scientists documented profound aging effects from young adulthood to old age, on neurocognitive ability and brain white matter measures. White matter actively affects how the brain learns and functions. Genetic material shared amongst biological relatives appears to predict the observed changes in brain function with age.
Participants were enrolled in the Genetics of Brain Structure and Function Study and drawn from large Mexican Americans families in San Antonio. Brain imaging studies were conducted at the University of Texas Health Science Center at San Antonio Research Imaging Institute directed by Peter Fox, M.D.
“The use of large human pedigrees provides a powerful resource for measuring how genetic factors change with age,” Blangero said.
By applying a sophisticated analysis, the scientists demonstrated a heritable basis for neurocognitive deterioration with age that could be attributed to genetic factors. Similarly, decreasing white matter integrity with age was influenced by genes., The investigators further demonstrated that different sets of genes are responsible for these two biological aging processes.
“A key advantage of this study is that we specifically focused on large extended families and so we were able to disentangle genetic from non-genetic influences on the aging process,” said Glahn.
(Source: txbiomed.org)