Neuro signals study gives new insight into brain disorders

ScienceDaily (Mar. 16, 2011) — Research into how the brain transmits messages to other parts of the body could improve understanding of disorders such as epilepsy, dementia, multiple sclerosis and stroke.

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Scientists at the University of Edinburgh have identified a protein crucial for maintaining the health and function of the segment of nerve fibres that controls transmission of messages within the brain.

The study, published in the journal Neuron, could help direct research into neurodegenerative disorders, in which electrical impulses from the brain are disrupted. This can lead to inability to control movement, causing muscles to waste away.

Professor Peter Brophy, Director of the University of Edinburgh's Centre for Neuroregeneration, said: "Knowing more about how signals in the brain work will help us better understand neurodegenerative disorders and why, when these illnesses strike, the brain can no longer send signals to parts of the body."

The brain works like an electrical circuit, sending impulses along nerve fibres in the same way that current is sent through wires.

These fibres can measure up to a metre, but the area covered by the segment of nerve that controls transmission of messages is no bigger than the width of a human hair.

Dr Matthew Nolan, of the University's Centre for Integrative Physiology, said: "At any moment tens of thousands of electrical impulses are transmitting messages between nerve cells in our brains. Identifying proteins that are critical for the precise initiation of these impulses will help unravel the complexities of how brains work and may lead to new insights into how brains evolved."

The research is funded by the Wellcome Trust and the Medical Research Council.

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Brain injuries rise sharply in minor hockey after bodychecking rules relaxed, Canadian study shows

ScienceDaily (Mar. 16, 2011) — Minor league hockey players in the Atom division are more than 10 times likely to suffer a brain injury since bodychecking was first allowed among the 9 and 10-year-olds, says a study led by St. Michael's Hospital neurosurgeon Dr. Michael Cusimano.

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The findings, published online in the journal Open Medicine, add to the growing evidence that bodychecking holds greater risk than benefit for youth and support widespread calls to ban the practice.

According to the researchers, led by Cusimano, director of the Injury Prevention Research Centre at St. Michael's Hospital in Toronto, the odds of visiting an emergency department due to a brain injury from bodychecking increased significantly among all minor hockey players after Hockey Canada relaxed bodychecking rules in the 1998/1999 season. At that time, the organization allowed, for the first time, body contact among 9 and 10 year-olds in the Atom division.

The team examined the records of 8,552 male youth 6-17 years-old who attended one of five emergency departments in Ontario for hockey related injuries that occurred before and after the rule change. Researchers found more than half of hockey-related injuries were a result of bodychecking. What's more, the risk of a head or neck injury, including concussions, increased across all minor hockey divisions.

"Our work confirmed the fact that body checking is the most common cause of injury in hockey. While proponents argue lowering the age for bodychecking helps players learn how to properly bodycheck and reduces injuries at older ages, our study clearly showed the opposite ― the risk of all injuries and especially, brain injuries, increases with exposure to bodychecking," Cusimano said. "While all age groups showed increases in injuries, the youngest were the most vulnerable and that bodychecking puts youth unnecessarily at the risk of the long-term effects of brain injuries, such as cognitive and social-behavioural problems."

For some time, researchers like Dr. Cusimano have called on organizations like the NHL to take more leadership in reducing the incidence of brain injuries. In recent weeks, pressure has mounted on the NHL after Pittsburgh Penquins captain Sidney Crosby and Montreal Canadiens' Max Pacioretty suffered serious concussions that sidelined both players.

"Ice hockey is a sport with great potential to increase the health of individuals but practices that increase the risk for the vast majority of players must be minimized," Cusimano adds. "It is now very clear that there is no benefit to any one or any group to continue to allow bodychecking. Hockey organizers, sponsors, the media, coaches, trainers, and players and parents must come together to advocate for multifaceted approaches that include changes to the rules to reduce the risk of injury."

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Self-administered light therapy may improve cognitive function after traumatic brain injury

ScienceDaily (Mar. 18, 2011) — At-home, daily application of light therapy via light-emitting diodes (LEDs) placed on the forehead and scalp led to improvements in cognitive function and post-traumatic stress disorder in patients with a traumatic brain injury (TBI), according to a groundbreaking study published in Photomedicine and Laser Surgery, a peer-reviewed journal published by Mary Ann Liebert, Inc.

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Margaret Naeser, PhD, LAc, VA Boston Healthcare System, Boston University School of Medicine, and colleagues from Massachusetts General Hospital, and Harvard-MIT Division of Health Sciences and Technology, in Boston, and MedX Health Inc. (Mississauga, ON, Canada), report on the use of transcranial LED-based light therapy to treat two patients with longstanding traumatic brain injury (TBI). Each patient applied LEDs nightly and demonstrated substantial improvement in cognitive function, including improved memory, inhibition, and ability to sustain attention and focus. One patient was able to discontinue medical disability and return to full-time work. These cognitive gains decreased if the patients stopped treatment for a few weeks and returned when treatment was restarted. Both patients are continuing LED treatments in the home. The findings are presented in "Improved Cognitive Function After Transcranial, Light-Emitting Diode Treatments in Chronic, Traumatic Brain Injury: Two Case Reports."

Low-level light therapy using lasers or externally placed LEDs to deliver red and near-infrared (NIR) light energy has been shown in cell-based studies to improve cellular metabolism and to produce beneficial physiological effects. In acute stroke in humans, for example, transcranial NIR light therapy applied less than 24 hours post-stroke was associated with improved outcomes.

"The results of this study will provide a basis for future therapeutic use of phototherapy to improve recovery after injury and facilitate management of other CNS disorders. The development of novel therapies to restore function after neurologic injury, stroke, or disease is an increasingly important goal in medical research as a result of an increase in non-fatal traumatic wounds and the increasing prevalence of dementias and other degenerative disorders in our aging population," says Raymond J. Lanzafame, MD, MBA, Editor-in-Chief of the Journal.

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Prognosis for brain damage

ScienceDaily (Mar. 18, 2011) — A Norwegian research centre is developing new magnetic resonance (MR) imaging techniques to study the brain. This could have impact for victims of brain damage as well as Alzheimer patients.

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"In a way, MR is like Lego blocks," says Asta Håberg, Professor of Neuro Imaging at the Medical Imaging Laboratory (MI Lab) in Trondheim. "There's a practically infinite number of combinations of what we can take images of, so we test out new combinations to see what we can find. This is how we arrived at the methods that enable us to perform faster, higher-quality MR imaging."

MI Lab is one of Norway's 14 original Centres for Research-based Innovation (SFI) which have received funding from the Research Council of Norway since 2007.

Professor Håberg is involved in a project to study brain damage from accidents, with the objective of finding the best MR variable for establishing prognoses for patients. In a follow-up study, researchers are studying 100 patients over four years. Using repeated MR imaging, they hope to find a clinical variable, present shortly after the accident, that predicts patients' condition one year later. A method that can determine long-term prognoses for victims of brain damage would be useful in individualising rehabilitation training.

Research on memory

The SFI centre's MR group is also running another exciting project related to memory functions. Problems with memory afflict patients suffering from multiple sclerosis, epilepsy, depression, Alzheimer's disease, schizophrenia and more. MI Lab scientists are working to locate the brain areas that are activated when we use our memory.

It turns out that the areas which first lose functionality with the onset of dementia are related to olfactory function, memory and directional sense. The brain areas that support these functions are located within the temporal lobe.

"Brain researchers believe it will eventually be possible to predict age-related dementia 10-20 years before onset by examining brain activity," says Professor Håberg. "With early diagnosis, disease progression can be slowed. But it will be some years before we have cracked all the necessary codes."

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Possible new target for treatment of multiple sclerosis

ScienceDaily (Mar. 28, 2011) — The immune system recognizes and neutralizes or destroys toxins and foreign pathogens that have gained access to the body. Autoimmune diseases result when the system attacks the body's own tissues instead. One of the most common examples is multiple sclerosis (MS). MS is a serious condition in which nerve-cell projections, or axons, in the brain and the spinal cord are destroyed as a result of misdirected inflammatory reactions. It is often characterized by an unpredictable course, with periods of remission being interrupted by episodes of relapse.

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A team of researchers led by LMU Munich Professor Martin Kerschensteiner of the Medical Center of the University of Munich and Professor Thomas Misgeld from the Technical University of Munich has now been able to explain how the damage is inflicted. Their results reveal that the inflammatory reaction can induce a previously unknown type of axonal degeneration, which they call "focal axonal degeneration" (FAD). In an animal model of MS, this process is reversible if it is recognized and treated early, so the researchers believe that it could serve as a potential target for therapeutic intervention. "Development of an effective treatment will be a long-term project," cautions Kerschensteiner. "As yet, we only have a superficial understanding of the underlying molecular mechanisms and, of course, finding effective therapies will require time-consuming screens and extensive trials of drug candidates."

Multiple sclerosis is a common and, in many cases seriously disabling, autoimmune disease that can lead to the disturbance or loss of sensory function, voluntary movement, vision and bladder control. Commonly, it is thought that the primary target of MS is the myelin sheath, an insulating membrane that enwraps axons, and increases the speed of signal transmission. However, damage to nerve fibers is also a central process, as whether autoimmune pathology ultimately leads to permanent disability depends largely on how many nerve fibers are damaged over the course of time.

The team led by Kerschensteiner and Misgeld set out to define precisely how the damage to the nerve axons occurs. As Misgeld explains, "We used an animal model in which a subset of axons is genetically marked with a fluorescent protein, allowing us to observe them directly by fluorescence microscopy." After inoculation with myelin, these mice begin to show MS-like symptoms. But the researchers found that many axons showing early signs of damage were still surrounded by an intact myelin sheath, suggesting that loss of myelin is not a prerequisite for axonal damage.

Instead a previously unrecognized mechanism, termed focal axonal degeneration (FAD), is responsible for the primary damage. FAD can damage axons that are still wrapped in their protective myelin sheath. This process could also help explain some of the spontaneous remissions of symptoms that are characteristic of MS. "In its early stages, axonal damage is spontaneously reversible," says Kerschensteiner. "This finding gives us a better understanding of the disease, but it may also point to a new route to therapy, as processes that are in principle reversible should be more susceptible to treatment."

However, one must remember that it takes years to transform novel findings in basic research into effective therapies. First the process that leads to disease symptoms must be elucidated in molecular detail. In the case of MS it has already been suggested that reactive oxygen and nitrogen radicals play a significant role in facilitating the destruction of axons. These aggressive chemicals are produced by immune cells, and they disrupt and may ultimately destroy the mitochondria. Mitochondria are the cell's powerhouses, because they synthesize ATP, the universal energy source needed for the build-up and maintenance of cell structure and function.

"In our animal model, at least, we can neutralize these radicals and this allows acutely damaged axons to recover," says Kerschensteiner. The results of further studies on human tissues, carried out in collaboration with specialists based at the Universities of Göttingen and Geneva, are encouraging. The characteristic signs of the newly discovered process of degeneration can also be identified in brain tissue from patients with MS, suggesting that the basic principle of treatment used in the mouse model might also be effective in humans.

Even if this turns out to be the case, it would not mean that a new therapy would soon be at hand. The chemical agents used in the mouse experiments are not specific enough and not tolerated well enough to be of clinical use. "Before appropriate therapeutic strategies can be developed, we need to clarify exactly how the damage arises at the molecular level," says Kerschensteiner. "We also want to investigate whether similar mechanisms play a role in later chronic stages of multiple sclerosis ."

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Healthy welders may be at increased risk for early brain damage

ScienceDaily (Apr. 6, 2011) — New research suggests that workers exposed to welding fumes may be at risk for developing brain damage in an area of the brain also affected in Parkinson's disease. The study is published in the April 6, 2011, online issue of Neurology®, the medical journal of the American Academy of Neurology.

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Fumes produced by welding contain manganese. Manganese is a chemical element that, even at low levels, has been linked to neurologic problems, including Parkinson's disease-like symptoms.

"There are over one million workers who perform welding as part of their job functions in the United States," said Brad A. Racette, MD, with Washington University School of Medicine in St. Louis and a Fellow with the American Academy of Neurology. "If a link between neurotoxic effects and these fumes were proven, it would have a substantial public health impact for the U.S. workforce and economy."

The study involved 20 welders with no symptoms of Parkinson's disease, 20 people with Parkinson's disease who were not welders and 20 people who were not welders and did not have Parkinson's. The welders were recruited from two Midwest shipyards and one metal fabrication company. All participants were given brain PET and MRI scans, motor skills tests and examined by a neurologist who specializes in movement disorders. The welders had an average of 30,000 hours of lifetime welding exposure. Their average manganese levels were found to be two times the upper limits of normal.

Scientists found that welders had an average 11.7 percent reduction in a marker of dopamine in one area of the brain on PET scans as compared to people who did not weld. Dopamine is a chemical messenger that helps nerve cells communicate and is decreased in specific brain regions in people with Parkinson's disease. The welders' motor skills test scores also showed mild movement difficulties that were about half of that found in the early Parkinson's disease patients.

"While these changes in the brain and dopamine dysfunction may be an early marker of neuron death related to welding exposure, the damage appeared to be different from those of people with full-fledged Parkinson's disease," said Racette. "MRI scans also revealed brain changes in welders that were consistent with manganese deposits in the brain."

"Although this study shows that these workers had dopamine dysfunction in the brain, the study authors could not determine whether this was specifically related to manganese," said W. R. Wayne Martin, MD, who wrote an accompanying editorial on the topic. Martin is with the University of Alberta in Edmonton, Alberta, Canada and a member of the American Academy of Neurology. "Will these individuals develop full-fledged Parkinson's disease? We can't answer that question based on the study but more research should be done to explore this possibility."

The study was supported by the Michael J. Fox Foundation, the National Institutes of Health, the American Parkinson Disease Association, Advanced Research Center at Washington University, the Great St. Louis Chapter of the ADPA, the McDonnell Center for Higher Brain Function and the Barnes-Jewish Hospital Foundation.

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Vehicle pollution significantly damages the brain, mouse study suggests

ScienceDaily (Apr. 13, 2011) — If mice commuted, their brains might find it progressively harder to navigate the maze of Los Angeles freeways. A new study reveals that after short-term exposure to vehicle pollution, mice showed significant brain damage -- including signs associated with memory loss and Alzheimer's disease.

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The mind-numbing toxin is not an exhaust gas, but a mix of tiny particles from burning of fossil fuel and weathering of car parts and pavement, according to the study to be published April 7 in the journal Environmental Health Perspectives.

Many studies have drawn a link between vehicle pollution and health problems. This is the first to explore the physical effect of freeway pollution on brain cells.

The authors found a way to recreate air laden with freeway particulate matter inside the laboratory. Whether in a test tube or in live mice, brain cells showed similar responses:

Neurons involved in learning and memory showed significant damage, The brain showed signs of inflammation associated with premature aging and Alzheimer's disease, Neurons from developing mice did not grow as well.

The freeway particles measured between a few dozen to 200 nanometers -- roughly one-thousandth the width of a human hair, and too small for car filtration systems to trap.

"You can't see them, but they are inhaled and have an effect on brain neurons that raises the possibility of long-term brain health consequences of freeway air," said senior author Caleb Finch, an expert in the effects of inflammation and holder of the ARCO/William F. Kieschnick Chair in the Neurobiology of Aging.

Co-author Constantinos Sioutas, of the USC Viterbi School of Engineering, developed the unique technology for collecting freeway particulates in a liquid suspension and recreating polluted air in the laboratory. This made it possible to conduct a controlled study on cultured brain cells and live animals.

Exposure lasted a total of 150 hours, spread over 10 weeks, in three sessions per week lasting five hours each.

"Of course this leads to the question, 'How can we protect urban dwellers from this type of toxicity?' And that's a huge unknown," Finch said.

The authors hope to conduct follow-up studies on issues such as:

Memory functions in animals exposed to freeway particulates, Effects on development of mice exposed prenatally, Lifespan of exposed animals, Interaction of particulates with other components of smog, such as heat and ozone, Potential for recovery between periods of exposure, Comparison of effects from artificially and naturally occurring nanoparticles, Chemical interactions between freeway particulates and brain cells.

If further studies confirm that freeway particulates pose a human health hazard, solutions will be hard to find.

Even an all-electric car culture would not solve the problem on its own, Finch said.

"It would certainly sharply decrease the local concentration of nanoparticles, but then at present electrical generation still depends upon other combustion processes -- coal -- that in a larger environment contribute nanoparticles anyway.

"It's a long-term global project to reduce the amount of nanoparticles around the world. Whether we clean up our cars, we still have to clean up our power generation."

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