New procedure to make brain surgery safer

ScienceDaily (May 27, 2011) — To increase patient safety in clinical practice and minimize risks and damage that may arise during surgery, computer support and digital medical imaging are key technologies. Before brain operations, neurosurgeons can now evaluate patient-specific surgical risks, achieve increased safety, and avoid unacceptable risks.

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Brain interventions must be planned so that the neurosurgeon can access and remove the tumor without causing unnecessary damage. Before the brain tumor can be removed, crucial questions must be answered. Where do the functional areas of the cortex (gray matter) of the patient lie? What are the paths of the nerve fiber tracts that connect them? Answering these questions is important because the functional areas of the brain are interconnected via nerve pathways, also known as nerve fiber tracts. These nerve tracts must be protected as much as possible; otherwise, permanent dysfunction could occur. Furthermore, nerve tracts can be pushed or infiltrated by the brain tumor itself. If nerve tracts become damaged during an operation, there is a risk that distant functional areas connected to the tumor-afflicted part of the brain could be affected and induce lasting sensory, motor, and cognitive impairment. Therefore, neurosurgeons attempt to answer these questions for each patient during the planning stage of the brain operation to minimize the risks present in the intervention. To do so, surgeons require medical imagery of each patient's brain anatomy and function that is as realistic and precise as possible. However, medical images contain inaccuracies that arise from the processing, modeling, and reconstruction of patient data.

Solving these problems requires more than merely improving existing imaging methods. Mathematical analysis and models must be integrated to produce information about the location of the tumor, functional areas, and nerve fiber tracts, to increase the accuracy of patient-specific data, and to give the surgeon dependable knowledge.

The Fraunhofer MEVIS Institute for Medical Image Computing in Bremen, Germany has pioneered a procedure that analyzes uncertainty in patient-specific images, modeling, and reconstruction and incorporates this information into reconstructions of patient data. This procedure allows safety margins around nerve tracts in the brain to be more accurately determined. In addition, the reliability of the reconstructed data is calculated to supply the surgeon with accurate information concerning nerve tract locations, paths, and intersections and to construct safety margins around the nerve fiber tracts. By integrating errors in measurement, reconstruction, and modeling, the exact locations of tracts in a space-occupying tumor are calculated. This gives the neurosurgeon a reliable prognosis concerning where the incision in the brain should be made and which safety margins should be chosen to avoid harming nerve tracts and irreversibly damaging important functional areas. Before an intervention, the surgeon can evaluate patient-specific risks. These software assistants will be refined and implemented for neuronavigation in future operations, providing the surgeon with updated information during surgery that can be compared to planning data.

The paths of nerve tracts in the brain and the functional areas that they connect can now be explored by visitors of the "New Paths in Medicine" exhibit on the MS Wissenschaft exhibition ship. The converted inland vessel is underway until September 29, 2011 and docks in 35 different cities. During the "Year of Health Research," visitors can familiarize themselves with the field's newest trends, developments, and research findings. The exhibit showcases a physical three-dimensional model of the brain produced through an innovative printing process based on the medical image data of a real person. This brain model can be touched and viewed from different angles thanks to its rotating base. Nerve tracts can be activated by touching sensors on the physical model that correspond to functional areas of the brain. The brain is displayed on a screen along with the activated nerve tracts that are responsible, for instance, for sight, speech, feeling, and motion. This new form of interactive exhibit was developed by Fraunhofer MEVIS in Bremen together with the Universum® Science Center in Bremen to demonstrate how modern image processing combined with mathematics and intelligent software can help make neurosurgical operations more predictable and safe. The three-dimensional print of the brain was produced by the Fraunhofer-Institut ITWM in Kaiserslautern.

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Changes in brain circuitry play role in moral sensitivity as people grow up

ScienceDaily (May 29, 2011) — People's moral responses to similar situations change as they age, according to a new study at the University of Chicago that combined brain scanning, eye-tracking and behavioral measures to understand how the brain responds to morally laden scenarios.

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Both preschool children and adults distinguish between damage done either intentionally or accidently when assessing whether a perpetrator had done something wrong. Nonetheless, adults are much less likely than children to think someone should be punished for damaging an object, especially if the action was accidental, said study author Jean Decety, the Irving B. Harris Professor in Psychology and Psychiatry at the University of Chicago and a leading scholar on affective and social neuroscience.

The different responses correlate with the various stages of development, Decety said, as the brain becomes better equipped to make reasoned judgments and integrate an understanding of the mental states of others with the outcome of their actions. Negative emotions alert people to the moral nature of a situation by bringing on discomfort that can precede moral judgment, and such an emotional response is stronger in young children, he explained.

"This is the first study to examine brain and behavior relationships in response to moral and non-moral situations from a neurodevelopmental perspective," wrote Decety in the article, "The Contribution of Emotion and Cognition to Moral Sensitivity: A Neurodevelopmental Study," published in the journal Cerebral Cortex. The study provides strong evidence that moral reasoning involves a complex integration between affective and cognitive processes that gradually changes with age.

For the research, Decety and colleagues studied 127 participants, aged 4 to 36, who were shown short video clips while undergoing an fMRI scan. The team also measured changes in the dilation of the people's pupils as they watched the clips.

The participants watched a total of 96 clips that portrayed intentional harm, such as someone being shoved, and accidental harm, such as someone being struck accidentally, such as a golf player swinging a club. The clips also showed intentional damage to objects, such as a person kicking a bicycle tire, and accidental damage, such as a person knocking a teapot off the shelf.

Eye tracking in the scanner revealed that all of the participants, irrespective of their age, paid more attention to people being harmed and to objects being damaged than they did to the perpetrators. Additionally, an analysis of pupil size showed that "pupil dilation was significantly greater for intentional actions than accidental actions, and this difference was constant across age, and correlated with activity in the amygdala and anterior cingulate cortex," Decety said.

The study revealed that the extent of activation in different areas of the brain as participants were exposed to the morally laden videos changed with age. For young children, the amygdala, which is associated the generation of emotional responses to a social situation, was much more activated than it was in adults.

In contrast, adults' responses were highest in the dorsolateral and ventromedial prefrontal cortex -- areas of the brain that allow people to reflect on the values linked to outcomes and actions.

In addition to viewing the video clips, participants were asked to determine, for instance, how mean was the perpetrator, and how much punishment should he receive for causing damage or injury. The responses showed a clear connection between moral judgments and the activation the team had observed in the brain.

"Whereas young children had a tendency to consider all the perpetrator malicious, irrespective of intention and targets (people and objects), as participants aged, they perceived the perpetrator as clearly less mean when carrying out an accidental action, and even more so when the target was an object," Decety said.

When recommending punishments, adults were more likely to make allowances for actions that were accidental, he said. The response showed that they had a better developed prefrontal cortex and stronger functional connectivity between this region and the amygdala than children. Adults were better equipped to make moral judgments. "In addition, the ratings of empathic sadness for the victim, which were strongest in young children, decreased gradually with age, and correlated with the activity in the insula and subgenual prefrontal cortex," which area areas associated with emotional behavior and automatic response to stresses, Decety said. Together, the results are consistent with the view that morality is instantiated by functionally integrating several distributed areas/networks.

The research was supported with a grant from the National Science Foundation. Joining Decety in writing the paper were Kalina Michalska, a postdoctoral scholar, and Katherine Kinzler, an assistant professor, both in the Department of Psychology.

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Iron key to brain tumor drug delivery

ScienceDaily (June 2, 2011) — Brain cancer therapy may be more effective if the expression of an iron-storing protein is decreased to enhance the action of therapeutic drugs on brain cancer cells, according to Penn State College of Medicine researchers.

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Malignant glioblastoma multiforme is a deadly brain tumor for which no long-term effective cure exists. Because drugs in the blood do not pass from the blood vessels to the brain, effective amounts of chemotherapy drugs do not reach the tumor. Increasing dosages damage normal brain tissue and cause significant neurological damage. These dosages also would likely be harmful to other organs in the body. However, by increasing the sensitivity of the cancer cells to drugs, the effectiveness of treatment can be increased.

"About half of all brain tumors are resistant to chemotherapy and new therapeutic strategies are urgently needed to treat this cancer," said James Connor, Ph.D., Distinguished Professor and vice-chairman of neurosurgery.

Connor and his graduate student Xiaoli Liu took advantage of the high iron requirements of the brain cancer cells to target ferritin, a protein that stores iron in all cells.

"High levels of iron are required in cancer cells to meet the energy requirements associated with their rapid growth," Connor said. "In addition, iron is essential for general cell health."

Working with Achuthamangalam Madhankumar, Ph.D., assistant professor of neurosurgery, the researchers used liposomes -- tiny lipid containers -- to deliver a fragment of RNA called interference or siRNA, to tumor cells. The siRNA targets the molecular machinery of the cell so that the protein cannot be made -- a process known as downregulation. By targeting and turning off ferritin in cancer cells, the protective function of H-ferritin disappears and the sensitivity to chemotherapy increases.

Using ferritin siRNA, the protein level decreases by 80 percent within 48 hours providing a window of opportunity for enhanced sensitivity to the chemotherapeutic agent. The researchers studied whether silencing ferritin would lower the effective dosage of BCNU, a chemotherapy drug used in brain tumor treatment and one of the few approved for brain cancer. While BCNU is effective, it has serious side effects limiting its use.

The use of siRNA reduces the amount of BCNU needed for tumor suppression by more than half in mice, according to the researchers, who published their findings in the journal Cancer Research.

"Our results further indicate that a nanoliposomal delivery mechanism can increase the efficacy of siRNA and optimize the amount of siRNA delivered," Connor said. "By silencing the ferritin gene, tumor sensitivity to chemotoxins was increased. The results from this project are a promising initial step toward the development of siRNA gene therapy involving ferritin for the treatment of multiple tumor types."

Other researchers contributing to this project were Becky Slagle-Webb, research assistant, and Jonas M. Sheehan, M.D., associate professor of neurosurgery, Penn State College of Medicine and Nodar Surguladze, Ph.D., deputy director, Institute of Molecular Biology and Biological Physics, Republic of Georgia.

The Tara Leah Witmer Foundation partially supported this research.

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A novel function of anti-diuretic hormone vasopressin in the brain

ScienceDaily (Jan. 20, 2011) — The anti-diuretic hormone "vasopressin" is released from the brain, and known to work in the kidney, suppressing the diuresis. Now, a Japanese research team led by Professor Yasunobu Okada, Director-General of National Institute for Physiological Sciences (NIPS), and Ms. Kaori Sato, a graduate student of The Graduate University for Advanced Studies, has clarified the novel function of "vasopressin" that works in the brain, as well as in the kidney via the same type of the vasopressin receptor, to maintain the size of the vasopressin neurons.

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It might be a useful result for clarification of the condition of cerebral edema which swells along with the brain trauma or the cerebral infarction, and for its treatment method development. This result of the study is reported in the Science Signaling magazine.

The research team focused on the vasopressin neurons which exist in a hypothalamus of the brain. The vasopressin is essentially released from the vasopressin neurons into blood circulation and acts on the kidney as anti-diuretic, when the blood plasma becomes more concentrated. In contrast, they ascertained that the vasopressin neurons release the vasopressin into the brain, not in blood, when the surrounding body fluid becomes more diluted than usual. Usually, the more diluted the body fluid becomes, the bigger the neuronal cell swells. However, their finding shows that the vasopressin in the brain maintains the size of the vasopressin neurons even when the body fluid becomes more diluted. In addition, it was clarified that the vasopressin sensor protein (receptor) which was currently considered to be only in the kidney, was related to this function in the brain.

This study became possible by labeling vasopressin neurons of the rat brain hypothalamus with green fluorescent protein (GFP)．(The transgenic rat was developed by Professor Yoichi Ueta; University of Occupational and Environmental Health, Japan.)

Professor Okada says that "It is a surprising result that the same type of the vasopressin receptor as the kidney exists in the brain and the vasopressin works on it. It can be expected to clarify the condition of cerebral edema which swells along with the brain trauma or the cerebral infarction, and to develop its treatment method.

This result is supported by Grants-in-Aid for Scientific Research, the MEXT, Japan.

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New era of advances in brain research: As recording technology rapidly improves, neurons give up their secrets cell by cell

ScienceDaily (Jan. 30, 2011) — Scientists at The Rehabilitation Institute of Chicago (RIC) report that, thanks to improvements in technology and data analysis, our understanding of the functional principles that guide the development and operation of the brain could improve drastically in the next few years. The advances could herald a neuroscientific revolution, much as increasing processor speeds paved the way for the computing revolution of the last half century.

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In the February, 2011 issue of Nature Neuroscience, the researchers, Dr. Ian H. Stevenson and Dr. Konrad P. Kording, performed a meta-analysis of 56 studies conducted since the 1950s (the advent of multi-electrode recordings) in which the activity of neurons was recorded in animals or humans. They found that the number of simultaneously recorded single neurons has grown exponentially since the 1950s, doubling approximately every seven years.

The researchers likened the progress in neuronal recording techniques to Moore's law, which describes the exponential growth of processing speed that has doubled approximately every two years, making computers smaller and technology accessible to more people.

"As it becomes easier for us to access and interpret information coming from the brain, we will be able to better help those with disabilities and conditions of the nervous system," said Dr. Kording. "Our goal is to take what we are learning about how and why the brain works so we can quickly and successfully use it to help patients. By decoding how neurons communicate with each other, we may one day be able to restore connections by conditioning different neurons to talk to each other, or to talk to each other in different ways, thereby restoring ability in our patients."

The "firing" or "spiking" of a neuron is really a signal sent along a gradient to other neurons and throughout the entire nervous system. These signals send messages and convey important information, including representations about the world and messages that control our behaviors and actions.

According to Dr. Kording, "Recording of only a single neuron at a time was possible in the late 1950s. Now, researchers can record activity from hundreds of neurons simultaneously, gathering valuable information about when and why neurons fire or do not fire."

In patients with conditions caused by lost connections in the brain, such as stroke or spinal cord injury, information from the brain sent via neurons cannot get relayed to certain limbs or parts of the body. Researchers at RIC are using data from neurons to pioneer research designed to restore connections and ability using novel technologies. In fact, RIC researchers recently reported that they have identified novel ways of potentially re-routing the flow of information in the nervous system using stimulation technology. Currently, RIC researchers are on the cutting-edge of exploring the use of novel brain-machine interface, functional electronic stimulation and virtual reality technology to restore function in individuals suffering from paralysis caused by spinal cord injuries or stroke.

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Neuroimaging shows how the brain learns mental skills

ScienceDaily (Feb. 9, 2011) — Movements become skilled and automatic with practise, so tasks like riding a bicycle can be performed without much attention or mental effort. New research by scientists at Royal Holloway, University of London provides evidence that the cerebellum, a part of the brain used to store memories for skilled movements, could also store memories important for mental skills -- such as the rules used to interpret traffic light signals.

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The prefrontal cortex, in the frontal lobe, uses problem-solving to establish the correct rules using attention, and the new research raises the possibility that the cerebellum then learns to implement them skilfully with little conscious attention, freeing the prefrontal cortex to direct attention to new problems.

The study, published in the Journal of Neuroscience, reports that brain imaging was used to scan volunteers during learning, and that in a part of the cerebellum known to be connected with the prefrontal cortex, activity changed from one practice trial to the next. The rate of change was faster for rules that became automatic more quickly. After practice, volunteers used simple rules quickly and accurately even when attention drawn away by a 'distractor' task performed at the same time.

Dr Ramnani, from the Department of Psychology at Royal Holloway said: "The study adds to the groundwork for understanding cognitive deficits in patients with cerebellar damage and improving strategies for their rehabilitation. It also raises the possibility that the cerebellum might be used for the skillful, automatic and unconscious use of mathematical and grammatical rules."

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New hybrid drug, derived from common spice, may protect, rebuild brain cells after stroke

ScienceDaily (Feb. 11, 2011) — Whether or not you're fond of Indian, Southeast Asian and Middle Eastern food, stroke researchers at Cedars-Sinai Medical Center think you may become a fan of one of their key spices.

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The scientists created a new molecule from curcumin, a chemical component of the golden-colored spice turmeric, and found in laboratory experiments that it affects mechanisms that protect and help regenerate brain cells after stroke. Research scientist Paul A. Lapchak, Ph.D., director of Translational Research in the Department of Neurology at Cedars-Sinai Medical Center, is presenting these findings at the American Heart Association International Stroke Conference in Los Angeles.

Only one drug is now approved for ischemic stroke, which occurs when a clot blocks blood flow to the brain. Commonly called a "clot-busting drug," tissue plasminogen activator (tPA) is injected intravenously to dissolve clots and reinstate blood flow. If blood and oxygen are restored in time, consequences of the stroke, such as speech, memory, movement and other impairments, may be reduced.

The new curcumin-hybrid compound -- CNB-001 -- does not attack clots but instead repairs stroke damage at the molecular level that feed and support the all-important brain cells, neurons.

Curcumin has been studied for its potential to treat brain injury and disease, and while the substance itself looks promising, it has several drawbacks, especially as an emergency stroke treatment, which must be quick to be effective: It is not well absorbed in the body, fails to reach its target in high concentrations, becomes depleted quickly, and is blocked from entering the brain by a natural protective mechanism called the blood-brain barrier.

"CNB-001 has many of the same benefits of curcumin but appears to be a better choice of compound for acute stroke because it crosses the blood-brain barrier, is quickly distributed in the brain, and moderates several critical mechanisms involved in neuronal survival," Lapchak says, adding that he and his colleagues expect the new drug to move to human clinical trials soon.

When brain tissue is deprived of blood and oxygen, a cascading series of interrelated events triggers at the molecular level, breaking down the normal electrical and chemical "signaling pathways" responsible for nourishing and supporting neurons. The environment quickly becomes toxic, killing brain cells and destroying their support structures.

Theoretically, interrupting these harmful events and restoring normal pathway function could prevent cell death and the memory and behavioral deficits that result, but it will take a cocktail of drugs or a drug capable of targeting many mechanisms to correct the many pathways damaged by stroke, Lapchak says. CNB-001protects brain cells from damage by repairing four major pathways. One mechanism also plays a major role in the growth and survival of neurons.

The drug reduced stroke-caused "motor deficits" -- problems of muscle and movement control -- in this laboratory study. It was effective when administered up to an hour after stroke, which correlates with about three hours in humans, the same time frame for which tPA is currently approved.

Lapchak and colleagues at the Salk Institute for Biological Studies used the same laboratory rabbit model to mimic human stroke that earlier researchers had employed before the clot-busting drug tPA entered clinical trials. Patrick D. Lyden, M.D., chairman of Cedars-Sinai's Department of Neurology, helped lead a major trial that resulted in the Food and Drug Administration's 1996 approval of tPA, still considered the stroke treatment gold standard.

Those who cook Indian, Thai, Malay and Persian dishes know turmeric well for its zesty flavor, use in curries and for the rich color it imparts to food. Turmeric also has a long history of use in Ayurvedic and Chinese traditional medicine.

Grants from the National Institute of Neurological Disorders and Stroke, part of the National Institutes of Health, supported the CNB-001 study (NS060685 to PAL).

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Early brain effects of HIV in mouse model

ScienceDaily (Mar. 2, 2011) — A new mouse model closely resembles how the human body reacts to early HIV infection and is shedding light on nerve cell damage related to the disease, according to researchers funded by the National Institutes of Health.

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The study in the Journal of Neuroscience demonstrates that HIV infection of the nervous system leads to inflammatory responses, changes in brain cells, and damage to neurons. This is the first study to show such neuronal loss during initial stages of HIV infection in a mouse model.

The study was conducted by a team of scientists from the University of Nebraska Medical Center, Omaha, and the University of Rochester Medical Center, N.Y. It was supported by the National Institute on Drug Abuse (NIDA), the National Institute of Neurological Disorders and Stroke, the National Institute of Mental Health, and the National Center for Research Resources.

"This research breakthrough should help us move forward in learning more about how HIV affects important brain functioning in its initial stages, which in turn could lead us to better treatments that can be used early in the disease process," said Dr. Nora D. Volkow, director of NIDA.

"The work contained within this study is the culmination of a 20-year quest to develop a rodent model of the primary neurological complications of HIV infection in humans," said Dr. Howard Gendelman, one of the primary study authors. "Previously, the rhesus macaque was the only animal model for the study of early stages of HIV infection. However, its use was limited due to expense and issues with generalizing results across species. Relevant rodent models that mimic human disease have been sorely needed."

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Multiple sclerosis blocked in mouse model: Barring immune cells from brain prevents symptoms

ScienceDaily (Mar. 7, 2011) — Scientists have blocked harmful immune cells from entering the brain in mice with a condition similar to multiple sclerosis (MS).

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According to researchers from Washington University School of Medicine in St. Louis, this is important because MS is believed to be caused by misdirected immune cells that enter the brain and damage myelin, an insulating material on the branches of neurons that conduct nerve impulses.

New insights into how the brain regulates immune cell entry made the accomplishment possible. Washington University scientists had borrowed an anti-cancer drug in development by the company ChemoCentryx simply to test their theories.

"The results were so dramatic that we ended up producing early evidence that this compound might be helpful as a drug for MS," says Robyn Klein, MD, PhD, associate professor of pathology and immunology, of medicine and of neurobiology. "The harmful immune cells were unable to gain access to the brain tissue, and the mice that received the highest dosage were protected from disease."

ChemoCentryx is now testing the drug in Phase I safety trials. The study is published in The Journal of Experimental Medicine.

Klein and her colleagues discovered a chemical stairway that immune cells have to climb down to enter the brain. Immune cells that exit the blood remain along the vessels on the tissue side, climbing down from the meninges into the brain where they can then cross additional barriers and attack myelin on the branches of neurons.

"The effect of immune cell entry into the brain depends on context," Klein says. "In the case of viral infection, immune cell entry is required to clear the virus. But in autoimmune diseases like multiple sclerosis, their entry is associated with damage so we need to find ways to keep them out."

The stairway is located on the tissue side of the microvasculature, tiny vessels that carry blood into the central nervous system. The steps are made of a molecule called CXCL12 that localizes immune cells, acting like stairs that slow them down so that they can be evaluated to determine if they are allowed to enter the brain. Klein's lab previously discovered that the blood vessel cells of the microvasculature display copies of this molecule on their surfaces.

Klein also found that MS causes CXCL12 to be pulled inside blood vessel cells in humans and mice, removing the stairway's steps and the checkpoints they provide. In the new paper, she showed that blocking the internalization of the molecule prevented immune cells from getting into the brain and doing harm.

Work by another lab called Klein's attention to CXCR7, a receptor that binds to CXCL12. She showed that the receptor is made by the same cells in the microvasculature that display CXCL12. They watched the receptor take copies of CXCL12 and dump them in the cells' lysosomes, pockets for breakdown and recycling of molecules the cell no longer needs.

"After it dumps its cargo in the lysosome, the receptor can go right back to the cell surface to pull in another copy of CXCL12," Klein says. "There likely exists an equilibrium between expression and disposal of CXCL12. Some of the proteins expressed by the immune cells in MS patients affect CXCR7 expression and activity, disrupting the equilibrium and stripping the steps from this immune cell stairway we're studying."

Klein contacted researchers at ChemoCentryx, who were developing a blocker of the CXCR7 receptor as a cancer treatment. When they gave it to the mouse model of MS, immune cells stopped at the meninges.

Klein also found that immune factors could cause microvasculature cells to make more or less of CXCR7, ramping up or down the number of steps on the chemical stairway. She is currently investigating additional immune factors that impact on CXCR7 activity within the blood vessel cell. Whether a given factor promotes or suppresses the receptor may also differ depending upon what part of the brain is being considered.

"One of the biggest questions in MS has been why the location, severity and progression of disease varies so much from patient to patient," Klein says. "Getting a better understanding of how these factors regulate immune cell entry will be an important part of answering that question."

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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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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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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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Study links inflammation in brain to some memory decline

ScienceDaily (Apr. 15, 2011) — High levels of a protein associated with chronic, low-grade inflammation in the brain correlate with aspects of memory decline in otherwise cognitively normal older adults, according to a study led by scientists at the University of California, San Francisco.

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The study is being reported in a poster session at the American Academy of Neurology annual meeting on April 13, 2011.

Inflammation is part of the body's natural immune response to tissue damage. However, chronic inflammation is associated with many diseases. In the brain, it is thought to play a role in aging and neurodegenerative diseases, such as Parkinson's and Alzheimer's. If further research determines that inflammation causes memory decline, anti-inflammatory drugs could prove useful in staving off the damage.

Studies in animals have shown that prolonged brain inflammation impairs function of the hippocampus, a region of the brain involved in storing and generating memory. It does so by disrupting the establishment of memories, a process known as long term potentiation.

The scientists in the study hypothesized that the presence of C-reactive protein (CRP), a marker of chronic low grade inflammation in the brain, would be associated with poorer memory creation and smaller medial-temporal lobes, which include the hippocampus.

They examined 76 women and men (mean age 71.8) with detectible levels of CRP in their blood, and 65 people (mean age 70.8) with undetectable levels. All participants were given a 16-word list learning task to measure verbal recall, and underwent magnetic resonance imaging, MRI, to measure volumes of regions of the medial temporal lobes, specifically the hippocampus, entorhinal cortex and parahippocampal cortex.

The results showed that adults with measureable levels of C reactive protein recalled fewer words and had smaller medial temporal lobes.

Scientists don't know if the inflammation indicated by the C reactive protein is the cause of the memory loss, if it reflects a response to some other disease process or if the two factors are unrelated. But if inflammation causes the cognitive decline, relatively simple treatments could help, said Joel H. Kramer, PsyD, UCSF clinical professor of neuropsychology and the director of the neuropsychology program at the UCSF Memory and Aging Center.

"Anti-inflammatory drugs available today could be used to treat low grade infections in the brain, and could be used more aggressively following surgery, which prompts a large inflammatory response," he said.

Kramer and his colleagues plan to monitor the participants until the end of their lives and to use additional inflammatory markers -- ones that tend to be more sensitive to acute changes than CRP.

"We think such a study will give us a better idea of what's driving the processes we've observed," he said. "If baseline levels of inflammatory markers predict change over time, we'd consider a clinical trial using anti-inflammatory drugs to treat inflammation."

Inflammation is just one of several possible factors that might be driving cognitive decline in normally aging adults, said Kramer. He and his colleagues are examining the possible impact of cardiovascular and stroke risk factors, as well. "We're also just starting to look at exercise, and want to study sleep," he said.

The study was funded by the National Institute on Aging.

Other co-authors of the study are Ralph Green and Joshua Miller, of UC Davis, and Reva Wilheim, Caroline Racine, Brianne Bettcher, Kristine Yaffe and Bruce Miller, of the UCSF Memory and Aging Center.

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Neurosurgeon pushes brain bypass to new heights

ScienceDaily (May 8, 2011) — On the cover of a recent edition of Neurosurgery, readers saw an artist's intricate depiction of the high-flow brain bypass technique developed by SLU professor of neurosurgery, Saleem Abdulrauf, M.D.

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Also in the March issue of the journal, Abdulauf shared details of a surgery he performed to treat a patient's brain aneurysm, a weak area in the wall of an artery that supplies blood to the brain.

Abdulrauf's high-flow procedure means improved outcomes for patients. His technique is less invasive and keeps more blood flowing in the brain than previous surgeries.

Abulrauf likens brain bypass to bypass surgery for the heart. When a patient has an aneurysm involving a brain blood vessel or a tumor at the base of the skull wrapping around a blood vessel, surgeons eliminate the problem vessel by replacing it with an artery from another part of the body.

Brain bypass surgery was first developed in the 1960's in Switzerland by M. Gazi Yasargil, M.D, who is considered the father of modern neurosurgery. Used for complex aneurysms and tumors deep in the base of the skull, Abdulrauf built upon the procedure developed by his mentor, Yasargil.

Instead of replacing a problem artery with a healthy one from the scalp, as the original procedure did, Abdulrauf used an artery from the arm to allow a larger vessel to be replaced.

"With this new technique, we can treat patients in a way that minimizes recovery time and offers the best chance at keeping their brains healthy," Abdulrauf said.

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Anti-depressants boost brain cells after injury in early studies

ScienceDaily (Apr. 22, 2011) — Anti-depressants may help spur the creation and survival of new brain cells after brain injury, according to a study by neurosurgeons at the University of Rochester Medical Center.

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Jason Huang, M.D., and colleagues undertook the study after noticing that patients with brain injuries who had been prescribed anti-depressants were doing better in unexpected ways than their counterparts who were not taking such medications. Not only did their depression ease; their memory also seemed improved compared to patients not on the medication.

"We saw these patients improving in multiple ways -- their depression was improved, but so were their memory and cognitive functioning. We wanted to look at the issue more, so we went back to the laboratory to investigate it further," said Huang, associate professor of Neurosurgery and chief of Neurosurgery at Highland Hospital, an affiliate of the University of Rochester Medical Center.

The team's findings were published online recently in the Journal of Neurotrauma.

Huang said many patients who have a traumatic brain injury also experience depression -- by some estimates, half of such patients are depressed. Doctors aren't sure whether the depression is a byproduct of the sudden, unfortunate change in circumstances that patients find themselves in, or whether the depression is a direct consequence of brain damage.

Previous research by other groups indicated that anti-depressants help generate new brain cells and keep them healthy in healthy animals. That, together with the experience of his patients, led Huang to study the effects of the anti-depressant imipramine (also known as Tofranil) on mice that had injuries to their brains.

Scientists found that imipramine boosted the number of neurons in the hippocampus, the part of the brain primarily responsible for memory. By one measure, mice treated with imipramine had approximately 70 percent more neurons after four weeks than mice that did not receive the medication.

That change was borne out on behavioral tests as well. The team tested mice by using what scientists call a novel object recognition test. Like human infants, mice tend to spend more time sizing up objects that they haven't encountered before -- or don't remember encountering -- than they do objects that they've seen before. This gives scientists a way to measure a mouse's memory.

The team found that mice that had been treated with imipramine had a better memory. They were more likely to remember objects they had seen previously and so spent more time exploring truly novel objects, compared to mice that did not receive the compound.

The benefits did not extend to the motor skills of the mice -- a finding that parallels what neurosurgeons like Huang have seen in their patients on anti-depressants, who don't show improved mobility after use of the medications.

Scientists aren't sure whether the drug helps spur the creation of more new neurons, or whether it helps newly created neurons survive -- or both. Some of the team's evidence indicates that the drug helps immature stems evolve into useful cells such as neurons and astrocytes, and to travel to the exact areas of the brain where they're needed.

In addition to sorting out those questions, investigators will try to identify the molecular pathway that prompts the brain to create more neurons in response to anti-depressants. The team suspects that a molecule known as BDNF or brain-derived neurotrophic factor may play a role.

Huang notes that one of his mentors, co-author Douglas H. Smith, M.D., of the University of Pennsylvania, has found that a brain injury itself also seems to prompt the brain to create more brain cells, perhaps as a way to compensate for injury.

"The brain has an intrinsic mechanism to repair itself to a certain extent," said Huang. "Our goal is to learn more about that mechanism and improve it, to help patients recover even more brain function than they can now, even with extensive work and rehabilitation."

Some of Huang's work is based on his experiences treating soldiers and civilians while working for four months as a neurosurgeon with the U.S. Army Reserve in Iraq, as well as more than a decade of experience treating patients affected by incidents like motor vehicle accidents.

He said that traumatic brain injury -- an injury experienced by approximately 1.4 million Americans each year -- must be treated aggressively. Often this involves surgery to relieve pressure on the brain, other procedures to protect the brain against immediate further injury, and then rehabilitation for months or years.

"It's exciting that the study involves a drug that is already safe and approved by FDA and is used clinically. If we could add a medication to the treatment regimen -- even a slight improvement would be a big gain for these patients. It's our hope that the work will ultimately make a difference in patient care," added Huang, who is also a scientist in the Center for Neural Development and Disease.

In addition to Huang, other authors at Rochester include post-doctoral associates Xiaodi Han, M.D., Ph.D., Jing Tong, M.D., and Jiankai Yang, M.D.; neurosurgery resident Arash Farahvar, M.D.,; and undergraduate Ernest Wang. Other authors include Jun Zhang, M.D., of the Chinese PLA General Hospital in Beijing; Uzma Samadani, M.D., Ph.D., of New York University; and Douglas H. Smith, M.D., of the University of Pennsylvania.

The work was funded by the National Institute of Neurological Disorders and Stroke and by the University of Rochester.

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Toward new medications for chronic brain diseases

ScienceDaily (Apr. 22, 2011) — A needle-in-the-haystack search through nearly 390,000 chemical compounds had led scientists to a substance that can sneak through the protective barrier surrounding the brain with effects promising for new drugs for Parkinson's and Huntington's disease. They report on the substance, which blocks formation of cholesterol in the brain, in the journal, ACS Chemical Biology.

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Aleksey G. Kazantsev and colleagues previously discovered that blocking cholesterol formation in the brain could protect against some of the damage caused by chronic brain disorders like Parkinson's disease. Several other studies have suggested that too much cholesterol may kill brain cells in similar neurodegenerative diseases. So they launched a search for a so-called "small molecules" -- substances ideal for developing into medicines -- capable of blocking formation of cholesterol.

They describe discovery of a small molecule that blocks the activity of a key protein involved in cholesterol production. It successfully lowered cholesterol levels in isolated nerve cells and brain slices from mice. If the molecule proves to be a good target for developing new drugs, the scientists note, "it could have a broader application in other neurological conditions, such as Alzheimer's disease, for which modulation of cholesterol and other associated metabolic pathways might be of therapeutic benefit."

The authors acknowledge funding from the Carmen Foundation, the RJG Foundation, the Michael J. Fox Foundation for Parkinson's Research, the CHDI Foundation, the Ecole Polytechnique Federale de Lausanne, and the Swiss National Science Foundation.

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Protein and calories can help lessen effects of severe traumatic brain injury, report says

ScienceDaily (Apr. 21, 2011) — To help alleviate the effects of severe traumatic brain injury (TBI), the U.S. Department of Defense should ensure that all military personnel with this type of injury receive adequate protein and calories immediately after the trauma and through the first two weeks of treatment, says a new report from the Institute of Medicine. Evidence from several studies of severely brain-injured patients shows that providing energy and protein to patients early reduces inflammation and improves their outcomes, said the committee of experts who wrote the report.

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This is the only nutrition-related approach to treating TBI that the committee recommended DOD implement at this time based on its review of the possible benefits of nutrients, dietary supplements, and specific diets to improve outcomes for TBI ranging from mild to severe. Several other nutritional approaches show potential for reducing the symptoms of brain injury, but there is not yet enough evidence about their effectiveness to recommend their adoption.

The committee identified the B vitamin choline, the amino acid-like compound creatine, n-3 fatty acids commonly known as EPA and DHA, and zinc as the most promising areas of investigation and recommended that DOD scientists and other researchers give them priority attention. These approaches are ones for which human clinical trials have been undertaken or are ongoing.

Other approaches, including antioxidants, flavonoids, ketogenic diets, and vitamin D, have less supporting evidence that has come solely from animal studies or from studies in people with different conditions. Although researchers must prioritize resources, DOD should continue to monitor the clinical literature for any new findings about the potential of these nutrients and diets in lessening brain injury effects, the report says.

The research priorities outlined in the report could generate information that provides health professionals with a fuller picture of which nutrients and dietary approaches work safely and most effectively. This information could also lead to new evidence-based clinical guidelines. There are few well-supported guidelines to inform health professionals' use of foods and dietary supplements to treat brain-injured patients, so clinicians employ a wide range of practices.

The IOM study focused on the potential role of nutrition in protecting against or treating the immediate and near-term effects of TBI. It did not evaluate the role of nutritional therapies in the rehabilitation phase or address long-term health effects associated with brain trauma, such as post-traumatic stress disorder, Alzheimer's disease, pain, and depression. A review of nutrition approaches to lessen long-term effects of TBI would be useful, the committee noted.

TBI is a significant cause of death and disability among personnel serving in the wars in Iraq and Afghanistan. It also contributes to nearly one-third of all injury-related deaths in the United States, making it a major health concern for the civilian population as well. According to recent estimates, between 1.6 million and 3.8 million sports-related TBIs occur annually, including those not treated by a health care provider.

The study was sponsored by the U.S. Army Medical Research and Materiel Command of the U.S. Department of Defense. Established in 1970 under the charter of the National Academy of Sciences, the Institute of Medicine provides independent, objective, evidence-based advice to policymakers, health professionals, the private sector, and the public. The National Academy of Sciences, National Academy of Engineering, Institute of Medicine, and National Research Council make up the National Academies.

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Neurorobotics reveals brain mechanisms of self-consciousness

ScienceDaily (Apr. 27, 2011) — A new study uses creative engineering to unravel brain mechanisms associated with one of the most fundamental subjective human feelings: self-consciousness. The research, published in the April 28 issue of the journal Neuron, identifies a brain region called the temporo-parietal junction (TPJ) as being critical for the feeling of being an entity localized at a particular position in space and for perceiving the world from this position and perspective.

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Recent theories of self-consciousness highlight the importance of integrating many different sensory and motor signals, but it is not clear how this type of integration induces subjective states such as self-location ("Where am I in space?") and the first-person perspective ("From where do I perceive the world?"). Studies of neurological patients reporting out-of-body experiences have provided some evidence that brain damage interfering with the integration of multisensory body information may lead to pathological changes of the first-person perspective and self-location. However, it is still not known how to examine brain mechanisms associated with self-consciousness.

"Recent behavioral and physiological work, using video-projection and various visuo-tactile conflicts showed that self-location can be manipulated in healthy participants," explains senior study author, Dr. Olaf Blanke, from the Ecole Polytechnique Fédérale de Lausanne in Switzerland. "However, so far these experimental findings and techniques do not allow for the induction of changes in the first-person perspective and have not been integrated with neuroimaging, probably because the experimental set-ups require participants to sit, stand, or move. This makes it very difficult to apply and film the visuo-tactile conflicts on the participant's body during standard brain imaging techniques."

Making use of inventive neuroimaging-compatible robotic technology that was developed by Dr. Gassert's group at the Swiss Federal Institute of Technology in Zurich, Dr. Blanke and colleagues studied healthy subjects and employed specific bodily conflicts that induced changes in self-location and first-person perspective while simultaneously monitoring brain activity with functional magnetic resonance imaging. They observed that TPJ activity reflected experimental changes in self-location and first-person perspective. The researchers also completed a large study of neurological patients with out-of-body experiences and found that brain damage was localized to the TPJ.

"Our results illustrate the power of merging technologies from engineering with those of neuroimaging and cognitive science for the understanding of the nature of one of the greatest mysteries of the human mind: self-consciousness and its neural mechanisms," concludes Dr. Blanke. "Our findings on experimentally and pathologically induced altered states of self-consciousness present a powerful new research technology and reveal that TPJ activity reflects one of the most fundamental subjective feelings of humans: the feeling that 'I' am an entity that is localized at a position in space and that 'I' perceive the world from here."

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