Researchers evaluate red wine compound for treating concussions in pro boxers

ScienceDaily (May 27, 2011) — UT Southwestern Medical Center researchers are engaging the help of professional boxers and trainers to study whether a component in red wine and grapes could help reduce the short- and long-term effects of concussions.

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Researchers plan to recruit about two dozen professional boxers to take the neuroprotective compound resveratrol after a fight to see if it reduces damage to the brain after impact and helps restore subtle brain functions and connections via its antioxidant effects. If successful, researchers hope the results may be applicable not only to concussions in other sports such as football and hockey, but also to everyday incidents such as falls, auto accidents and other blows to the head.

"We know from animal studies that if we give the drug immediately after or soon after a brain injury, it can dramatically and significantly reduce the damage you see long term," said Dr. Joshua Gatson, assistant professor of surgery in Burn/Trauma/Critical Care and principal investigator for the study. "There haven't been any completed human studies yet, so this is really the first look at resveratrol's effect on traumatic brain injury."

Resveratrol is already being studied as an agent to lower blood sugar levels, for use against cancer, to protect cardiovascular health, and in stroke and Alzheimer's disease treatments.

"Even though resveratrol is found in red wine, you would need 50 glasses of wine to get the required dose to get the protection you would need," said Dr. Gatson.

He came up with the idea for the trial, called the REPAIR study, while watching ESPN. Being a sports fan, he saw frequent concussion issues in football.

"The only treatment available is rest and light exercise, but there is no drug therapy to protect the brain from consecutive concussions, which are actually a lot worse than the initial one," said Dr. Gatson, who investigates biomarkers and novel therapies for traumatic brain injury. "There's been a lot of work with resveratrol showing that it also protects the brain, so we thought this might be the ideal drug."

In this study, researchers are administering the required oral dose once a day for seven days. Pro boxers will take a supplement form of resveratrol within two hours of their match. Researchers will then use neurocognitive tests and novel MRI protocols to track subtle brain activity, inflammation, and restoration of cells and connections.

"The main goal of our research is to protect the brain after each episode so that we can decrease the cumulative effect of these sports concussions," Dr. Gatson said.

Because boxers can have several fights in a short period of time, the researchers decided to target pro boxers with the help of Joseph Mohmed, the study research coordinator, and a coach for USA Boxing, the governing body for all amateur boxing, including the Olympics. Mr. Mohmed also is a former facilities manager at UT Southwestern.

According to the American Association of Neurological Surgeons, 2009 figures showed that 446,788 sports-related head injuries were treated at U.S. hospital emergency rooms, an increase of nearly 95,000 from the year before, in sports ranging from diving and cycling to baseball, basketball, soccer and football. The annual incidence of football-related concussion in the U.S. is estimated at 300,000, with about 47,000 football-related head injuries treated in hospital emergency rooms. In addition, more than 85,000 people were treated for bicycle-related head injuries; about two-thirds of 600 bicycling deaths a year are attributed to traumatic brain injury.

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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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Blast-related injuries detected in the brains of US military personnel

ScienceDaily (June 2, 2011) — An advanced imaging technique has revealed that some U.S. military personnel with mild blast-related traumatic brain injuries have abnormalities in the brain that have not been seen with other types of imaging.

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The abnormalities were found in the brain's white matter, the wiring system that nerve cells in the brain use to communicate with each other.

The study is reported June 2 in The New England Journal of Medicine by scientists at Washington University School of Medicine in St. Louis and the Landstuhl Regional Medical Center in Landstuhl, Germany.

They evaluated 84 U.S. military personnel evacuated to Landstuhl from Iraq and Afghanistan after exposure to many types of explosive blasts. Abnormalities were found in 18 of 63 patients diagnosed with mild traumatic brain injury, but not among 21 injured in other ways.

Traumatic brain injuries are estimated to have affected as many as 320,000 military personnel in the wars in Iraq and Afghanistan. Most of these are classified as mild traumatic brain injuries, also known as concussions.

"We call these injuries 'mild', but in reality they sometimes can have serious consequences," says senior author David L. Brody, MD, PhD, assistant professor of neurology at Washington University School of Medicine in St. Louis.

In the new study, white matter abnormalities were detected using an advanced magnetic resonance imaging method called diffusion tensor imaging. Diffusion tensor imaging allows scientists to assess the movement of water in tissue. Changes in the patterns of water movement are often linked to injury or disease, but the significance of the abnormalities seen in the military service personnel is not yet fully understood.

Mild traumatic brain injury has been a controversial topic, and the new approach may provide an additional tool to help resolve some of the debate. Much of the controversy has revolved around whether symptoms following mild traumatic brain injuries are due to structural injury to the brain, disruptions in brain chemistry, psychological factors or a combination of these.

"There is still a lot more work to be done before we fully understand whether these abnormalities truly represent significant damage to the brain white matter," says lead author Christine L. Mac Donald, PhD, research instructor in neurology at Washington University. "And if so, how this damage affects attention, memory, emotional regulation, balance, coordination, sleep and other functions. Likewise, the relationship between mild traumatic brain injury and post-traumatic stress disorder is especially important. Our ongoing studies will hopefully start to answer some of these questions."

Researchers have used diffusion tensor imaging to study mild civilian brain injuries previously and did not see abnormalities in the areas highlighted by the new study. These regions included the orbitofrontal cortex, an area involved in emotional regulation and reward-based behaviors, and the cerebellum, an area linked to coordination, movement, organization and planning.

These regions were predicted to be especially vulnerable to blasts based on previously published computer simulations. The results suggest that there may be fundamental differences between blast-related traumatic brain injuries and the sorts of mild traumatic brain injuries sustained by civilians, such as those caused by car accidents, falls, blows to the head and sports injuries.

In addition, advanced imaging also showed abnormalities in parts of the brain known to be harmed in civilian trauma.

Military personnel in the study all had blast-related injuries plus other injuries such as falls, motor vehicle crashes or being struck by blunt objects. The exact contribution of blast effects versus other injuries could not be fully determined in the study.

Up to a year after injury, the white matter abnormalities were still detectible, though their appearance on the scans had changed over time.

The results come from a collaborative team that included Mac Donald, who lived at Landstuhl for five and a half months to work on the study; Col. Stephen F. Flaherty, MD (now retired); and Lt. Col. Raymond Fang, MD, of the military medical staff at Landstuhl Regional Medical Center. The Landstuhl Regional Medical Center has been the central triage point for the wars in Iraq and Afghanistan for many years and is the closest hospital with a reliable MRI scanner.

Brody emphasizes that mild traumatic brain injury is still a diagnosis based on a history of an injury to the head that causes loss of consciousness, memory loss, confusion or other disruption in the function of the brain.

"A negative MRI scan, even with these advanced methods, does not rule out mild traumatic brain injury," he says. "These MRI-based methods show great promise, but are not yet ready to be used in routine clinical practice."

Brody said he believes the approach used in the study may prove helpful in military and civilian contexts and in children and adults.

"Our hope is that these advanced MRI-based methods will one day help make more accurate diagnoses, assist with triage and allow treatment interventions to start early for people with traumatic brain injuries," he says.

Mac Donald CL, Johnson AM, Cooper D, Nelson EC, Werner NJ, Shimony JS, Snyder AZ, Raichle ME, Witherow JR, Fang R, Flaherty SF, Brody DL. Detection of blast-related traumatic brain injury in U.S. military personnel. The New England Journal of Medicine, June 2, 2011.

Funding from the Congressionally Directed Medical Research Program and the National Institutes of Health (NIH) supported this research.

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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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People who have had head injuries report more violent behavior

ScienceDaily (June 2, 2011) — Young people who have sustained a head injury during their lifetime are more likely to engage in violent behavior, according to an eight-year study from the University of Michigan School of Public Health.

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Further, the research found that young people who suffered a recent head injury (within a year of being questioned for the study) were even more likely to report violent behavior.

The report, which appears in the current issue of the journal Pediatrics, is one of the few studies to examine long-term effects of head injuries in a general population of young adults. Most other similar studies were conducted in prison populations.

There's been a recent blitz of media and research attention regarding youth, college and professional athletes who suffer head injuries and concussions while playing. This study is broader, but confirms previous findings about the connection between violence and head injuries, says lead author Sarah Stoddard, a research assistant professor at the School of Public Health.

"These are not necessarily sports-playing injuries," said Stoddard, who also is a research fellow at the U-M School of Nursing. "They could be from a car accident or from previous violent behavior, but it does support some of the sports research that's been going on with concussions."

Stoddard used data from the School of Public Health's Flint Adolescent Study, which looks at many issues regarding urban youth. Marc Zimmerman, professor of public health and chair of the U-M Department of Health Behavior and Health Education, is the principal investigator on that study.

The researchers followed a group of ninth-graders from four schools in Flint, Mich., into young adulthood. They conducted annual interviews over eight years. In years five and six, participants were asked if they had ever sustained a head injury. Those who said yes -- about 23 percent -- reported more violent behavior in year eight of the study.

Moreover, Stoddard and Zimmerman examined the proximal relationship between a head injury and violent behavior and found that an injury reported in year seven of the study predicted violent behavior in year eight.

"We found that the link between a head injury and later violence was stronger when a head injury was more recent, even after controlling for other factors including previous violent behavior," Stoddard said.

The results also suggest that adolescents and young adults who have suffered a head injury that did not interfere with their ability to participate in an hour-long interview may still experience significant adverse developmental or behavioral effects.

The researchers defined a head injury as having been knocked unconscious or sustaining a concussion or a fractured skull.

Traumatic brain injury is a serious public health issue, they say. An estimated 1.7 million people annually sustain a TBI, and that only includes people who get medical care, so the number is likely much higher. Roughly 75 percent of head injuries are mild and many do not receive medical attention, but any TBI disrupts the function of the brain. Long-term impact can include changes in cognition, language and emotion, including irritability, impulsiveness and violence.

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How does anesthesia disturb self-perception?

ScienceDaily (Jan. 24, 2011) — An Inserm research team in Toulouse, led by Dr Stein Silva (Inserm Unit 825 "Brain imaging and neurological handicaps"), working with the "Modelling tissue and nociceptive stress" Host Team (MATN IFR 150), were interested in studying the illusions described by many patients under regional anaesthetic. In their work, to be published in the journal Anesthesiology, the researchers demonstrated that anaesthetising an arm affects brain activity and rapidly impairs body perception.

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The ultimate aim of the work is to understand how neuronal circuits are reorganised at this exact moment in time and to take advantage of anaesthesia to reconfigure them correctly following trauma. This would allow anaesthetic techniques to be used in the future to treat pain described by amputated patients in what are known as "phantom limbs."

Neuroscience research in recent years has shown that the brain is a dynamic structure. Phenomena such as learning, memorising or recovery from stroke are made possible by the brain's plastic properties. Brain plasticity does not, however, always have a beneficial effect.

For example, some amputated patients suffering from chronic pain (known as phantom limb pain) feel as though their missing limb were "still there." Such "phantom limb" illusions are related to the appearance in the brain of incorrect representations of the missing body part.

Persons under regional anaesthetic describe these very same false images.

Based on these observations, Inserm's researchers wished to discover whether anaesthesia could, in addition to fulfilling its primary function, induce comparable phenomena in the brain. If this were so, anaesthetics could be used as new therapeutic tools capable of modulating brain activity.

With this in mind, a team headed by Dr Stein Silva monitored 20 patients who were to have one of their arms anaesthetised before surgery. The patients were shown 3D images of the hand, shot from different angles, and their ability to distinguish the right hand from the left was assessed. Results showed how anaesthesia affected the patients' ability to perceive their body correctly.

The researchers observed three phenomena based on these tests:

All the patients described false sensations in their arm (swelling, difference in size and shape, imagined posture). In general, patients under anaesthetic took longer to distinguish between a left and right hand and made far more mistakes than persons not under anaesthetic. The best results were obtained when the anaesthetised limb was visible.

In other words, anaesthetising the hand (peripheral deafferentation ) modifies brain activity and rapidly changes the way we perceive the outside world and our own body. The teams are now using functional brain imaging to characterise the regions concerned in the brain. They also hope that it will be possible to use anaesthesia for therapeutic purposes in the future by modulating post-lesional plasticity (chronic pain in amputated patients, improved recovery in those suffering from brain lesions).

Inserm researcher Stein Silva, an anaesthetist and the chief author of the study, believes that it will no doubt be necessary to develop new anaesthetic techniques to inhibit or directly stimulate the brain images associated with painful phenomena.

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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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Culprit found for increased stroke injury with diabetes

ScienceDaily (Jan. 24, 2011) — Strokes are a leading cause of mortality and adult disability. Those that involve intracerebral hemorrhage (bleeding in the brain) are especially deadly, and there are no effective treatments to control such bleeding. Moreover, diabetes and hyperglycemia (high blood glucose levels) are associated with increases in bleeding during hemorrhagic stroke and worse clinical outcomes.

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But Joslin Diabetes Center researchers now have identified one key player that contributes to this increased bleeding, a discovery that may pave the way toward treatments that minimize adverse stroke outcomes both for people with pre-existing diabetes and those with hyperglycemia identified at the time of stroke.

Studies in the lab of Joslin Investigator Edward Feener, Ph.D., pinpointed a new mechanism involving a protein called plasma kallikrein that interferes with the normal clotting process in the brain following blood vessel injury with diabetes. Their work is reported online in the journal Nature Medicine.

The scientists began by injecting a small amount of blood into the brains of rats with diabetes and of control animals without diabetes. The difference was dramatic -- the diabetic animals bled over a much greater area of the brain.

Work in the Feener lab had previously implicated plasma kallikrein in diabetic eye complications. When the experimenters pre-treated the diabetic animals with a molecule that inhibits the protein's effects, brain damage from the blood injections dropped to levels similar to that in the control animals. Conversely, when pure plasma kallikrein was injected into the brain, it produced little impact on the control animals but rapidly increased major bleeding in the animals with diabetes.

Further studies by the Joslin researchers showed that normalizing blood glucose levels in diabetic animals could block the effect from plasma kallikrein, and that rapidly inducing hyperglycemia in control animals mimicked the effects of diabetes on brain hemorrhage. This suggests that high blood sugar at the time of brain hemorrhage, rather than diabetes per se, is responsible for the increased bleeding.

"Given the prevalence of strokes and the damage they inflict, these findings are exciting because they suggest the possibility that rapid control of blood sugar levels may provide an opportunity to reduce intracerebral hemorrhage, which is a clinical situation that has very limited treatment options," says Dr. Feener, who is also an associate professor of medicine at Harvard Medical School. "This work could have broad implications since about half of patients with acute hemorrhagic stroke have hyperglycemia, whether or not they have pre-existing diabetes."

The work also raises the possibility of developing drugs that target plasma kallikrein and may provide protective measures in people with diabetes or others at high risk for stroke. Such drugs might also prove useful for patients suffering from the more common ischemic strokes, which usually begin as blocked vessels in the brain but can transform into hemorrhages.

Surprisingly, while plasma kallikrein has been studied for decades, the Joslin scientists found that the protein boosts brain bleeding through a previously unknown mechanism -- by blocking platelet activation near damaged blood vessels.

Joslin's Jia Liu and Ben-Bo Gao were co-lead authors on the Nature Medicine paper. Other contributors include Joslin's Allen Clermont, and Price Blair and Robert Flaumenhaft of Beth Israel Deaconess Medical Center, and Tamie Chilcote and Sukanto Sinha of ActiveSite Pharmaceuticals. Lead funding came from the National Institutes of Health and the American Heart Association.

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A psychopath lacks empathy just like a person with frontal head injury, study suggests

ScienceDaily (Jan. 25, 2011) — People diagnosed as psychopathic have difficulty showing empathy, just like patients who have suffered frontal head injury. This has been shown in a new study from the University of Haifa. "Our findings show that people who have psychopathic symptoms behave as though they are suffering frontal brain damage," said Dr. Simone Shamay-Tsoory, who conducted the study.

See Also:Mind & BrainBrain InjuryIntelligenceDisorders and SyndromesNeurosciencePsychologyBehaviorReferenceEmpathyAntisocial personality disorderEmotional detachmentBrain damage

Psychopathy is a personality disorder that finds expression in extreme anti-social behavior and intentional harm to others, including a lack of compassion and empathy. An existing explanation for such behavior suggests inability to comprehend the existence of emotions in others. However, the fact that many psychopaths act with sophistication and deceit with intention to harm others, indicates that they actually have a good grasp of the mental capacity of others -- and are even capable of using that knowledge in order to cause them harm.

Earlier research by Dr. Shamay-Tsoory has examined individuals with frontal head injury, i.e., damage to parts of the brain that are responsible for emotional functioning. She has shown that people suffering this type of brain damage have difficulty showing empathy. Having observed similar emotional deficiency in psychopathic behavior, she set out to see if there is in fact a similarity between the two cases.

The current study assessed 17 people who had been diagnosed by psychiatrists as psychopathic -- and not suffering from any known brain damage; and another 25 individuals suffering frontal lobe injury. Each of the participants underwent a computerized test examining cognitive ability to recognize feelings in another and the ability to demonstrate empathy for another's emotions. They were also tested to gage their capacity to understand another's thoughts. The results of these tests showed that both groups demonstrated a similar difficulty in showing empathy, while two control groups of individuals with no known mental disorders or brain damage and individuals with non-frontal brain damage both showed different results with positive empathy capabilities.

"Seeing as psychopathic behavior is similar to that of a person with brain damage, it could be that it could benefit from similar forms of treatment," Dr. Shamay-Tsoory noted.

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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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Retired NFL players misuse painkillers more than general population, study finds

ScienceDaily (Jan. 30, 2011) — Retired NFL players use painkillers at a much higher rate than the rest of us, according to new research conducted by investigators at Washington University School of Medicine in St. Louis.

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The researchers say the brutal collisions and bone-jarring injuries associated with football often cause long-term pain, which contributes to continued use and abuse of painkilling medications.

The study is published online in the journal Drug and Alcohol Dependence. It involved 644 former NFL players who retired from football between 1979 and 2006. Researchers asked them about their overall health, level of pain, history of injuries, concussions and use of prescription pain pills.

The study found that 7 percent of the former players were currently using painkilling opioid drugs. That's more than four times the rate of opioid use in the general population. Opioids are commonly prescribed for their analgesic, or pain-relieving, properties. Medications that fall within this class of drugs include morphine, Vicodin, codeine and oxycodone.

"We asked about medications they used during their playing careers and whether they used the drugs as prescribed or whether they had ever taken them in a different way or for different reasons," says principal investigator Linda B. Cottler, PhD, professor of epidemiology in psychiatry at Washington University. "More than half used opioids during their NFL careers, and 71 percent had misused the drugs. That is, they had used the medication for a different reason or in a different way than it was prescribed, or taken painkillers that were prescribed for someone else."

Those who misused the drugs during their playing days were more likely to continue misusing them after retiring from football. Some 15 percent of those who misused the drugs as active players still were misusing them in retirement. Only 5 percent of former players who took the drugs as prescribed misused them after they retired from the NFL.

Cottler, director of the Epidemiology and Prevention Research Group in the Department of Psychiatry, says it's not clear from the study whether retired players became dependent on the drugs. What is clear from the survey, she says, is that retired NFL players continue to live with a lot of pain.

"The rate of current, severe pain is staggering," she says. "Among the men who currently use prescription opioids -- whether misused or not -- 75 percent said they had severe pain, and about 70 percent reported moderate-to-severe physical impairment."

Pain was one of the main predictors of current misuse. Another was undiagnosed concussion. Retired NFL players in the study experienced an average of nine concussions each. Some 49 percent had been diagnosed with a concussion at some point during their playing careers, but 81 percent suspected they had concussions that were not diagnosed. Some players believed they may have had up to 200 concussions during their playing days.

"Many of these players explained that they didn't want to see a physician about their concussions at the time," says Simone M. Cummings, PhD, a senior scientist in psychiatry who conducted phone interviews with the former players. "These men said they knew if they reported a concussion, they might not be allowed to play. And if you get taken out of a game too many times, you can lose your spot and get cut from the team."

She says players with suspected-but-undiagnosed concussions reported they borrowed pills from teammates, friends or relatives to treat the pain themselves, thus misusing opioids in an attempt to remain in the NFL. Although 37 percent of the retired players reported that they had received opioids only from a doctor, the other 63 percent who took the drugs during their NFL careers admitted that on occasion they got the medication from someone other than a physician.

Retired players currently misusing opioid drugs also are more likely to be heavy drinkers, according to Cottler.

"So these men are at elevated risk for potential overdose," she says. "They reported more than 14 drinks a week, and many were consuming at least 20 drinks per week, or the equivalent of about a fifth of liquor."

The ESPN sports television network commissioned the study, which also was funded by the National Institute on Drug Abuse. The ESPN program "Outside the Lines" spoke informally to many retired players about their use of painkillers. One reported taking up to 1,000 Vicodin tablets per month. Another reported ingesting 100 pills per day and spending more than $1,000 per week on painkillers.

Former St. Louis Rams offensive lineman Kyle Turley said in a statement to ESPN that he knew of many players who took drugs to help them deal with the pain inflicted by the injuries they sustained in the NFL.

"I know guys that have bought thousands of pills," Turley said. "Tons of guys would take Vicodin before a game."

The researchers say offensive linemen had particularly high rates of use and misuse of opioids.

"The offensive linemen were twice as likely as other players to use or misuse prescription pain medicines during their NFL careers," Cottler says. "In addition, this group tends to be overweight and have cardiovascular problems, so they represent a group of former players whose health probably should be monitored closely."

In fact, Cottler says it would be a good idea to continue monitoring everyone who has played in the NFL. She says this study revealed that some 47 percent of retired players reported having three or more serious injuries during their NFL careers, and 61 percent said they had knee injuries. Over half, 55 percent, reported that an injury ended their careers.

"These are elite athletes who were in great physical condition when their playing careers began," she says. "At the start of their careers, 88 percent of these men said they were in excellent health. By the time they retired, that number had fallen to 18 percent, primarily due to injuries. And after retirement, their health continued to decline. Only 13 percent reported that they currently are in excellent health. They are dealing with a lot of injuries and subsequent pain from their playing days. That's why they continue to use and misuse pain medicines."

Cottler LB (WU), Abdallah AB (WU), Cummings SM (WU), Barr J (ESPN), Banks R (ESPN), Forchheimer R (ESPN). Injury, pain and prescription opioid use among former NFL football players, Drug and Alcohol Dependence, vol. 113(3), Jan. 28, 2011.

This work was commissioned and supported by a grant from ESPN, with additional funding from the National Institute on Drug Abuse of the National Institutes of Health.

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Snakes and spiders: Revealing the wiring that allows us to adapt to the unexpected

ScienceDaily (Jan. 31, 2011) — Wouldn't life be easy if everything happened as we anticipated? In reality, our brains are able to adapt to the unexpected using an inbuilt network that makes predictions about the world and monitors how those predictions turn out. An area at the front of the brain, called the orbitofrontal cortex, plays a central role and studies have shown that patients with damage to this area confuse memories with reality and continue to anticipate events that are no longer likely to happen.

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The brain's ability to react adaptively, becomes crucial for survival, when faced with potential dangers, such as snakes and spiders, so to what extent does the harmfulness of an anticipated outcome affect our brain's event monitoring system? Not at all, reveals a new study published in the February 2011 issue of Elsevier's Cortex: the processes are the same, regardless how scary the anticipated event.

The team of researchers, supervised by Prof. Armin Schnider of the University Hospitals of Geneva in Switzerland, recorded functional magnetic resonance images (fMRI) while healthy volunteers performed a task in which they repeatedly saw a pair of faces and had to predict on which face a target was about to appear. The target could be a simple black disk (neutral stimulus) or a spider (potentially harmful stimulus). The researchers found a strong activation of the brain's visual areas whenever the spider appeared. However, irrespective of whether the disk or the spider was the target, its unexpected absence activated a cerebral network including the orbitofrontal cortex.

The findings show that, while the potential harmfulness of an event strongly affects brain responses, it does not influence the way the brain reacts when the expected event does not occur. The study supports the notion that the orbitofrontal cortex is "at the centre of a specific cerebral network which functions as a generic outcome monitoring system," says Louis Nahum, the first author of the study. "This capacity is probably as old in evolution as the instinctive reaction to threatening stimuli; its failure deprives the brain of the ability to remain in phase with reality," notes Armin Schnider.

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The changing roles of two hemispheres in stroke recovery

ScienceDaily (Jan. 31, 2011) — Most people who survive a stroke recover some degree of their motor, sensory and cognitive functions over the following months and years. This recovery is commonly believed to reflect a reorganisation of the central nervous system that occurs after brain damage. Now a new study, published in the February 2011 issue of Elsevier's Cortex, sheds further light on the recovery process through its effect on language skills.

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For almost all right-handed people and for about 60% of left-handers, damage to the left side of the brain causes a condition known as aphasia, an acute or chronic impairment of language skills. The syndrome is strongly associated with damage to the left hemisphere of the brain; however, there is a long-standing controversy regarding the involvement of parts of the right hemisphere in language functions and their contribution to recovery from aphasia. The majority of experts stress the role of the dominant left side in language recovery, while others argue for a complementary (or compensatory) function of the right hemisphere.

Odelia Elkana, from the Hebrew University, Jerusalem, and colleagues investigated the systematic patterns of reorganisation in the brain's language functions, and their relation to linguistic performance, in patients recovering from childhood brain damage to the left hemisphere. They used functional MRI to detect patterns of brain activity while patients performed various linguistic tasks inside the scanner. The new study focused on a rare group of children whose brain damage had occurred after they had already developed language skills but while the brain was still developing, and therefore most able to reorganise its language functions.

According to the authors, the findings suggest that "recovery is a dynamic, ongoing process, may last for years after onset and is reflected in an increasing proficiency of inter-hemispheric coordination, rather than just in an increase of activation in one side or the other. Therefore, the role of each hemisphere in the recovery process is not only dependent on the stage of recovery (acute, sub-acute or chronic stage), but also within each of these stages it may continuously change over time."

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Rural underage binge drinkers put their health at risk, German study finds

ScienceDaily (Feb. 6, 2011) — Binge drinking is often considered to be a problem of towns and cities but new research published in BioMed Central's open access journal BMC Public Health shows that binge drinking in rural areas is more of a problem than previously thought.

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Dr Carolin Donath, from the Psychiatric University Clinic Erlangen, looked at the drinking patterns of over 44,000 15 and 16 year olds in Germany and found that more than 93% of the young people from the countryside and over 86% of those from urban areas had tried alcohol. Of the adolescents who had drunk alcohol in the last month, 78% from rural areas and 74% from cities admitted to binge drinking (5 or more drinks at one time).

Dr Carolin Donath says that, "Whilst there is awareness of the problems of binge drinking in towns and cities, this study demonstrates that both drinking and binge drinking are as much of a problem for rural teenagers."

Binge drinking in school children has social ramifications as well as increasing health risks. Not only does alcohol abuse affect school work, and hence job prospects, but being drunk increases the likelihood of accidents among traffic and of unsafe sexual behaviour. This pattern of drinking also causes long term damage to the brain resulting in permanent brain damage, including memory problems and cognitive defects, and increasing risk of heart disease and cancer.

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Hope for stroke victims

ScienceDaily (Feb. 8, 2011) — Much of the devastation of stroke and head trauma is due to damage caused the overproduction of a substance in the brain called glutamate. Preventing this damage has been impossible, until now, as many drugs don't cross the so-called blood-brain barrier, and those that do often don't work as intended. But a method originally devised at the Weizmann Institute of Science may, in the future, offer a way to avert such glutamate-induced harm.

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Prof. Vivian I. Teichberg of the Institute's Neurobiology Department first demonstrated a possible way around these problems in 2003. Glutamate -- a short-lived neurotransmitter -- is normally all but absent in brain fluids. After a stroke or injury, however, the glutamate levels in brain fluid become a flood that over-excites the cells in its path and kills them. Instead of attempting to get drugs into the brain, Teichberg had the idea that one might be able to transport glutamate from the brain to the blood using the tiny "pumps," or transporters, on the capillaries that work on differences in glutamate concentration between the two sides. Decreasing glutamate levels in blood would create a stronger impetus to pump the substance out of the brain. He thought that a naturally-occurring enzyme called glutamate-oxaloacetate transaminase (GOT, for short) could "scavenge" blood glutamate, significantly lowering its levels. By 2007, Teichberg and his colleagues had provided clear evidence of the very strong brain neuroprotection that oxolacetate (a chemical similar to GOT) afforded rats exposed to a head trauma.

Two new studies -- conducted by Francisco Campos and others from the lab of Prof. Jose Castillo in the University of Santiago de Compostela, Spain -- now provide a definitive demonstration of Teichberg's results. In the first, the scientists conclusively showed that oxoloacetate injected into rats with stroke-like brain injuries reduces glutamate levels both in the blood and in the affected brain region, while significantly lessening both cell death and the swelling that can accompany stroke. In the second, a team of neurologists in two different hospitals checked the levels of glutamate and GOT in several hundred stroke victims who were admitted to their hospitals. They found that the most significant predictor of the prognosis -- how well they would recover at three months and how much brain damage they would suffer -- was the levels of these two substances. High glutamate levels correlated with a poor outcome, high GOT levels with a better one.

The overall implication of these two papers is that administering GOT might improve a patient's chances of recovering, as well as speeding up the process. In addition to stroke and head trauma, a number of diseases are characterized by an accumulation of glutamate in the brain, including Alzheimer's disease, Parkinson, multiple sclerosis, epilepsy, glaucoma, certain brain tumors and amyotrophic lateral sclerosis, and there is hope that, in the future, treatments to scavenge glutamate could relieve the symptoms and improve the outcomes for a number of neurological problems. Yeda, the technology transfer arm of the Weizmann Institute, holds a patent for this method.

Prof. Vivian I. Teichberg's research is supported by the Nella and Leon Benoziyo Center for Neurosciences; the Carl and Micaela Einhorn-Dominic Brain Research Institute; and the Legacy Heritage Fund Program of the Israel Science Foundation. Prof. Teichberg is the incumbent of the Louis and Florence Katz-Cohen Professorial Chair of Neuropharmacology.

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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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Advanced macular degeneration is associated with an increased risk of bleeding stroke, study finds

ScienceDaily (Feb. 10, 2011) — Older people with late-stage, age-related macular degeneration (AMD) appear to be at increased risk of brain hemorrhage (bleeding stroke), but not stroke caused by brain infarction (blood clot), according to research presented at the American Stroke Association's International Stroke Conference 2011.

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"Other studies have found there are more strokes in older individuals with late AMD, but ours is the first to look at the specific types of strokes," said Renske G. Wieberdink, M.D., study researcher and epidemiologist at Erasmus Medical Center in Rotterdam, the Netherlands. "We found the association is with brain hemorrhage, but not brain infarction."

AMD is degeneration of the macula, which is the part of the retina responsible for the sharp, central vision needed to read or drive. Because the macula primarily is affected in AMD, central vision loss may occur. Age-related macular degeneration usually produces a slow, painless loss of vision. Early signs of vision loss from AMD include shadowy areas in your central vision or unusually fuzzy or distorted vision.

Because the number of brain hemorrhages observed in the study was small, the findings will need to be corroborated in a larger group, Wieberdink said.

"These findings should be considered preliminary," she said. "Patients and physicians must be very careful not to over-interpret them. We don't know why there are more brain hemorrhages in these patients or what the relationship with AMD might be. This does not mean that all patients with late-stage AMD will develop brain hemorrhage."

Beginning in 1990, the Rotterdam Study is a prospective, population-based cohort investigation into factors that determine the occurrence of cardiovascular, neurological, ophthalmological, endocrinological and psychiatric diseases in older people.

The researchers tallied stroke incidence among 6,207 participants 55 years and older. All of the participants were stroke-free at the study's outset. AMD was assessed during scheduled eye examinations, and participants with the condition were divided into five different stages of AMD, and whether their condition was wet AMD or dry AMD. Participants were tracked for an average of 13 years. Of the 726 persons who suffered a stroke in that time, 397 were brain infarctions, 59 were brain hemorrhages and the stroke type was not available for 270.

Late AMD (stage 4) was associated with a 56 percent increased risk of any type of stroke. Late AMD, both the dry and the wet form, was strongly associated with more than six times the risk of brain hemorrhage, but not with brain infarction. Early AMD (stages 1-3) did not increase the risk of any stroke. Associations were adjusted for possible confounders, such as diabetes, blood pressure, anti-hypertensive medications, smoking status, body mass index, alcohol use and C-reactive protein levels.

"We cannot yet say if there is a common causal pathway or mechanism of action yet -- this association needs to be further investigated," Wieberdink said. "But I don't think it is a causal relationship. It seems more likely that late AMD and brain hemorrhage both result from some as yet unknown common mechanism."

If the findings are replicated, it may be possible to develop some stratification of risk among such patients, Wieberdink said.

Co-authors are: Lintje Ho, M.D.; Kamran Ikram, M.D., Ph.D.; Peter Koudstaal, M.D., Ph.D.; Albert Hofman, M.D., Ph.D.; Hans Vingerling, M.D., Ph.D.; and Monique Breteler, M.D., Ph.D. Author disclosers and funding information are on the abstract.

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Ischemic stroke hospitalizations decline in middle-aged, elderly, increases in young

ScienceDaily (Feb. 9, 2011) — The number of acute ischemic stroke hospitalizations among middle-aged and older men and women fell between 1994 and 2007, but sharply increased among those under age 35 -- including teens and children -- according to research presented at the American Stroke Association's International Stroke Conference 2011.

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Analysts at the U.S. Centers for Disease Control and Prevention (CDC), reviewing hospitalization data by age and gender, identified declining rates of 51 percent in girls 0-4 years and 25 percent in men and 29 percent in women over 45.

However, the number of ischemic stroke hospitalizations increased 51 percent in males between ages 15 and 34 during the period studied. The rate increased 17 percent in females between 15 and 34.

Among children and teens, they found a 31 percent increase in boys between 5 to 14 years and a 36 percent increase among girls 5 to 14 years.

Among the younger middle-aged set, they found a 47 percent increase among men 35-44 and a 36 percent increase among women 35-44.

"I believe this is the first large study to report these findings, stratified by age and gender," said Xin Tong, M.P.H., a health statistician with the CDC's Division for Heart Disease and Stroke Prevention in Atlanta.

"We cannot link anything in particular to the trend in younger patients, but I believe the role of obesity and hypertension will prompt a big discussion. Unfortunately, right now we can't speculate on the causes."

The unit of analysis was hospitalization, so researchers couldn't draw any firm connections or determine what factors are driving the increase in ischemic stroke cases among the young. Ischemic stroke occurs when blood supply to the brain becomes obstructed, usually by a clot or narrowing of the arteries. The risk of long-term brain damage can be reduced significantly if patients receive the clot-busting tissue plasminogen activator (tPA) within three or four and a half hours after stroke onset.

Hospitals and physicians should be aware of the rising risk of stroke in young people, and the necessity to educate them about stroke symptoms, Tong said.

"Acute ischemic stroke is currently considered something that mostly happens to older people, but awareness of rising rates in the young is important or else tPA and other important stroke treatment may be unnecessarily delayed in younger patients," she said.

Tong said her group is pursuing additional investigation on this subject.

Co-authors are: Elena V. Kuklina, M.D., Ph.D.; Cathleen Gillespie, M.S.; and Mary G. George, M.D., M.S.P.H.

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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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How adult stem cell therapy reduces inflammatory damage

ScienceDaily (Feb. 14, 2011) — Medical researchers from The University of Texas Health Science Center at Houston (UTHealth) presented new research results at the American Heart Association International Stroke Conference that demonstrated how MultiStem®, a novel stem cell therapy being developed by Athersys, Inc. provided multiple benefits when administered in preclinical models of ischemic stroke. The study, conducted by leading researchers from the Department of Neurology at the UTHealth Medical School working in collaboration with scientists at Athersys, illustrated the potential benefits of MultiStem therapy for treating stroke. Researchers observed that intravenous administration of MultiStem one day after a stroke reduced inflammatory damage in the brain and resulted in a significant improvement in motor skills.

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"We are seeing a paradigm shift in the way some types of stem cells may enhance recovery from stroke," said Sean I. Savitz, M.D., principal investigator and associate professor of neurology at UTHealth. "The stem cells may actually exert some of their effects on other organs such as the spleen. The spleen seems to play an important role in some neurological disorders by contributing, for example, to ongoing inflammation and brain injury after stroke. We're finding these stem cells are working on dampening inflammation involving the spleen."

According to the American Heart Association, approximately 800,000 individuals suffer a stroke each year in the United States, and an estimated 2 million individuals suffer a stroke each year in the U.S., Japan, and major European countries combined. Approximately 85% of strokes are ischemic, meaning they are caused by a blockage of blood flow in the brain, which occurs as a result of a clot or "thrombus." Currently there is only one FDA-approved drug therapy for the treatment of ischemic stroke, the thrombolytic tPA, which helps to dissolve the flow-impeding blood clot. However, tPA must be administered within several hours from when the stroke has occurred in order to be effective. Due to its limited window, only about 5% of all patients who could potentially benefit from therapy with tPA actually receive treatment. Given the lack of effective therapies, many patients who suffer a stroke require extensive physical therapy or experience significant or permanent disability, and as a result, must receive long-term institutional care or be cared for by a family member. As a consequence of an aging population, recent forecasts from the American Heart Association project that the prevalence of stroke will increase by 25% in the next 20 years, and the total estimated annual cost for treating and caring for stroke survivors will skyrocket from $64 billion in 2010 to $140 billion in 2030, representing a substantial increase in cost to the national healthcare system.

In the rat model of stroke used in the study, animals that received treatment with MultiStem showed statistically significant improvement in motor skills relative to animals that received placebo, and also showed reduced cell death, reduction of inflammatory cytokines and an increase in anti-inflammatory cytokines. Interestingly, researchers found that animals treated with placebo showed a reduction in spleen size and an increase in inflammatory cytokines in the blood, whereas animals that were treated with MultiStem showed normal spleen size and increased levels of anti-inflammatory cytokines in the blood. The spleen is believed to play a significant role in promoting and sustaining the inflammation that can result in substantial long-term damage following brain injury.

"Ischemic stroke represents an enormous clinical, economic and social burden that is expected to increase dramatically in the years ahead as a result of an aging population, and the corresponding increase in the number of individuals that are susceptible to all forms of cardiovascular disease," said Gil Van Bokkelen, Chairman and Chief Executive Officer of Athersys. "MultiStem appears to have profound effects in multiple neurological injury models, by reducing inflammation, protecting at-risk brain tissue, and promoting tissue repair. If we can develop new, more effective therapies that meaningfully extend the treatment window for stroke victims, we can improve clinical care, reduce long-term health care costs, and improve the quality of life for millions of people."

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Reduced levels of an important neurotransmitter found in multiple sclerosis patients

ScienceDaily (Feb. 11, 2011) — Researchers at the University of Illinois at Chicago have shown for the first time that damage to a particular area of the brain and a consequent reduction in noradrenaline are associated with multiple sclerosis.

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The study is available online in the journal Brain.

The pathological processes in MS are not well understood, but an important contributor to its progression is the infiltration of white blood cells involved in immune defense through the blood-brain barrier.

Douglas Feinstein, research professor in anesthesiology at the UIC College of Medicine, and his colleagues previously showed that the neurotransmitter noradrenaline plays an important role as an immunosuppressant in the brain, preventing inflammation and stress to neurons. Noradrenaline is also known to help to preserve the integrity of the blood-brain barrier.

Because the major source of noradrenaline is neurons in an area of the brain called the locus coeruleus, the UIC researchers hypothesized that damage to the LC was responsible for lowered levels of noradrenaline in the brains of MS patients.

"There's a lot of evidence of damage to the LC in Alzheimer's and Parkinson's disease, but this is the first time that it has been demonstrated that there is stress involved to the neurons in the LC of MS patients, and that there is a reduction in brain noradrenaline levels," said Paul Polak, research specialist in the health sciences in anesthesiology and first author on the paper.

For the last 15 years, Feinstein and his colleagues have been studying the importance of noradrenaline to inflammatory processes in the brain.

"We have all the models for studying this problem, so in some ways it was a small step to look at this question in MS," said Polak.

The researchers found that LC damage and reduced levels of noradrenaline occur in a mouse model of MS and that similar changes could be found in the brains of MS patients.

The findings suggest that LC damage, accompanied by reduction in noradrenaline levels in the brain, may be a common feature of neurologic diseases, Polak said.

"There are a number of FDA-approved drugs that have been shown to raise levels of noradrenaline in the brain, and we believe that this type of therapeutic intervention could benefit patients with MS and other neurodegenerative diseases, and should be investigated," he said.

Sergey Kalinin, post-doctoral research associate in anesthesiology, also contributed to the study. This study was supported by grants from the Department of Veteran Affairs and Partners for Cures.

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Acute anemia linked to silent strokes in children

ScienceDaily (Feb. 12, 2011) — Silent strokes, which have no immediate symptoms but could cause long-term cognitive and learning deficits, occur in a significant number of severely anemic children, especially those with sickle cell disease, according to research presented at the American Stroke Association's International Stroke Conference 2011.

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One-quarter to one-third of children with sickle cell disease have evidence of silent strokes in their brains, according to Michael M. Dowling, M.D., Ph.D., lead author of the study and assistant professor of pediatrics and neurology at the University of Texas Southwestern Medical Center in Dallas.

"These are 5- to 10-year-old children who have brains that look like the brains of 80-year-olds," Dowling said. "These strokes are called 'silent' because they don't cause you to be weak on one side or have any obvious neurologic symptoms. But they can lead to poor academic performance and severe cognitive impairments."

Sickle cell disease is a blood disorder characterized by low levels of hemoglobin, the iron-containing component of red blood cells that carries oxygen. Low hemoglobin causes anemia. In sickle cell disease, the blood cells are misshapen (sickle-shaped) and may form clots or block blood vessels. About 10 percent of children with sickle cell disease suffer a stroke. Blood transfusions can reduce the high risk of repeat strokes.

Dowling and colleagues hypothesized that silent strokes occur during severe anemia and may be detectable by MRI. They used MRI on the brains of 52 hospitalized children 2- to 19-years-old at Children's Medical Center Dallas with hemoglobin concentrations dropping below 5.5 g/dL. They compared severely anemic children with sickle cell disease to a group of children without sickle cell disease who had hemoglobin levels below 5.5 g/dL.

They identified silent strokes in about 20 percent of the children with sickle cell disease who were experiencing acute anemia. They also saw evidence of silent strokes, though not as often, in severely anemic children who didn't have sickle cell disease.

The many reasons, besides sickle cell disease, why children could have anemia include trauma, surgery, iron deficiency or cancer such as leukemia.

"These are brain injuries that go unnoticed by doctors, unless the children have testing with a special MRI," he said. "We looked at every child who went to the hospital for a 30-month period and identified about 400 children that came in with hemoglobin below 5.5 g/dL. That represented about 12 percent of the admissions for sickle cell disease and about 1 percent of the total admissions to Children's Medical Center."

The findings suggest that children with or without sickle cell disease who have acute anemia could be suffering undetected brain damage. The researchers suggest that all children with severe anemia need careful examination for silent strokes.

Improved recognition and timely transfusion to increase blood hemoglobin levels could prevent permanent brain damage in children with silent strokes, according to the study.

Future studies should look at larger groups of children for longer periods to better understand the impact of acute anemia on children, Dowling said.

Co-authors are: Charles T. Quinn, M.D., M.S; Patricia Plumb, R.N., M.S.N.; Zora R. Rogers, M.D.; Nancy Rollins, M.D.; Korgun Koral, M.D.; Robert Barber, Ph.D. and George R Buchanan, M.D.

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Swedish discovery could lead to new stroke therapy

ScienceDaily (Feb. 18, 2011) — The opportunities to treat a stroke have long been limited to the hours after an attack. The loss of brain function caused by the stroke has previously been regarded as permanent. Brain researchers at Lund University have now discovered a substance that opens up the possibility of treatment up to two days after a stroke.

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The only acute treatment for a stroke currently available is thrombolysis. This uses drugs that dissolve the blood clot responsible for the stroke, but it only reaches around 10 per cent of stroke patients in time to prevent lasting damage. For other patients, there are no other effective drugs that reduce the loss of brain function following a stroke.

Researchers at the Laboratory for Experimental Brain Research in Lund, together with American researchers, have discovered a substance that reinforces the brain's self-healing functions after a stroke. It has long been known that people affected by a stroke can regain some lost function during the first six months. Professor Tadeusz Wieloch and his colleagues have found a way to activate a protein in the brain, the sigma-1 receptor, which plays an important role in the brain's recovery during the critical period after the injury.

The study, which is published in the scientific journal Brain, began with experiments on rats. The animals were subjected to a stroke and then placed in different environments -- an enriched cage with extra stimulation in the form of several levels of tubes, beams and ladders, and a normal cage.

"After performing a genetic analysis of the rats that stayed in the normal cage and those that were in an enriched cage, we found that many genes were activated by the enriched environment. One of these genes coded for the protein sigma-1 receptor. We then injected the rats with a specific substance that activated the sigma-1 receptor and found that the rats regained their function more quickly than the untreated animals," explains Professor Wieloch.

The idea is to recreate and reinforce the brain's natural response to an enriched environment. By injecting the activating substance, brain repair is stimulated. This result of Swedish basic research, which started over 15 years ago, has led to a clinical trial on stroke patients by a Japanese pharmaceutical company.

"We are very pleased that our research on stroke here in Lund has made it all the way from our experiments in the lab to an international clinical trial," says Professor Wieloch.

"This is an excellent example of how basic research can be translated into a healthcare setting and possibly lead to new and better therapies. It also exemplifies the fact that, within medical research, it is a long journey from experimental studies to results that benefit the patient," says Professor Wieloch.

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Value of therapeutic hypothermia after cardiac arrest confirmed by new research

ScienceDaily (Feb. 18, 2011) — Mayo Clinic researchers confirmed that patients who receive therapeutic hypothermia after resuscitation from cardiac arrest have favorable chances of surviving the event and recovering good functional status. In therapeutic hypothermia, a patient's body temperature is cooled to 33 degrees Celsius following resuscitation from cardiac arrest, in order to slow the brain's metabolism and protect the brain against the damage initiated by the lack of blood flow and oxygenation.

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This study was published in the December 2010 issue of Annals of Neurology.

"Therapeutic hypothermia is a neuroprotective strategy. Brain recovery is the main determinant of outcome for patients who survive cardiac resuscitation," says Alejandro Rabinstein, M.D., a Mayo Clinic neurologist. "For a number of years, we have collected information about what determines whether or not a patient is going to wake up after resuscitated cardiac arrest. However, most of this information comes from the time when patients were not treated with therapeutic hypothermia, which now has become the standard of care for many cases of cardiac arrest. We wanted to know whether hypothermia therapy changed what we knew before about how to estimate neurological prognosis in these patients."

In this study, Dr. Rabinstein and his team identified 192 patients, more than 100 of whom were treated with therapeutic hypothermia. Detailed neurologic exams were performed, including electroencephalograms, brain CT scans, and measurement of neuron-specific enolase (NSE). NSE is a substance detected in the blood that provides information about the extent of brain damage. "The results of the study mainly validated what we knew about prognosis following cardiac arrest from non-hypothermia cases. The findings on physical examination on the days following cardiac arrest remain most valuable in estimating the prognosis," says Dr. Rabinstein.

High NSE level in the blood was shown to reliably predict poor outcome after cardiac arrest in patients not treated with hypothermia. However, less is known about the value of this marker in patients who are cooled after the cardiac arrest. Although in this study the presence of elevated levels of NSE was statistically associated with worse outcomes in patients treated with hypothermia, Dr. Rabinstein concluded that the NSE level was not sufficiently reliable to estimate the prognosis in this group of patients because elevated levels were also seen in some patients who recovered well. Therefore, the NSE level should not be used in isolation to define prognosis in patients treated with hypothermia. "That was a remarkable finding of our study that deserves more attention," he says.

"It's important for people to know that among patients treated with therapeutic hypothermia following resuscitated cardiac arrest, up to two-thirds of them may go home with good function," says Dr. Rabinstein. "We are still examining how these patients recover in terms of higher intellectual faculties, but certainly these are results that were not even conceivable prior to the application of therapeutic hypothermia."

Other members of the Mayo team included Jennifer Fugate, D.O.; Eelco Wijdicks, M.D., Ph.D.; Jay Mandrekar, Ph.D.; Daniel Claassen, M.D.; Edward Manno, M.D.; Roger White, M.D.; and Malcolm Bell, M.D.

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Gene variant affects stroke prognosis in humans

ScienceDaily (Mar. 1, 2011) — A small difference in DNA sequence predicts the degree of disability after a stroke, according to a paper published online on February 28 in the Journal of Experimental Medicine. Stroke, the consequence of disturbed blood flow to the brain, can impair speech, movement and vision, but it is currently difficult for clinicians to predict the severity of these side effects or the long-term prognosis.

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Strokes result in the death of brain cells called neurons. Angeles Almeida and co-workers found that variations in a gene known to control cell death -- Tp53 -- influence stroke outcome.

Tp53 comes in two flavors in humans: R and P. The R variant triggers cell death more efficiently. In two distinct groups of stroke patients, those exclusively expressing the R variant suffered more severe disability several months after the stroke. Neurons expressing the R variant were more vulnerable to death caused by oxygen deprivation, a condition that mimics the brain environment during stroke.

Future work is needed to determine if this Tp53 variation can also predict prognosis of patients with other disorders characterized by neuronal death, such as Alzheimer's or Parkinson's disease.

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New U.S. national study finds boxing injuries on the rise; Youth head injury rates also concerning

ScienceDaily (Mar. 2, 2011) — The risk and nature of injury in the sport of boxing has generated a great deal of controversy in the medical community, especially in relation to youth boxing. A new study, conducted by researchers in the Center for Injury Research and Policy of The Research Institute at Nationwide Children's Hospital, examined boxing injuries among participants 6 years of age and older from 1990 to 2008.

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During the 19-year study period, an average of 8,700 boxing injuries were treated in United States emergency departments each year, and approximately 2,500 of those injuries were to children and adolescents 6 to 17 years of age. The number of boxing injuries each year increased 211 percent during the study, climbing from 5,361 injuries in 1990 to nearly 17,000 injuries in 2008.

According to the study, released online February 28, 2011 by the American Journal of Preventive Medicine, the most common injury diagnosis was a fracture (28 percent). The hand was the most frequently injured body region (33 percent), followed by the head and neck (23 percent). While the majority of injuries occurred at a sports or recreation facility (54 percent), one-third of the injuries (34 percent) occurred at home.

The most concerning discovery from the study was the similar proportion of concussions/closed head injuries (CHIs) among the age groups (9 percent among 12-17 year olds, 8 percent among 18-24 year olds and 9 percent among 25-34 year olds).

"We expected a smaller proportion of concussions/CHIs among younger boxers, since they generate a lower punch force," said Gary Smith, MD, DrPH, senior author of the study and director of the Center for Injury Research and Policy at Nationwide Children's Hospital. "The fact that young boxers are experiencing a similar proportion of concussions and CHI's as older boxers is extremely concerning given the potential risk of developing chronic traumatic encephalopathy (CTE) with repetitive brain trauma. These repetitive blows to the head may be placing boxers under 18 years of age at risk for neurological impairment and psychological problems due to CTE."

The findings from this study support the position of medical societies that oppose boxing, especially among youth.

"Although there is risk of injury with most sports, boxing is unique because participants are rewarded for intentionally striking their opponent in the face and head with the intent of harming or incapacitating them," said Dr. Smith, also a professor of Pediatrics at The Ohio State University College of Medicine. "The increasing number of boxing injuries, coupled with the potential long-term consequences of these injuries, suggests that increased injury prevention efforts are needed."

This is the first nationally representative study to examine boxing injuries treated in emergency departments. Data for this study were obtained from the National Electronic Injury Surveillance System (NEISS), which is operated by the U.S. Consumer Product Safety Commission. The NEISS dataset provides information on consumer product-related and sports and recreation-related injuries treated in hospital emergency departments across the country. Boxing participation data were obtained from the Superstudy of Sports Participation.

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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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