USA Football and Steelers' staff had a host of recommendations for increasing concussion safety for area youth football players at Saturday's coaches clinic at the UPMC Sports Complex in Pittsburgh. Know the signs and symptoms. Teach proper tackling technique. Limit full-contact padded practices. "The whole idea is to help our kids play the game of football the right way," Steelers president Art Rooney II said to nearly 100 youth coaches, according to the Pittsburgh-Post Gazette. The Centers for Disease Control and Prevention estimates there are 3.8 million sports and recreation-related concussion annually. Most injuries are sustained while bicycling, followed by organized contact sports such as football and ice hockey and playground mishaps. Last month, data were released on the forces incurred over the course of a full season by 7- and 8-year-old football players in northern Virginia. The magnitude of the hits were measured using accelerometers placed inside several helmets. Many were comparable to forces felt in a pillow fight, but some were on par with those sustained by high school or collegiate players. The higher magnitude forces typically occurred during practices, not games. Ed Passino, Northeast regional manager for USA Football urged coaches to limit full-contact practices. "One thing that we're teaching throughout the country is that you don't have to hit every day in practice," Passino said. "It's not 1950 anymore. Update the way you handle practice. "Maybe you only hit one day a week, you can still conduct form tackling without full-on collisions." The eight Ivy League presidents, two of whom are medical doctors, limited contact practices for their football teams last summer, allowing fewer than the NCAA. USA Football concussion safety information Source: Concussions at head of youth coaches camp -- Pittsburgh-Post Gazette -- May 20, 2012 Questions/comments? contact Jean Rickerson at jean@SportsConcussions.org 7 completed 18 scheduled

Alzheimer’s disease and Chronic Traumatic Encephalopathy (CTE) are both “neurodegenerative diseases.” That is, they are brain diseases that result in the progressive destruction of brain cells, eventually leading to cognitive, behavioral, and other impairments. Both diseases also lead to dementia. The distinction between Alzheimer’s and dementia is very often misunderstood, even by many doctors. “Dementia” is a clinical syndrome defined by memory and other cognitive impairments that are severe enough to cause difficulties in social and/or occupational functioning (i.e., reduced independence in functioning). Dementia is not an illness or a disease. Dementia is not a “mild” form of Alzheimer’s. Rather, it is analogous to “fever,” in that it tells you that you are sick, but doesn’t say what is causing the problem. Similarly, dementia means that there is something wrong with the brain’s functioning, but not what is causing it. Several illnesses and diseases can lead to dementia, including Alzheimer’s disease which accounts for approximately 75% of all cases of dementia. However, several other neurodegenerative diseases result in dementia, including CTE. Alzheimer’s and CTE are distinct diseases. Both Alzheimer’s and CTE can only be accurately diagnosed postmortem through a neuropathological examination of the brain. There have been several new scientific breakthroughs over the past few years that now allow doctors and scientists to be much more accurate in diagnosing Alzheimer’s during life. However, at this time, there is no method of diagnosing CTE during life, although our group at the Boston University Center for the Study of Traumatic Encephalopathy (CSTE) recently received a grant from the National Institutes of Health to begin developing these types of tests. One of the major differences between Alzheimer’s and CTE involves what causes each of the diseases. There is no known specific risk factor that leads to Alzheimer’s. For CTE, however, it is believed that repetitive brain trauma (including concussions and subconcussive blows to the head) is a necessary, but not sufficient risk factor. That is, everyone that has been found to have CTE in postmortem examination has had a history of repetitive brain trauma, including athletes (e.g., football and hockey players, boxers and wrestlers), as well as others, such as combat military personnel, developmentally disabled individuals who repeatedly bang their heads, and victims of domestic abuse. Boxers and football players (especially lineman) appear to be the most likely to get the disease because of the repetitive brain trauma exposure. But, it is important to note that not everyone with a history of repetitive brain trauma will develop CTE. Our center is currently conducting research into the other potential additive risk factors, such as genetics, age of initial brain trauma exposure, frequency and overall duration of exposure, etc. This research will hopefully lead us to understand why one person gets the disease and another person does not. This line of investigation, along with our new study to develop methods of diagnosing CTE during life, will eventually lead to effective treatments and prevention strategies. Robert A. Stern, Ph.D. is a Professor of Neurology and Neurosurgery; Co-Director, Center for the Study of Traumatic Encephalopathy; Director, Clinical Core, BU Alzheimer's Disease Center, Boston University School of Medicine.

Like emergency workers rushing to a disaster scene, cells called microglia speed to places where the brain has been injured, to contain the damage by ‘eating up’ any cellular debris and dead or dying neurons. Scientists at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, have now discovered exactly how microglia detect the site of injury, thanks to a relay of molecular signals. Their work, published May 24, 2012 in Developmental Cell, paves the way for new medical approaches to conditions where microglia’s ability to locate hazardous cells and material within the brain is compromised. “Considering that they help keep our brain healthy, we know surprisingly little about microglia,” says Francesca Peri, who led the work. “Now, for the first time, we’ve identified the mechanism that allows microglia to detect brain injury, and how that emergency call is transmitted from neuron to neuron.” When an emergency occurs, cries can alert bystanders, who will dial the emergency number. A call will go out over the radio, and ambulances, police or fire engines in the area will respond as needed. In the brain, Peri and colleagues found, injured neurons send out their own distress cry: they release a molecule called glutamate. Neighbouring neurons sense that glutamate and respond by taking up calcium. As glutamate spreads out from the injury site, this creates a wave of calcium swallowing. Along that wave, as neurons take up calcium they release a third molecule, called ATP. When the wave comes within reach, a microglia cell detects that ATP and takes it as a call to action, moving in that direction – essentially tracing the wave backwards until it reaches the injury. . Lost alert: when microglia (green) cannot detect ATP (bottom), they don’t move to the injury site as they usually would (top).Photo credit: EMBL/Peri Scientists knew already that microglia can detect ATP, but this molecule doesn’t last long outside of cells, so there were doubts about how ATP alone could be a signal that carried far enough to reach microglia located far from the site of injury. The trick, as Peri and colleagues discovered, is the long-lasting glutamate-driven calcium wave that can travel the length of the brain. Thanks to this wave, the ATP signal is not just emitted by the injured cells, but is repeatedly sent out by the neurons along the way, until it reaches microglia. Dirk Sieger and Christian Moritz in Peri’s lab took advantage of the fact that zebrafish have transparent heads, which allow scientists to peer down a microscope straight into the fish’s brain. They used a laser to injure a few of the fish’s brain cells, and watched fluorescently-labelled microglia move in on the injury. When they genetically engineered zebrafish to make neurons’ calcium levels traceable under the microscope, too, the scientists were able to confirm that when the calcium wave reached microglia, these cells immediately started moving toward the injury. Knowing all the steps in this process, and how they feed into each other, could help to design treatments to improve microglia’s detection ability, which go awry in conditions such as Alzheimer’s and Parkinson’s diseases. Source: Sieger, D, Moritz, C., Ziegenhals, T., Prykhozhij, S. & Peri, F. Long-range Ca2+ waves transmit brain damage signals to microglia.Developmental Cell, published online 24 May 2012. Questions/comments? contact Jean Rickerson at jean@SportsConcussions.org

MINNEAPOLIS – A new study suggests that head impacts experienced during contact sports such as football and hockey may worsen some college athletes’ ability to acquire new information. The research is published in the May 16, 2012, online issue of Neurology®, the medical journal of the American Academy of Neurology. The study involved college athletes at three Division I schools and compared 214 athletes in contact sports to 45 athletes in non-contact sports such as track, crew and Nordic skiing at the beginning and at the end of their seasons. The contact sport athletes wore special helmets that recorded the acceleration speed and other data at the time of any head impact. The contact sport athletes experienced an average of 469 head impacts during the season. Athletes were not included in the study if they were diagnosed with a concussion during the season. All of the athletes took tests of thinking and memory skills before and after the season. A total of 45 contact sport athletes and 55 non-contact sport athletes from one of the schools also took an additional set of tests of concentration, working memory and other skills. “The good news is that overall there were few differences in the test results between the athletes in contact sports and the athletes in non-contact sports,” said study author Thomas W. McAllister, MD, of The Geisel School of Medicine at Dartmouth in Lebanon, N.H. “But we did find that a higher percentage of the contact sport athletes had lower scores than would have been predicted after the season on a measure of new learning than the non-contact sport athletes.” A total of 22 percent of the contact sport athletes performed worse than expected on the test of new learning, compared to four percent of the non-contact sport athletes. McAllister noted that the study did not find differences in test results between the two groups of athletes at the beginning of the season, suggesting that the cumulative head impacts that contact athletes had incurred over many previous seasons did not result in reduced thinking and memory skills in the overall group. “These results are somewhat reassuring, given the recent heightened concern about the potential negative effects of these sports,” he said. “Nevertheless, the findings do suggest that repetitive head impacts may have a negative effect on some athletes.” McAllister said it’s possible that some people may be genetically more sensitive to head impacts. The study was supported by the National Institutes of Health and the National Operating Committee on Standards for Athletic Equipment. Source: American Academy of Neurology -- May 16, 2012 Questions/comments? contact Jean Rickerson at Jean@SportsConcussions.org Photo courtesy of JamieLWilliams (c)2006 CreativeCommons.com

NFL Hall of Famer "Iron Mike" Webster's life ended in 2002 when he suffered a heart attack at age 50. Four Super Bowl rings, nine Pro Bowls, and voted to the NFL's all-time team in 2000, the driven, ultra-competitive Steelers' center drifted into a life of drug use, homelessness, and enormous suffering after retiring in 1988. In 2005, his son Garrett told ESPN that the only way his father could get to sleep was to taser himself into unconsciousness. Former teammates and friends offered assistance over the years but it wasn't enough. After Webster's death, forensic neuropathologist Dr. Bennet Omalu was determined to find neurological reasons for his cognitive decline. Seventeen years in the NFL at a time when safety precautions and concussion awareness were both minimal had resulted in thousands of impacts to his head. Though his brain looked normal at autopsy, Omalu pressed on until he found the abnormalities that we now call Chronic Traumatic Encephalopathy, or CTE. CTE and Alzheimer's CTE and Alzheimer's are both “neurodegenerative diseases.” That is, they are brain diseases that result in the progressive destruction of brain cells, eventually leading to cognitive, behavioral, and other impairments. Both Alzheimer’s and CTE can only be accurately diagnosed postmortem through a neuropathological examination of the brain and their progression has remained elusive. But clues about how Alzheimer's spreads from neuron to neuron are now emerging. Whether the same process of progression applies to CTE is currently unclear. Photo: Alzheimer's infects from neuron to neuron The inexorable spread of Alzheimer’s disease through the brain leaves dead neurons and forgotten thoughts in its wake. Researchers at Linköping University in Sweden are the first to show how toxic proteins are transferred from neuron to neuron. Through experiments on stained neurons, the research team – under the leadership of Martin Hallbeck, associate professor of Pathology – has been able to depict the process of neurons being invaded by diseased proteins that are then passed on to nearby cells. “The spread of Alzheimer’s, which can be studied in the brains of diseased patients, always follows the same pattern. But until now how and why this happens has not been understood,” says Hallbeck, who along with his research group has now published their results in The Journal of Neuroscience. The illness starts in the entorhinal cortex – a part of the cerebral cortex, and then spreads to the hippocampus. Both of these areas are important for memory. Gradually, pathological changes take place in more and more areas of the brain, while the patient becomes even sicker. Two proteins have been identified in connection with Alzheimer’s: beta amyloid and tau. Normally tau is found in the axons – the outgrowths that connect between neurons – where it has a stabilising function, while beta amyloid seems to have a role in the synapses where the neurons transfer signal substances to each other. But in Alzheimer’s patients, something happens with these proteins; autopsies reveal abnormal accumulations of both. Why they become abnormal is still unknown, but what is known is that it’s not the large accumulations, or plaques, that damage the neurons. Instead, smaller groups of beta amyloid – called oligomeres – seem to be the toxic form that gradually destroy the neurons and shrink the brain. “We wanted to investigate whether these oligomeres can spread from neuron to neuron, something many researchers tried earlier but didn’t succeed,” Hallbeck says. The study was inaugurated with an experiment on neuron cultures, where researchers injected oligomeres stained with a phosphorescent red substance called TMR using a very thin needle. The next day the neighbouring, connected neurons were also red, which showed that the oligomeres had spread. To test whether a sick neuron can “infect” others, they conducted a round of experiments with mature human neurons stained green and mixed with others that were red after having taken up stained oligomeres. After a day, approximately half of the green cells had been in contact with a few of the red ones. After two more days, the axons had lost their shape and organelles in the cell nucleus had started to leak. “Gradually more and more of the green cells became sick. Those that hadn’t taken up the oligomeres, on the other hand, weren’t affected,” Hallbeck says. The study is a breakthrough in understanding Alzheimer’s and its progress. If a way of stopping the transfer can be found, it could lead to a more effective inhibitor against the disease. Article: Spreading of neurodegenerative pathology via neuron-to-neuron transmission of beta-amyloid by Sangeeta Nath, Lotta Agholme, Firoz Kurudenkandy, Björn Granseth, Jan Marcusson and Martin Hallbeck. The Journal of Neuroscience, 27 June 2012. Photo: Alzheimer's infects from neuron to neuron: Two nerve cells, each about 10 micrometers large, are visible as shadows in this picture. From the beginning only the right one (yellow arrow) contained the toxic, red stained, oligomeric beta-amyloid. When these sick cells make contacts with the healthy, green labeled cells (black arrow), toxic beta-amyloid will spread through the neuronal projections (white arrow). Subsequently, also the green cell will become sick. Credit: Martin Hallbeck Source: The above story is reprinted from materials provided by Linköping University. Questions/comments? contact Jean Rickerson at jean@SportsConcussions.org

It is not yet known why girls suffer concussions at a higher rate than boys. The most prevalent theories range from lesser neck and upper body strength, to better reporting among females, to hormonal differences. Researchers at Emory University in Atlanta are currently in the third phase of a clinical trial designed to determine if the hormone progesterone, normally associated with female reproductive processes, can protect damaged neurons. Administered within four hours of the injury and lasting for three days, results of the treatment have been positive so far. Although catastrophic injuries in sports are rare, the question regarding applicability of a related treatment for concussion remains open. Pilot study highlighted efficacy Every 15 seconds, someone in the United States sustains a significant traumatic brain injury. Approximately 2 million adults and children in the United States suffer from traumatic brain injuries each year - leading to 50,000 deaths and 80,000 new cases of long-term disability, according to the Centers for Disease Control and Prevention. Despite the enormity of the problem, scientists have failed to identify effective medications to improve outcomes following a traumatic brain injury. Emory researchers, however, concluded in an earlier pilot clinical trial that giving progesterone to trauma victims shortly following brain injury appears to be safe and may reduce the risk of death and long-term disability. Their previous three-year study, called ProTECT I (Progesterone for Traumatic brain injury--Experimental Clinical Treatment), enrolled 100 participants at Grady Memorial Hospital. It was designed to evaluate whether progesterone can be administered intravenously in a safe and reliable way. "We found evidence that progesterone is not only safe for use in patients suffering from traumatic brain injuries," says Wright. "We also found a 50 percent reduction in mortality in those patients treated with progesterone. Even though this was a small pilot study, we found signs that progesterone improved functional outcomes and reduced disability in patients with moderate brain injury. "By expanding our test sites to 17 major trauma centers across 15 states and enrolling more than 1,000 patients, we hope to confirm these preliminary findings and determine if progesterone benefits victims of acute traumatic brain injury," says Wright. Progesterone common in males and females Progesterone is naturally present in small but measurable amounts in the brains of males and females. Human brain tissue is loaded with progesterone receptors. Laboratory studies suggest that progesterone is critical for the normal development of neurons in the brain and exerts protective effects on damaged brain tissue. Donald G. Stein, PhD, Asa G. Candler Professor of Emergency Medicine, Emory School of Medicine, and director of Emory's Department of Emergency Medicine Brain Research Laboratory, pioneered discoveries regarding the effect of progesterone following traumatic brain injury - first discovering the neuro-protective properties of progesterone in the laboratory more than 25 years ago. "The results that we are now seeing, and hope to continue validating, are an incredible and gratifying reward for more than 25 years of concentrated research," says Stein. "My work first started when I began to notice evidence that women tended to respond to treatment and recover better than men after suffering from brain injury and stroke. Many people do not realize that it's not just a female hormone; both men and women produce progesterone directly in the brain, as well as other tissue. "Ultimately, we learned that progesterone basically does in brain injuries what it also does during fetal development - protect cells and tissue," says Stein. "To now witness the translation of this laboratory research into a treatment that may have life-saving benefits is breathtaking." Source: A Hormonal Remedy for Brain Injuries is Explored --The New York Times -- June 21, 2012 Atlanta To Serve as National Epicenter for Promising Phase III Brain Injury Treatment Trial - Emory University Photo courtesy of (c) 2008 Eddy Grady@creativecommons.com Questions/comments? contact Jean Rickerson at jean@SportsConcussions.org

CHICAGO, May 24, 2012 -- Riddell Sports and USA Football today announced a renewed commitment to educating athletes and parents about concussion awareness. Starting today every new Riddell football helmet shipped to retailers and customers will include a hangtag offering concussion education that includes information from the Centers for Disease Control and Prevention (CDC) Heads Up program. Riddell's concussion education hangtag is the first of its kind among sports helmet manufacturers. "We have a longstanding commitment to player protection and continue to look for new ways to educate athletes and parents. As the leading manufacturer of football helmets, Riddell has raised concussion awareness through on-helmet labels and informational hangtags for over a decade," said Dan Arment, President of Riddell. "The new hangtag contains valuable information from the CDC and is the latest example of how Riddell will address concussion awareness with athletes and parents." Approximately three million American children age 6-14 play organized tackle football, placing it among the country's most popular youth sports. Since May 2009, 35 states and the District of Columbia have passed legislation to strengthen concussion education across youth and high school sports. Riddell's new hangtag will be attached to each helmet through an ear hole. The tag is titled "Raise Your Concussion Awareness" and lists concussion signs and symptoms, including CDC guidelines on what to do if a concussion is suspected. "Riddell shares USA Football's commitment to player safety and concussion awareness," USA Football Executive Director Scott Hallenbeck said. "Every parent who has a child playing youth football should ask their league two questions: 'How are your coaches trained to teach my child?' and 'Are your coaches educated on the symptoms and management of concussion?' Helmet hangtags will make certain that Riddell customers have a baseline of knowledge in this area and are directed on where they can learn more online." Riddell is the official football helmet and protective equipment partner of USA Football, the sport's national governing body in the United States. USA Football has partnered with the CDC to advance concussion education since 2007, particularly in high school and youth football. About USA Football: USA Football, the sport's national governing body in the United States, hosts more than 100 football training events annually offering education for coaches, skill development for players and resources for youth football league commissioners. The independent non-profit is the official youth football development partner of the NFL, its players and each of the league's 32 teams. Indianapolis-based USA Football manages U.S. national teams within the sport for international competition and provides $1 million annually in equipment grants and subsidizes youth league volunteer background checks. Endowed by the NFL and NFL Players Association in 2002 through the NFL Youth Football Fund, USA Football is chaired by former NFL team executive Carl Peterson. About Riddell: Founded in 1929, Riddell is a premier designer and developer of protective sports equipment and a recognized leader in helmet technology and innovation. One of Easton-Bell Sports, Inc.'s most well-known brands and the Official Helmet of the NFL®, Riddell is the leading manufacturer of football helmets, shoulder pads and reconditioning services (cleaning, repairing, repainting and recertifying existing equipment). SOURCE: Riddell Questions/comments? Contact Jean Rickerson at jean@SportsConcussions.org

SportsConcussions.org Named One of Constant Contact’s 2011 All Stars SportsConcussions.org recognized for achieving exemplary marketing results SEQUIM, Wash. — April 4, 2012 – SportsConcussions.org, a non-profit concussion education organization, has received the 2011 All Star Award from Constant Contact®, Inc., the trusted marketing advisor to more than half a million small organizations worldwide. Each year, a select group of Constant Contact customers are honored with the All Star Award for their exemplary marketing results. SportsConcussions.org’s results ranked among the top 10% of Constant Contact’s customer base. “We’re pleased to be recognized by Constant Contact for achieving strong marketing results, said Jean Rickerson, CEO and Founder of SportsConcussions.org. “Constant Contact’s tools have helped us reach a large audience with the all-important message regarding sports-related concussions in a very efficient way. We look forward to increasing our communication efforts even more in the coming year, to help protect more athletes. We are very grateful to all of our customers who follow us on our website, on social media and through our weekly newsletter. Our goal is to provide them with ideas and resources so they can protect athletes in their local communities.” Constant Contact looked at the following criteria to select this year’s All Stars: · Frequency of campaigns, events, and surveys · Open, bounce, and click-through rates · Event registration rates · Survey completion rates · Use of social features · Use of mailing list sign-up tools “There is nothing we like more than to see our customers finding success. It’s the reason Constant Contact was founded, and it’s a thrill to see the fantastic results that our All Stars are achieving,” said Gail Goodman, CEO of Constant Contact. “This group is really leading the charge when it comes to delivering relevant, engaging content that drives real business results. We salute this year’s All Stars for their success, and are honored to have played a part in their achievements.” About SportsConcussions.orgSportsConcussions.org is a non-profit organization dedicated to raising awareness about sports-related concussions. According to the Centers for Disease Control and Prevention (CDC) up to 3.8 million people suffer from a recreation- or –sport related concussion each year. SportsConcussions.org is anchored by a website that is update daily, featuring news, ideas and resources for school districts, leagues, coaches, parents and athletes. The organization also holds community workshops and conferences, and establishes baseline testing programs. About Constant Contact, Inc. Constant Contact is revolutionizing the success formula for small organizations through affordable, easy-to-use Engagement MarketingTM tools that help create and grow customer relationships. More than half a million small businesses, nonprofits, and associations worldwide rely on Constant Contact to drive ongoing customer dialogs through email marketing, social media marketing, event marketing, and online surveys. All Constant Contact products come with unrivaled KnowHow, education, and free coaching with a personal touch, including award-winning customer support.

As the on-ice passion of the NHL playoff games intensifies so do the penalties, particularly for vicious hits to the head. Saturday's games resulted in three separate incidents that will highlight the league's commitment to cracking down on illegal hits that may, and often do, cause concussions. Brendan Shanahan, Senior Vice President, Player Safety and Operations held hearings on two of the three violations Sunday afternoon. The third is scheduled for Monday. The hits are reviewed on video and the suspensions are explained in great detail by Shanahan on the NHL network (see videos below). Shanahan suspended New York Rangers forward Carl Hagelin for an illegal hit that forced opponent Daniel Alfredsson's head into the glass. Alfredsson, the Senators captain, left the game for evaluation and his status for the rest of the playoffs is uncertain. On Monday the team announced he had suffered a concussion on the play. This is Hagelin's first major penalty. The Wall Street Journal reports that disciplinary action against Hagelin may increase if Alfredsson, who has a history of concussions, is unable to return to the series. A one-game suspension was also issued Sunday for Ottawa Senators defenseman Matt Carkner for continuing to pummel an "unwilling opponent," Rangers forward Brian Boyle, who was knocked to the ice after Carkner delivered two powerful blows to his head. Carkner continued to hit Boyle as he lay on the ice. Boyle did not return the punches. Carkner was classified as an "aggressor" under NHL rules and was assessed a minor penalty for instigating, a major penalty for fighting and a game misconduct. Blackhawks forward Andrew Shaw is scheduled for a hearing on Monday for a shoulder-to-head hit on Coyotes goalie Mike Smith that left him down on the ice writhing in pain. Shaw earned a charging major and game misconduct on the play. Smith remained in the game. Last Thursday, Vancouver Canucks forward Byron Bitz was suspended for two games for a vicious hit to the head on Los Angeles Kings forward Kyle Clifford the night before. Clifford's head was shoved into the glass causing him to miss at least one game. In addition to the suspension Bitz was assessed a major penalty for boarding and a game misconduct the night of the game. Carl Hagelin/ Daniel Alfredsson Matt Carkner/ Brian Boyle Byron Bitz/ Kyle Clifford Source: NHL Network Questions/comments? Contact Jean Rickerson at jean@SportsConcussions.org