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Brandon P. Lucke-Wold, Ryan C. Turner, Aric F. Logsdon, Linda Nguyen, Julian E. Bailes, John M. Lee, Matthew J. Robson, Bennet I. Omalu, Jason D. Huber and Charles L. Rosen

, Harvey L , Dixon CE , Sun D : ER stress and effects of DHA as an ER stress inhibitor . Transl Stroke Res 4 : 635 – 642 , 2013 4 Begum G , Yan HQ , Li L , Singh A , Dixon CE , Sun D : Docosahexaenoic acid reduces ER stress and abnormal protein accumulation and improves neuronal function following traumatic brain injury . J Neurosci 34 : 3743 – 3755 , 2014 5 Blaylock RL , Maroon J : Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis . Surg Neurol Int 2 : 107 , 2011 6

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Vin Shen Ban, Christopher J. Madden, Julian E. Bailes, H. Hunt Batjer and Russell R. Lonser

), including chronic traumatic encephalopathy (CTE). Specifically, high-profile cases of athletes or former athletes who were thought to have suffered or died as a consequence of the cumulative nature of the head impacts they sustained during their careers have been highlighted in the media. 6 , 7 , 13 , 25 The increased media exposure related to CTE has underscored important questions surrounding the pathogenesis, incidence and prevalence, and natural history of CTE, but it has also led to common misperceptions due to lack of scientifically substantiated data

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Bennet Omalu, Jennifer L. Hammers, Julian Bailes, Ronald L. Hamilton, M. Ilyas Kamboh, Garrett Webster and Robert P. Fitzsimmons

. Chronic traumatic encephalopathy is the cumulative outcome of repeated subconcussive and concussive brain injuries, and in this instance, it is our opinion that the decedent sustained repeated subconcussive and concussive brain injuries primarily from exposures from blasts and secondarily from training activities and noncombat activities as a marine. Other possible tertiary nonmilitary contributory factors to his cumulative risk of developing CTE may have included a remote traumatic history of nasal bone fracture and engagement in contact sports such as football and

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Matthew L. Dashnaw, Anthony L. Petraglia and Julian E. Bailes

cytokine release. 77 , 79 In normal reactions to a single mild TBI, over time microglia eventually enter a reparative phase composed of phagocytic activity to repair any debris and damaged cells, and ultimately return to their resting state. 8 With repeated brain injury, microglia may enter a constitutively activated state and become neurodestructive, which may translate into risk for chronic traumatic encephalopathy. 8 Sequelae of Repetitive Mild TBI In the past decade, there has been an increased interest in laboratory research focused on repetitive mild TBI

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James Pan, Ian D. Connolly, Sean Dangelmajer, James Kintzing, Allen L. Ho and Gerald Grant

-term neurological consequences and represents a spectrum of disorders. The most remarkable outcome of mTBI is termed chronic traumatic encephalopathy (CTE), a clinical syndrome that is associated with neurodegeneration and behavioral, cognitive, and/or motor deficits. Although this disease has distinct pathological features, CTE is considered a diagnosis of exclusion because only postmortem biopsies can confirm the diagnosis. Therefore, new diagnostic methods need to be developed to: 1) inform patients of a definitive diagnosis, 2) better understand the epidemiology and risk

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Julian E. Bailes, Anthony L. Petraglia, Bennet I. Omalu, Eric Nauman and Thomas Talavage

literature from 1900 to 2011 using various search engines, including MEDLINE, PubMed, Google Scholar, and the Cochrane Database. Initially, potential articles were identified using a combination of the following search terms: “subconcussion,” “subconcussive head injury,” “concussion,” “mild traumatic brain injury,” “TBI,” “animal models,” “repetitive traumatic brain injury,” “pathophysiology,” “chronic traumatic encephalopathy,” “neurodegeneration,” “head impacts,” “accelerometer,” “neuropsychology,” “neuroimaging,” “magnetic resonance imaging,” “functional magnetic

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Lonnie Schneider, Ethan Reichert, Jenna Faulkner, Brielle Reichert, Joshua Sonnen and Gregory W. J. Hawryluk

I t has long been known that victims of traumatic brain injury (TBI) are at increased risk of dementia. 13 , 34 The relatively recent description of chronic traumatic encephalopathy (CTE) 29 , 30 has dramatically increased medical, scientific, and societal attention to late neurodegenerative sequelae of central nervous system (CNS) trauma. 4 The mechanisms underlying the dementia that can follow CNS trauma are not well understood, however, impeding the development of targeted treatments. In considering possible etiologies for the dementias that follow CNS

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Jonathan G. Hobbs, Jacob S. Young and Julian E. Bailes

reticular activating system. 67 There is also a growing interest in the role of inflammation in the pathogenesis of disease following a concussion, particularly with regard to postconcussive disease, which spans a spectrum of diseases including postconcussion syndrome (PCS), prolonged PCS (PPCS), chronic traumatic encephalopathy (CTE), mild cognitive impairment, and dementia pugilistica. 11 , 116 Briefly, following an SRC, the traumatic event in the CNS recruits neutrophils and monocytes, which in combination with the microglia and astrocytes already residing in the

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Charles H. Tator, Hannah S. Davis, Paul A. Dufort, Maria Carmella Tartaglia, Karen D. Davis, Ahmed Ebraheem and Carmen Hiploylee

etiological features of PCS in a large retrospective cohort and to identify any predictors. We also aimed to determine whether there were any differences in predictors if the ICD-10 or DSM-IV definitions were used. Our long-term aims are to develop strategies to prevent and treat PCS and to determine whether PCS is an antecedent to chronic traumatic encephalopathy (CTE). Methods Study Design and Patients This study was a retrospective chart review approved by the Research Ethics Board of the University Health Network in Toronto, Canada. All consecutive patients

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Heather S. Spader, Douglas C. Dean III, W. Curt LaFrance Jr., Neha P. Raukar, G. Rees Cosgrove, Stephanie A. Eyerly-Webb, Anna Ellermeier, Stephen Correia, Sean C. L. Deoni and Jeffrey Rogg

T raumatic brain injury affects an estimated 1.7 million people in the United States annually, 8 with approximately 75% of these injuries categorized as mild. Football is responsible for one of the highest frequencies of mild traumatic brain injury (mTBI) in athletics; approximately 5% of high school and collegiate football players are diagnosed with an mTBI annually. 20 Approximately 20% of these athletes will have disabling symptoms beyond 3 months postinjury. 37 Repeated mTBIs have also been recently linked to chronic traumatic encephalopathy (CTE), a